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This study aimed to investigate the levels of serum, gingival crevicular fluid (GCF), and salivary adipokines and their possible relationship with periodontitis and obesity. An electronic search was conducted in the following databases: PubMed/ Medline, Scopus, and EBSCOhost through February 2023. Two independent reviewers screened the titles, abstracts, and full text of all the studies. Studies comparing the levels of adipokines in GCF, serum, and/or saliva in subjects with obesity and periodontitis (group 1), subjects with normal weight and periodontitis (group 2), and subjects with obesity and gingival health (group 3) were included. Meta‐analyses and meta‐regression were performed on the data from included studies. Seventeen studies with study participants ranging from 30 to 120 were included with subjects in each group ranging from 10 to 40. There was a significant increase in levels of serum TNF‐α, leptin, IL‐6, and CRP between groups 1 and 2 (p <.05). In GCF, TNF‐α and resistin levels were significantly higher (p <.05) in Group 1 vs. 2. Serum level of leptin was higher for group 1 vs. 3 (p <.05). Meta‐regression analysis revealed that the obesity definition (body mass index (BMI) cut‐off value >25 or >30) was significant for serum resistin (p <.05) and GCF resistin (p <.05) between group 1 and 2. The current analysis indicates that both periodontitis and obesity can modulate the pro‐inflammatory cytokines at systemic and local levels. This bidirectional interaction of periodontitis and obesity via the inflammation pathway seems likely plausible. Further studies are required to elucidate this mechanism in more detail. [ABSTRACT FROM AUTHOR]

Heart failure with preserved ejection fraction (HFpEF) is one of the major subtypes of heart failure (HF) and no effective treatments for this common disease exist to date. Cardiac fibrosis is central to the pathology of HF and a potential avenue for the treatment of HFpEF. To explore key fibrosis‐related genes and pathways in the pathophysiological process of HFpEF, a mouse model of HFpEF was constructed. The relevant gene expression profiles were downloaded from the Gene Expression Omnibus database, and single‐sample Gene Set Enrichment Analysis (ssGSEA) was performed targeting fibrosis‐related pathways to explore differentially expressed genes (DEGs) in healthy control and HFpEF heart tissues with cross‐tabulation analysis of fibrosis‐related genes. Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed on the identified fibrosis‐related genes. The two most significant DEGs were selected, and further validation was conducted in HFpEF mice. The results indicated that myocardial fibrosis was significantly upregulated in HFpEF mice compared to healthy controls, while the ssGSEA results revealed significant differences in the enrichment of nine fibrosis‐related pathways in HFpEF myocardial tissue, with 112 out of 798 DEGs being related to fibrosis. The in vivo results demonstrated that expression levels of resistin‐like molecule gamma (Relmg) and adenylate cyclase 1 (Adcy1) in the heart tissues of HFpEF mice were significantly higher and lower, respectively, compared to healthy controls. Taken together, these results suggest that Relmg and Acdy1 as well as the fibrosis process may be potential targets for HFpEF treatment. [ABSTRACT FROM AUTHOR]

Aims/Introduction: Gene–environment interactions are considered to critically influence type 2 diabetes mellitus development; however, the underlying mechanisms and specific interactions remain unclear. Given the increasing prevalence of low birthweight (LBW) influenced by the intrauterine environment, we sought to investigate genetic factors related to type 2 diabetes development in individuals with LBW. Materials and Methods: The interaction between 20 reported type 2 diabetes susceptibility genes and the development of type 2 diabetes in LBW (<2,500 g) individuals in a population‐based Japanese cohort (n = 1,021) was examined by logistic regression and stratified analyses. Results: Logistic regression analyses showed that only the G/G genotype at the rs1862513 locus of the resistin gene (RETN), an established initiator of insulin resistance, was closely related to the prevalence of type 2 diabetes in individuals with LBW. Age, sex and current body mass index‐adjusted stratified analyses showed a significant interaction effect of LBW and the RETN G/G genotype on fasting insulin, homeostatic model assessment 2‐insulin resistance, Matsuda index and the prevalence of type 2 diabetes (all P‐values for interaction <0.05). The adjusted odds ratio for type 2 diabetes in the LBW + G/G genotype group was 7.33 (95% confidence interval 2.43–22.11; P = 0.002) compared with the non‐LBW + non‐G/G genotype group. Similar results were obtained after excluding the influence of malnutrition due to World War II. Conclusions: Simultaneous assessment of LBW and the RETN G/G genotype can more accurately predict the risk of future type 2 diabetes than assessing each of these factors alone, and provide management strategies, including early lifestyle intervention in LBW population. [ABSTRACT FROM AUTHOR]

Resistin is a protein involved in inflammation and angiogenesis processes and may play a role in the progression of colorectal cancer (CRC). However, it remains unclear whether resistin is associated with increased mortality after CRC diagnosis. We examined pre‐diagnostic serum resistin concentrations in relation to CRC‐specific and all‐cause mortality among 1343 incident CRC cases from the European Prospective Investigation into Cancer and Nutrition cohort. For CRC‐specific mortality as the primary outcome, hazard ratios (HRs) and 95% confidence intervals (95% CI) were estimated from competing risk analyses based on cause‐specific Cox proportional hazards models and further in sensitivity analyses using Fine–Gray proportional subdistribution hazards models. For all‐cause mortality as the secondary outcome, Cox proportional hazards models were used. Subgroup analyses were performed by sex, tumor subsite, tumor stage, body mass index and time to CRC diagnosis. Resistin was measured on a median of 4.8 years before CRC diagnosis. During a median follow‐up of 8.2 years, 474 deaths from CRC and 147 deaths from other causes were observed. Resistin concentrations were not associated with CRC‐specific mortality (HRQ4vsQ1 = 0.95, 95% CI: 0.73–1.23; Ptrend =.97; and HRper doubling of resistin concentration = 1.00; 95% CI: 0.84–1.19; P =.98) or all‐cause mortality. Results from competing risk (sensitivity) analysis were similar. No associations were found in any subgroup analyses. These findings suggest no association between pre‐diagnostic circulating resistin concentrations and CRC‐specific or all‐cause mortality among persons with CRC, and the potential insignificance of resistin in CRC progression. [ABSTRACT FROM AUTHOR]

Summary: Obesity is reported to increase stroke risk, with adipocyte‐derived cytokines or adipokines implicated as mediators. However, the relationship between adipokines and stroke is not well clarified. Thus, we aimed to evaluate the association of adipokines with stroke using fully adjusted risk estimates that incorporated body mass index in a meta‐analysis. Data from 52 studies (62,428 patients) were pooled in a random‐effects meta‐analysis. Adiponectin was independently associated with a lower risk of pre‐existing stroke (adjusted odds ratio: 0.64 [95% confidence interval: 0.46–0.88], p < 0.01), whereas leptin (1.08 [1.00–1.17], p = 0.04), resistin (1.06 [1.04–1.08], p < 0.01) and visfatin (1.04 [1.01–1.07], p = 0.01) are associated with a higher risk of stroke, but none with incident stroke. Adipokines independently associated with an ischaemic stroke subtype were adiponectin (0.48 [0.30–0.77], p < 0.01), leptin (1.10 [1.01–1.20], p = 0.04), and resistin (1.06 [1.04–1.08], p < 0.01). Fatty acid‐binding protein‐4 (FABP‐4) independently predicted 6‐month poor functional outcomes in stroke patients (adjusted hazard ratio: 1.09 [1.06–1.12], p < 0.01); whereas both FABP‐4 (1.17 [1.03–1.34], p = 0.01) and visfatin (1.24 [1.00–1.55], p = 0.05) were predictive of 6‐month mortality. Adipokines are associated with a greater risk of pre‐existing stroke, but not with the relationship with incident stroke. Adipokines, such as FABP‐4 and visfatin, may serve as biomarkers of stroke severity and worsening of stroke outcomes. [ABSTRACT FROM AUTHOR]

Cancer‐related fatigue is a frequent, burdensome and often insufficiently treated symptom. A more targeted treatment of fatigue is urgently needed. Therefore, we examined biomarkers and clinical factors to identify fatigue subtypes with potentially different pathophysiologies. The study population comprised disease‐free breast cancer survivors of a German population‐based case‐control study who were re‐assessed on average 6 (FU1, n = 1871) and 11 years (FU2, n = 1295) after diagnosis. At FU1 and FU2, we assessed fatigue with the 20‐item multidimensional Fatigue Assessment Questionnaire and further factors by structured telephone‐interviews. Serum samples collected at FU1 were analyzed for IL‐1ß, IL‐2, IL‐4, IL‐6, IL‐10, TNF‐a, GM‐CSF, IL‐5, VEGF‐A, SAA, CRP, VCAM‐1, ICAM‐1, leptin, adiponectin and resistin. Exploratory cluster analyses among survivors with fatigue at FU1 and no history of depression yielded three clusters (CL1, CL2 and CL3). CL1 (n = 195) on average had high levels of TNF‐α, IL1‐β, IL‐6, resistin, VEGF‐A and GM‐CSF, and showed high BMI and pain levels. Fatigue in CL1 manifested rather in physical dimensions. Contrarily, CL2 (n = 78) was characterized by high leptin level and had highest cognitive fatigue. CL3 (n = 318) did not show any prominent characteristics. Fatigued survivors with a history of depression (n = 214) had significantly higher physical, emotional and cognitive fatigue and showed significantly less amelioration of fatigue from FU1 to FU2 than survivors without depression. In conclusion, from the broad phenotype "cancer‐related fatigue" we were able to delineate subgroups characterized by biomarkers or history of depression. Future investigations may take these subtypes into account, ultimately enabling a better targeted therapy of fatigue. [ABSTRACT FROM AUTHOR]

Summary: Midlife obesity and late‐life weight loss confer a greater risk for developing dementia and Alzheimer's disease (AD), but the exact mechanisms behind this phenomenon are currently unknown. The answer could lie on the involvement of gastrointestinal factors, such as adipokines (e.g., leptin, adiponectin, and resistin) and ghrelin. In this context, we conducted a pre‐registered systematic review and meta‐analysis of 42 cross‐sectional and 13 longitudinal studies targeting the associations between leptin, adiponectin, resistin, and ghrelin and the prevalence of general dementia, AD, and mild cognitive impairment (MCI). We also examined the relationship between the four gastrointestinal factors and neurocognitive outcomes and AD‐related cerebrospinal fluid biomarkers. Patients with AD had lower blood leptin and higher resistin levels than cognitively normal participants. Lower leptin and higher resistin were associated with higher degree of cognitive impairment. Additionally, lower late‐life leptin levels might be associated with higher prospective risk of dementia and AD, although more studies are needed to corroborate this. Results in ghrelin and adiponectin were not conclusive, with age, sex distribution, obesity, and severity of dementia seemingly acting as moderators across several analyses. Our work might contribute to the identification of new preclinical blood markers of MCI and AD. [ABSTRACT FROM AUTHOR]

Background: A role for resistin in the pathogenesis of polycystic ovarian syndrome (PCOS) and related features were described for various ethnicities. As its expression is partly inherited, a role for RETN polymorphisms in regulating resistin levels and PCOS risk was shown, but with varied results. Aim: To investigate the association of rs34124816 (–537A>C), rs1862513 (–420C>G), rs3219175 (–358G>A), rs3745367 (+299G>A), rs3745369 (+1263G>C), and rs1423096 (+4965C>T) RETN SNPs with PCOS. Methods: Study subjects included 583 women with PCOS, and 713 eumenorrheic women serving as controls. Genotyping was done by real‐time PCR. Results: Higher minor allele frequency (MAF) of rs34124816, rs3219175, and rs3745369, and lower MAF of rs1862513 and rs1423096 were seen in PCOS cases. Reduced PCOS risk was found with rs3745367 minor‐allele homozygotes and rs1423096 minor‐allele homozygotes, while increased risk was linked with rs3745367 heterozygotes, and with rs3745369 heterozygotes and minor‐allele homozygotes. While it did not reach statistical significance, serum resistin levels were elevated in PCOS cases than in control women and major‐allele homozygotes of rs34124816 and rs1862513, and in rs1423096 minor‐allele‐containing carriers. Carriage of rs34124816 correlated positively with age and LH, whereas rs1862513 positively and rs3745367 negatively correlated with fasting glucose. Six‐locus (rs34124816‐rs1862513‐rs3219175‐rs3745367‐rs3745369‐rs1423096) haplotype analysis demonstrated a significant reduction in AGGGGG and a marked increase in AGGGCG haplotypes between cases and controls, thus assigning PCOS protective and susceptible nature to these haplotypes, respectively. Conclusions: This study is the first to document the contribution of rs34124816 and rs1423096 RETN variants to the risk of PCOS. The varied association of RETN gene variants with PCOS suggests an ethnic contribution of RETN association with PCOS. [ABSTRACT FROM AUTHOR]

White adipose tissue (WAT) is not only an energy storage reservoir that is critical in energy homeostasis but is also a highly metabolically active endocrine organ. WAT can secrete a variety of adipocytokines, including leptin (LEP), adiponectin (APN), resistin, visfatin, tumor necrosis factor‐α (TNF‐α), interleukin‐6 (IL‐6), and osteopontin (OPN). It can also synthesize and secrete exosomes, which enhance intercellular communication and participate in various physiological processes in the body. It can also synthesize and secrete exosomes to enhance intercellular communication and participate in a variety of physiological processes in the body. The skeleton is an important organ for protecting internal organs. It forms the scaffolding of the body and gives the body its basic form. It drives muscle contraction to produce movement under the regulation of the nervous system. It is also an important hematopoietic organ; and it is regulated by the cytokines secreted by WAT. As research related to the release of adipocytokines from WAT to affect the skeleton continues to progress, an inextricable link between bone lipid regulation has been identified. In this paper, we review the literature to summarize the structure, function and metabolism of WAT, elaborate the specific molecular mechanisms by which WAT‐secreted hormones, cytokines and exosomes regulate skeletal cells, provide a theoretical basis for the in‐depth study of WAT cross‐organ regulation of bone, and provide new ideas for finding new adipose‐secreted targeting factors for the treatment of skeletal diseases. [ABSTRACT FROM AUTHOR]

Aim/Introduction: Resistin, which induces insulin resistance, is mainly expressed in monocytes/macrophages in humans. We reported previously that serum resistin was highest in the G–A haplotype defined by resistin single nucleotide polymorphisms (SNPs) at −420 (rs1862513) and − 358 (rs3219175). As sarcopenic obesity is associated with insulin resistance, we aimed to examine whether serum resistin and its haplotypes were associated with sarcopenic obesity at a latent stage. Materials and Methods: We cross‐sectionally analyzed 567 community‐dwelling Japanese participants attending annual medical check‐ups in which the sarcopenic obesity index was evaluated. The age‐ and gender‐matched normal glucose tolerance subjects with G–A homozygotes and those with C–G homozygotes were examined via RNA‐sequencing and pathway analysis (each n = 3), and RT‐PCR (each n = 8). Results: In multivariate logistic regression analyses, the fourth quartile (Q4) of serum resistin and G–A homozygotes were both associated with the latent sarcopenic obesity index defined by a visceral fat area of ≥ 100 cm2 and grip strength Q1 after adjustment for age and gender, with or without other confounding factors. RNA sequencing and pathway analysis showed that tumor necrosis factor (TNF) was involved in the top five pathways in the whole blood cells of G–A homozygotes compared with C–G homozygotes. RT‐PCR revealed that TNF mRNA was higher in G–A homozygotes than in C–G homozygotes. Conclusions: The G–A haplotype was associated with the latent sarcopenic obesity index defined by grip strength in the Japanese cohort, could be mediated by TNF‐α. [ABSTRACT FROM AUTHOR]

Summary: Obesity is recognized as a risk factor for adverse outcome in COVID‐19, but the molecular mechanisms underlying this relationship remain unknown. Adipose tissue functions as an endocrine organ by secreting multiple pro‐inflammatory and anti‐inflammatory factors, known as adipocytokines, which could be involved in COVID‐19 severity. We explored the role of adipocytokines in COVID‐19 and its association with BMI, clinical outcome, and inflammation. This is an observational study in 195 hospitalized COVID‐19 patients. Serial plasma concentrations of the adipocytokines leptin, adiponectin, resistin, and various inflammatory cytokines were assessed. Adipocytokines were compared between patients with normal weight (BMI: 18.5–24.9 kg/m2), overweight (BMI: 25.0–29.9 kg/m2), and obesity (BMI ≥ 30 kg/m2), between patients admitted to the ICU and to non‐ICU clinical wards, and between survivors and non‐survivors. Patients with overweight and obesity displayed higher leptin concentrations and lower adiponectin concentrations throughout hospital admission (p <.001), whereas resistin concentrations were not different from patients with normal weight (p =.12). Resistin concentrations correlated with inflammatory markers and were persistently higher in ICU patients and non‐survivors compared to non‐ICU patients and survivors, respectively (both p <.001), whereas no such relationships were found for the other adipocytokines. In conclusion, leptin and adiponectin are associated with BMI, but not with clinical outcomes and inflammation in COVID‐19 patients. In contrast, resistin is not associated with BMI, but high concentrations are associated with worse clinical outcomes and more pronounced inflammation. Therefore, it is unlikely that BMI‐related adipocytokines or differences in the inflammatory response underlie obesity as a risk factor for severe COVID‐19. [ABSTRACT FROM AUTHOR]

Background: Achieving an acceptable neurological outcome in cardiac arrest survivors remains challenging. Ischemia‐reperfusion injury induces inflammation, which may cause secondary neurological damage. We studied the association of ICU admission levels of inflammatory biomarkers with disturbed 48‐hour continuous electroencephalogram (cEEG), and the association of the daily levels of these markers up to 72 h with poor 6‐month neurological outcome. Methods: This is an observational, post hoc sub‐study of the COMACARE trial. We measured serum concentrations of procalcitonin (PCT), high‐sensitivity C‐reactive protein (hsCRP), osteopontin (OPN), myeloperoxidase (MPO), resistin, and proprotein convertase subtilisin/kexin type 9 (PCSK9) in 112 unconscious, mechanically ventilated ICU‐treated adult OHCA survivors with initial shockable rhythm. We used grading of 48‐hour cEEG monitoring as a measure for the severity of the early neurological disturbance. We defined 6‐month cerebral performance category (CPC) 1–2 as good and CPC 3–5 as poor long‐term neurological outcome. We compared the prognostic value of biomarkers for 6‐month neurological outcome to neurofilament light (NFL) measured at 48 h. Results: Higher OPN (p =.03), MPO (p <.01), and resistin (p =.01) concentrations at ICU admission were associated with poor grade 48‐hour cEEG. Higher levels of ICU admission OPN (OR 3.18; 95% CI 1.25–8.11 per ln[ng/ml]) and MPO (OR 2.34; 95% CI 1.30–4.21) were independently associated with poor 48‐hour cEEG in a multivariable logistic regression model. Poor 6‐month neurological outcome was more common in the poor cEEG group (63% vs. 19% p <.001, respectively). We found a significant fixed effect of poor 6‐month neurological outcome on concentrations of PCT (F = 7.7, p <.01), hsCRP (F = 4.0, p <.05), and OPN (F = 5.6, p <.05) measured daily from ICU admission to 72 h. However, the biomarkers did not have independent predictive value for poor 6‐month outcome in a multivariable logistic regression model with 48‐hour NFL. Conclusion: Elevated ICU admission levels of OPN and MPO predicted disturbances in cEEG during the subsequent 48 h after cardiac arrest. Thus, they may provide early information about the risk of secondary neurological damage. However, the studied inflammatory markers had little value for long‐term prognostication compared to 48‐hour NFL. [ABSTRACT FROM AUTHOR]

Some studies proposed the anti‐inflammatory effect of soy protein and soy isoflavones by changing the serum adiponectin and resistin levels. The purpose of this research was to determine the impact of soy isoflavones and soy protein on blood adiponectin and resistin levels in adults. Scopus, PubMed, Cochrane Library, ISI Web of Science, and ClinicalTrials.gov databases were searched until April 2022. The effect size was computed by the mean changes from the beginning for intervention and comparison groups and their standard deviation. In the case of significant heterogeneity, DerSimonian and Laird random‐effects model was used. Six and five clinical trials were selected for the systematic review and meta‐analysis, respectively. The overall estimate indicated that soy isoflavones in combination with soy protein did not significantly change serum adiponectin level (weighted mean differences (WMD) = 0.36 μg/ml; 95% confidence interval (CI): −0.26, 0.99; p =.25), but significantly increased serum resistin level (WMD = 0.64 ng/ml, 95% CI: 0.25, 1.04; p =.001). In combination with soy protein, soy isoflavones nonsignificantly increased serum adiponectin levels, but significantly increased resistin levels. New intervention studies with a high dose of soy isoflavones and soy protein in different parts of the world and an updated meta‐analysis are needed to confirm the results of our study. [ABSTRACT FROM AUTHOR]

Background and aims: Antipsychotic treatment may contribute to low vitamin D levels and have impact on direct anti‐inflammatory activity such as adiponectin activity and indirect proinflammatory activity such as leptin and resistin activity. However, vitamin D levels and adipokines mediated effect on weight gain and increased adiposity are not well evaluated. This study, therefore, assessed vitamin D and adipokines‐mediated obesity among Ghanaian psychiatric patients. Methods: This comparative cross‐sectional study was conducted at psychiatric unit of Komfo Anokye Teaching Hospital, Kumasi, Ghana. Anthropometric measurements, sociodemographic and previous medical history were taken from 300 antipsychotics treatment naïve and active patients. Obesity was classified using World Health Organization (WHO) body mass index (BMI)‐specific cut‐offs. Blood samples were collected for serum vitamin D and adipokines (adiponectin, leptin, and resistin) analysis using enzyme‐linked immunosorbent assay. Statistical analyses were done using SPSS version 26.0 and GraphPad Prism version 8.0. Results: We observed higher prevalence of obesity among treatment active psychiatric patients (40.7%) compared to treatment naïve group (16.8%). Vitamin D insufficiency and deficiency prevalence were significantly higher among the treatment active group (25.3%; 39.5%; p < 0.001) and associated with increased odds of obesity (91.8%; cOR = 91.84, 95% confidence interval [CI]: 24.94–338.13). Moreover, adiponectin (84.2%: cOR = 14.15, 95% CI: 5.52–36.27), leptin (55.6% cOR = 2.20, 95% CI: 1.04–4.67), and resistin (79.4%: cOR = −8.34, 95% CI: 3.39–20.55) were significantly associated with increased odds of obesity among treatment active psychiatric. Furthermore, treatment active psychiatric patients exhibited inverse correlation for adiponectin and leptin with BMI (r = −0.62; −0.24), and WHtR (r = −0.53; −0.24); however, a moderate positive correlation for resistin with BMI (r = 0.80), HC (r = 0.67), and WHtR (r = 0.65). Conclusion: Obesity is more prevalent in psychiatric patients on antipsychotics such as Olanzapine and Clozapine. Obesity among treatment active psychiatric patients is associated with vitamin D insufficiency and deficiency, low adiponectin and leptin levels but higher resistin level. [ABSTRACT FROM AUTHOR]

Objective: Adiponectin, which is secreted from adipose tissue, is a protein hormone. Although a large body of studies have found that circulating adiponectin levels increase in anorexia nervosa (AN) and caloric restriction, the effect of subtypes of AN and modifiers of adiponectin in AN are not yet known. Methods: A systematic search of electronic databases was performed using the search terms "adiponectin," "anorexia nervosa," and "eating disorder" up to January 2021. All studies published in peer‐reviewed journals, which included cases and control groups, were selected. The main outcome was the pooled standardized mean difference (SMD) in adiponectin levels between cases and controls, using the random‐effects model. Modifiers of SMD were tested via meta‐regression. Heterogeneity and publication bias were evaluated. Results: Thirty‐four studies met all eligibility criteria. The total sample of AN participants (Hedges' g =.765, p <.0001), and specifically the binge‐eating/purging (Hedges' g = 1.211, p <.00001) and restrictive subtypes (Hedges' g =.913, p <.00001) of AN have increased adiponectin plasma levels compared with healthy controls. Meta‐regression determined that insulin, IGF‐1, BMI, triglyceride, resistin, glucose, IL‐6 levels are significant modifiers of adiponectin levels. Discussion: Compared with controls, adiponectin levels are higher in AN overall, and specifically in the binge‐eating/purging and the restrictive AN subtypes. Many of metabolic parameters of glucose metabolism and pro‐inflammatory molecules modify the relationship between AN and adiponectin levels. Adipose tissue is important to maintain metabolic stability. Public Significance: Anorexia nervosa is a psychiatric disorder associated with a severe decrease in body weight and multiple metabolic abnormalities, including an increase in the hormone adiponectin. In this paper, we used meta‐analysis, a powerful statistical method, to aggregate data from 34 rigorously selected research reports. This enabled us to understand the value of adiponectin to differentiate clinical subtypes of anorexia nervosa and the relations between adiponectin and other important metabolic parameters. [ABSTRACT FROM AUTHOR]

Aims: Resistin is a circulating inflammatory biomarker that is associated with cardiovascular disease. We investigated the associations of resistin and incident heart failure (HF) and its subtypes, as well as specific measures of subclinical HF (myocardial fibrosis and relevant biomarkers). Methods: We analysed data from 1968 participants in the Multi‐Ethnic Study of Atherosclerosis with measurements of plasma resistin levels at clinic visits from 2002 to 2005. Participants were subsequently followed for a median of 10.5 years for HF events. The associations between resistin levels and incident HF, HF with reduced ejection fraction (HFrEF), and HF with preserved ejection fraction (HFpEF) were examined using multivariable Cox proportional hazards models. Linear regression models assessed the associations between resistin levels and myocardial fibrosis from cardiac magnetic resonance imaging, as well as hs‐cTnT and NT‐proBNP. Results: The mean age of the cohort was 64.7 years, and 50.0% were female. Seventy‐four participants (4%) developed incident HF during follow‐up. In a Cox proportional hazards model adjusted for age, gender, education level, race/ethnicity, and traditional risk factors, higher resistin levels were significantly associated with incident HF (HR 1.44, CI 1.18–1.75, P = 0.001) and HFrEF (HR 1.47, CI 1.07–2.02, P = 0.016), but not with HFpEF (HR 1.25, CI 0.89–1.75, P = 0.195). Resistin levels showed no significant associations with myocardial fibrosis, NT‐proBNP, or hs‐cTnT levels. Conclusions: In a multi‐ethnic cohort free of cardiovascular disease at baseline, elevated resistin levels were associated with incident HF, more prominently with incident HFrEF than HFpEF, but not with subclinical myocardial fibrosis or biomarkers of HF. [ABSTRACT FROM AUTHOR]

Background: The single nucleotide polymorphism (SNP) (rs10401670) of the RETN gene has been associated with metabolic disorder in obese subjects and has scarcely been evaluated after dietary interventions. The present study aimed to analyse the effects of the rs10401670 RETN gene polymorphism on metabolic changes secondary to weight loss and secondary to a high‐fat hypocaloric diet with a Mediterranean dietary pattern. Methods: A Caucasian population comprising 284 obese patients without diabetes mellitus was analysed. Before and after 3 months of a high‐fat hypocaloric diet with a Mediterranean pattern, an anthropometric evaluation, an assessment of nutritional intake and a biochemical analysis were performed. A statistical analysis was conducted for the combined CT and TT as a group and for wild‐type CC as a second group. Results: Decreases in weight, body mass index (BMI), fat mass, systolic blood pressure and waist circumference were similar in both genotypes groups. In T allele carriers, insulin, homeostatic model assessment for insulin resistance (HOMA‐IR), triglycerides and C‐reactive protein levels were decreased. The decrease in these parameters was statistically significant for triglycerides (−22.3 ± 9.3 mg dl–1: p = 0.03), C‐reactive protein (−2.8 ± 0.5 mg dl–1: p = 0.03), insulin (−7.4 ± 2.9 mUI L–1: p = 0.03) and HOMA‐IR (−2.4 ± 1.0: p = 0.02). Leptin levels were decreased in both genotypes groups after the hypocaloric diet, as well as the anthropometric parameters BMI, weight, waist circumference and fat mass. Resistin and adiponectin levels remained unchanged in both groups. Conclusions: In the present study, we have detected a significant association between the T allele of this SNP and a better response of insulin resistance, triglycerides and C‐reactive protein compared to non T allele carriers after weight loss with a high‐fat hypocaloric diet and a Mediterranean diet. Key points: In T allele carriers of the rs10401670 variant, insulin, homeostatic model assessment for insulin resistance (HOMA‐IR), triglycerides and C‐reactive protein levels were decreased.Leptin levels were decreased in both genotypes groups (carriers and non T allele carriers) after the hypocaloric diet, as well as the anthropometric parameters body mass index, weight, waist circumference and fat mass.Resistin and adiponectin levels remained unchanged in both groups. [ABSTRACT FROM AUTHOR]

The clinical relevance of blood levels of adipokines in individuals with postmenopausal osteoporosis (PMOP) has not been previously clarified. We performed this meta‐analysis to clarify the association between three common adipokines levels and the occurrence of PMOP. PubMed, Embase, Cochrane library, and China National Knowledgement Infrastructure (CNKI) were searched for collecting articles published before 31 October 2021, without language and status restrictions. Fourteen studies met the selection criteria. Meta‐analysis revealed that blood leptin level was remarkably lower (mean difference [MD], −1.94; 95% confidence interval [CI], −3.83 to −0.06; I2 = 96%) and adiponectin level was remarkably higher (MD, 3.48; 95% CI, 2.36 to 4.60; I2 = 90%) in individuals with PMOP than healthy individuals with normal bone mineral density (BMD). However, the statistical difference in leptin level was changed after eliminating the confounding influence of leptin sources and assay approaches. Furthermore, a positive association (r = 0.28) between leptin level and body mass index (BMI) as well as a negative association (r = −0.33) between adiponectin level and BMD was found. Moreover, adiponectin had the highest probability of predicting PMOP (84%). Current evidence suggests that leptin positively affects BMI and adiponectin negatively affects BMD, and adiponectin is the most relevant adipokine negatively associated with PMOP. [ABSTRACT FROM AUTHOR]

Background: Acne vulgaris (AV) is the most prevalent inflammatory skin disease and develops on the face and upper trunk. Resistin, a member of the cysteine‐rich secretory proteins family, is an adipokine expressed primarily in macrophages and monocytes; it has a role to play in the inflammatory period. Aims: This study's purpose was to detect whether known resistin gene (−420 C > G) polymorphism plays a role in the pathogenesis of AV. Methods: Patients with AV (n = 94) and healthy controls (n = 94) were enrolled in this investigation. Resistin gene (−420 C > G) polymorphism was decided by PCR‐RFLP procedure. Results: The distribution of genotype frequencies of resistin gene (−420 C > G) polymorphism was significantly different between the AV and healthy controls (p = 0.002). We found that the resistin gene (−420 C > G) CG genotype exhibited a significant association with decreased acne vulgaris risk. Conclusions: Our study is the first report investigating the relationship between the risk of AV and resistin gene (−420 C > G) polymorphism in the Turkish population. Resistin gene (−420 C > G) polymorphism is related to AV pathogenesis. CG genotype has a protective role and may be linked to a reduced risk of AV development. Furthermore, studies are needed to verify these findings in other populations. [ABSTRACT FROM AUTHOR]

Objective: To investigate the potential association between neutrophil degranulation and patterns of myocardial dysfunction in a cohort of patients with type 2 diabetes mellitus (T2DM). Background: Two distinct phenotypes of diabetic cardiomyopathy have been described: a restrictive phenotype with diastolic dysfunction (restrictive/DD) and a dilative phenotype with systolic dysfunction (dilative/SD). However, the underlying determinants of these two patterns are not yet recognized. Methods: In this single‐centre, observational, cross‐sectional study, 492 patients were recruited. Ultrasonographic measurements were performed by two experienced sonographers, blinded to the clinical data of the participants. Serum biomarkers of neutrophil degranulation were measured by enzyme‐linked immunosorbent sandwich assay (ELISA). Results: After adjustment for confounders, resistin, myeloperoxidase, matrix metalloproteinase 8 and matrix metalloproteinase 9/tissue inhibitor of metalloproteinases 1 complex were positively associated with the restrictive/DD pattern compared with the normal pattern. Similarly, MPO was positively associated with the dilative/SD pattern compared with the normal pattern, and resistin was negatively associated with the dilative/SD pattern compared with the restrictive/DD pattern. Conclusions: Neutrophil degranulation is associated with the restrictive/DD echocardiographic pattern in patients with T2DM, but not with the normal pattern and dilative/SD patterns. Neutrophils could have a pivotal role in the pathogenesis of myocardial dysfunction, and particularly diastolic dysfunction, in patients with T2DM. [ABSTRACT FROM AUTHOR]

Background: Increasing protein intake (above the Recommended Dietary Amount) alone or with resistance‐based exercise is suggested to improve cardiometabolic health; however, randomized controlled trials (RCTs) are needed to confirm this. Methods: The Liverpool Hope University‐Sarcopenia Aging Trial (LHU‐SAT) was a 16 week RCT (ClinicalTrials.gov Identifier: NCT02912130) of 100 community‐dwelling older adults [mean age: 68.73 ± 5.80 years, body mass index: 27.06 ± 5.18 kg/m2 (52% women)] who were randomized to four independent groups [Control (C), Exercise (E), Exercise + Protein (EP), Protein (P)]. E and EP completed supervised and progressive resistance‐based exercise (resistance exercise: two times per week, functional circuit exercise: once per week), while EP and P were supplemented with a leucine‐enriched whey protein drink (three times per day) based on individual body weight (0.50 g/kg/meal, 1.50 g/kg/day). Outcome measures including arterial stiffness (pulse wave velocity), fasting plasma/serum biomarkers [glucose/glycated haemoglobin, total cholesterol, low‐density lipoprotein (LDL), high‐density lipoprotein, insulin, resistin, leptin, adiponectin, C‐reactive protein, tumour necrosis factor‐alpha, interleukin‐6, cystatin‐C, & ferritin], insulin resistance (HOMA‐IR), and kidney function (eGFR) were measured before and after intervention. Results: Total protein intake (habitual diet plus supplementation) increased to 1.55 ± 0.69 g/kg/day in EP and to 1.93 ± 0.72 g/kg/day in P, and remained significantly lower (P < 0.001) in unsupplemented groups (E: 1.08 ± 0.33 g/kg/day, C: 1.00 ± 0.26 g/kg/day). At 16 weeks, there was a group‐by‐time interaction whereby absolute changes in LDL‐cholesterol were lower in EP [mean difference: −0.79 mmol/L, 95% confidence interval (CI): −1.29, −0.28, P = 0.002] and P (mean difference: −0.76 mmol/L, 95% CI: −1.26, −0.26, P = 0.003) vs. C. Serum insulin also showed group‐by‐time interactions at 16 weeks whereby fold changes were lower in EP (mean difference: −0.40, 95% CI: −0.65, −0.16, P = 0.001) and P (mean difference: −0.32, 95% CI: −0.56, −0.08, P = 0.009) vs. C, and fold changes in HOMA‐IR improved in EP (mean difference: −0.37, 95% CI: −0.64, −0.10, P = 0.007) and P (mean difference: −0.27, 95% CI: −0.53, −0.00, P = 0.048) vs. C. Serum resistin declined in P only (group‐by‐time interaction at 16 weeks: P = 0.009). No other interactions were observed in outcome measures (P > 0.05), and kidney function (eGFR) remained unaltered. Conclusions: Sixteen weeks of leucine‐enriched whey protein supplementation alone and combined with resistance‐based exercise improved cardiometabolic health markers in older adults. [ABSTRACT FROM AUTHOR]

Hypoxia-induced apoptosis of cementoblasts (OCCM-30) may be harmful to orthodontic treatment. Hypoxia-inducible factor 1-alpha (HIF-1a) mediates the biological effects during hypoxia. Little is known about the survival mechanism capable to counteract cementoblast apoptosis. We aimed to investigate the potential roles of HIF-1a, as well as the protein-protein interactions with ERK1/2, using an in-vitro model of chemical-mimicked hypoxia and adipokines. Here, OCCM-30 were co-stimulated with resistin, visfatin or ghrelin under CoCl2-mimicked hypoxia. In-vitro investigations revealed that CoCl2-induced hypoxia triggered activation of caspases, resulting in apoptosis dysfunction in cementoblasts. Resistin, visfatin and ghrelin promoted the phosphorylated ERK1/2 expression in OCCM-30 cells. Furthermore, these adipokines inhibited hypoxia-induced apoptosis at different degrees. These effects were reversed by pre-treatment with ERK inhibitor (FR180204). In cells treated with FR180204, HIF-1a expression was inhibited despite the presence of three adipokines. Using dominant-negative mutants of HIF-1a, we found that siHIF-1a negatively regulated the caspase-8, caspase-9 and caspase-3 gene expression. We concluded that HIF-1a acts as a bridge factor in lengthy hypoxia-induced apoptosis in an ERK1/2-dependent pathway. Gene expressions of the caspases-3, caspase-8 and caspase-9 were shown to be differentially regulated by adipokines (resistin, visfatin and ghrelin). Our study, therefore, provides evidence for the role of ERK1/2 and HIF-1a in the apoptotic response of OCCM-30 cells exposed to CoCl2-mimicked hypoxia, providing potential new possibilities for molecular intervention in obese patients undergoing orthodontic treatment. [ABSTRACT FROM AUTHOR]

Background: Acne vulgaris is a disease that inflames the sebaceous gland with multiple etiologies. Many proinflammatory adipokines contribute to this pathogenesis. Resistin is a proinflammatory mediator that activates kappa B, a nuclear factor, and c‐Jun N‐terminal kinases pathways inducing toll‐like receptor‐2, interleukin‐1, 6, and tumor necrosis factor alpha. Resistin gene affects the promoter and intron regions' polymorphisms' expression levels. We aimed to study the association of resistin gene polymorphisms (RETN ‐420 C/G) and the development of acne vulgaris and whether it is associated with serum resistin levels and disease severity. Subjects and methods: Resistin (RETN) gene (rs1862513) genotypes were identified using restriction fragment length polymorphism (RFLP), and serum resistin presence was assessed by enzyme‐linked immunosorbent assay in 40 patients with acne vulgaris and 40 age‐ and sex‐matched healthy controls as a cross‐reference. Patients were divided into mild, moderate, and severe groups. Global Acne Grading System (GAGS) was used to assess the severity of acne vulgaris. Results: CG and GG genotypes were present in cases (P = 0.006) odds ratio (OR)1 = 4.43; 95% confidence interval (CI) (1.53, 12.7) and OR2 = 5.47; 95% CI (0.99, 30.1); G‐allele statistically dominated in the patient group where P = 0.001 and OR = 3.57; 95% CI (1.63, 7.80). A positive significant relationship between RETN genotypes and serum resistin levels and GAGS score was present. Conclusion: RETN genes rs1862513 GG and G allele are correlated to acne vulgaris development and severity in a sample of the Egyptian population. This study comprised a small sample size. The cases may not accurately represent the general population; only one clinic was enrolled in the study. [ABSTRACT FROM AUTHOR]

Aims: We aimed to assess ethnic differences in inflammatory markers and their relationships with insulin sensitivity and regional adiposity between white European and black African men. Methods: A total of 53 white European and 53 black African men underwent assessment of inflammatory markers alongside Dixon‐magnetic resonance imaging to quantify subcutaneous and visceral adipose tissue and intrahepatic lipid. A hyperinsulinaemic‐euglycaemic clamp was used to measure whole‐body and adipose tissue insulin sensitivity. To assess ethnic differences in relationships, the statistical significance of an interaction term between adipokines and ethnic group was tested in multivariable regression models. Results: The black African men exhibited significantly lower adiponectin and tumour necrosis factor‐α (TNF‐α) and greater interleukin‐10 (IL‐10) compared to white European men (all p < 0.05). There were no statistically significant ethnic differences in leptin, resistin, IL‐6, interferon‐γ, IL‐13, IL‐1β, IL‐8 and vascular endothelial growth factor. Several relationships differed significantly by ethnicity such that they were stronger in white European than black African men including IL‐6 with visceral adipose tissue; adiponectin with subcutaneous adipose tissue; leptin with intrahepatic lipid; adiponectin, IL‐6 and TNF‐α with whole‐body insulin sensitivity and TNF‐α with adipose tissue insulin sensitivity (all pinteraction <0.05). Leptin significantly predicted whole‐body insulin sensitivity in white European (R2 = 0.51) and black African (R2 = 0.29) men; however, adiponectin was a statistically significant predictor in only white European men (R2 = 0.22). Conclusions: While adiponectin is lower in black African men, its insulin sensitising effects may be greater in white men suggesting that the role of adipokines in the development of type 2 diabetes may differ by ethnicity. [ABSTRACT FROM AUTHOR]

Aim: Salivary biomarkers can help in assessment of periodontitis; however, concentrations may be altered in the presence of diabetes. Hence, the ability of salivary biomarkers to discriminate periodontally healthy type II diabetics (T2DM) from T2DM who have periodontitis was examined. Methods: Ninety‐two participants (29 with T2DM with chronic periodontitis, DWP; 32 T2DM without chronic periodontitis, DWoP; and 31 Not Periodontitis, NP) provided saliva and clinical parameters of periodontal health were recorded. Salivary concentrations of interleukin (IL)‐1β, IL‐6, matrix metalloproteinase‐8 (MMP‐8), macrophage inflammatory protein‐1α (MIP‐1α), adiponectin and resistin were measured by immunoassay. Results: Salivary analyte concentrations for IL‐1β, MMP‐8 and resistin correlated with clinical parameters of periodontitis, with MMP‐8 demonstrating the strongest positive correlation with PD ≥5 mm (p < 0.0001). Periodontal health was reflected in salivary analyte concentrations by group, with concentrations of IL‐1β and MMP‐8 showing significant associations with periodontitis (p ≤ 0.04) that increased in concentration from health to DWoP to DWP. Odds ratio (OR) analyses showed that MMP‐8 discriminated periodontitis from NP (OR of 8.12; 95% CI: 1.01–65.33; p = 0.03) and in the presence of T2DM (DWP vs DWoP, OR = 5.09; 95% CI: 1.24–20.92; p = 0.03). Conclusion: Salivary MMP‐8 and IL‐1β discriminate periodontitis in T2DM. [ABSTRACT FROM AUTHOR]

Background: Resistin is known as a potential mediator of obesity‐associated insulin resistance. The high resistin level disrupts nitric oxide (NO)‐mediated relaxation which is also important in erectile function. An antioxidant alkaloid, Boldine, is known as anti‐diabetic and protects endothelial functions. Objectives: We aimed to investigate resistin expression in penile tissue in the presence of insulin resistance (IR) and the effect of Boldine treatment on erectile functions in the metabolic syndrome (MetS) rat model. Materials and methods: Wistar rats were randomly divided into three groups: Control, MetS, and boldine treated MetS group. MetS parameters were assessed by serum triglycerides (TG), uric acid (UA), glucose, insulin levels, HOMA index, and waist circumference (WC)/tibia length (TL) ratio. To evaluate erectile functions, intracavernous pressure (ICP)/mean arterial pressure (MAP) ratio was performed during cavernous nerve stimulation. Protein expressions of resistin, endothelial nitric oxide synthase (eNOS), p(S1177) eNOS, and insulin receptor‐β were evaluated by Western blotting. Results: TG, glucose, insulin levels, weight, WC/TL ratio, HOMA index and resistin expression in penile tissue were significantly increased and ICP/MAP values, and p (S1177) eNOS expression in penile tissue were decreased in MetS group. Boldine treatment enhanced ICP/MAP values, insulin receptor‐β and p(S1177) eNOS expressions compared with the MetS group. Discussion and Conclusion: MetS caused a deterioration in erectile function accompanied by an increase in resistin expression and a reduction in eNOS enzyme activation in the rat penile tissues. Boldine treatment resulted in an improvement in erectile function, independent of resistin expression. [ABSTRACT FROM AUTHOR]

Summary: In the current study, a systematic review and meta‐analysis were conducted to summarize and assess whether short sleep duration is associated with appetite‐regulating hormones and adipokine levels. Reference databases were searched for studies related to sleep and appetite‐regulating hormones and adipokines. Qualitative and quantitative syntheses were conducted to evaluate the relationship between sleep duration and the level of appetite‐regulating hormones and adipokines, including leptin, ghrelin, adiponectin, resistin, and orexin. Twenty‐one of 3536 studies, covering a total of 2250 participants, met the inclusion criteria. Leptin, ghrelin, and adiponectin were included in the meta‐analysis. Ghrelin levels were higher in the short sleep group (standard mean difference [SMD] = 0.14, 95% CI [0.03, 0.25], p = 0.01). Significant differences between the short sleep group and recommended sleep group were also noted in leptin level experimental subgroup studies (SMD = 0.19, 95% CI [0.03, 0.35], p = 0.02) and ghrelin level cross‐sectional subgroup studies (SMD = 0.14, 95% CI [0.02, 0.27], p = 0.03). A rise in leptin and ghrelin levels were also observed in sleep deprivation groups (SMD = 0.24, 95% CI [0.10, 0.39], p = 0.001 and SMD = 0.18, 95% CI [0.04, 0.33], p = 0.01, respectively). In conclusion, short sleep duration is associated with an increased ghrelin level, while sleep deprivation had a significant effect on the levels of both leptin and ghrelin. [ABSTRACT FROM AUTHOR]

Background/Objectives: Atopic dermatitis (AD) is an inflammatory chronic skin disorder. The etiology of AD is not fully understood. Therefore, we aimed by this study to shed light on the potential role of resistin in an etiopathogenesis of AD through investigation of resistin rs3745367 single nucleotide polymorphism (SNP) and resistin serum levels, and their relation to leukocytic count in a sample of Egyptian patients having atopic dermatitis. Methods: This case‐control study included 45 patients having AD and 40 controls. SCORAD index was assessed to evaluate the severity of AD. CBC, ELISA, and PCR‐RFLP were performed to detect leukocytic count, resistin serum level, and resistin rs3745367 SNP, respectively. Results: Atopic dermatitis patients had significant low serum resistin concentrations (P =.036) and a significantly high frequency of leukocytosis (P =.003). Low resistin serum levels were significantly related to AD disease severity (P <.001) and the presence of leukocytosis (P <.001). Resistin rs3745367 GG genotype (P =.030), as well as its G allele (P =.019), was expressively associated with AD development, and both increased the risk of AD by 3‐ and 2‐fold, respectively. Resistin rs3745367 GG genotype was significantly linked to low resistin serum levels (P <.001), AD‐positive family history (P =.015), and the presence of leukocytosis (P <.001). Conclusions: Resistin rs3745367 gene polymorphism may contribute to the development of AD. Resistin may have an immune‐modulating active character in the AD etiopathogenesis that could be mediated through its anti‐inflammatory effect. From this piece of work, we may suggest resistin as a new therapy to mitigate the pro‐inflammatory environment found in AD. [ABSTRACT FROM AUTHOR]

Background: Inflammatory biomarkers are useful in detecting patients with sepsis. The prognostic role of resistin and myeloperoxidase (MPO) has been investigated in sepsis. Materials and Methods: Plasma resistin and MPO were measured on days 1, 2 and 7 in 957 patients enrolled in the Albumin Italian Outcome Sepsis (ALBIOS) trial. The association between resistin and MPO levels on day 1, 2 and 7 and 90‐day mortality was assessed. Results: Plasma resistin and MPO concentrations were higher at day 1 and decreased until day 7. Both biomarkers were positively correlated with each other and with physiological parameters. Higher levels of resistin and MPO on day 1 were associated with the development of new organ failures. Patients experiencing death at 90 days showed higher levels of resistin and MPO compared with survivors. At day 1, only MPO in the 4th quartile (Q4), but not resistin, was found to predict 90‐day death (adjusted hazard ratio [aHR] 1.55 vs Q1). At day 2, resistin in the Q3 and Q4 predicted a > 40% increase in mortality as also did MPO in the Q4. On day 7, Q4 resistin was able to predict 90‐day mortality, while all quartiles of MPO were not. Conclusions: High levels of MPO, but not of resistin, on day 1 were able to predict 90‐day mortality. These findings may either suggest that early hyper‐activation of neutrophils is detrimental in patients with sepsis or reflect the burden of the inflammatory process caused by sepsis. Further studies are warranted to deepen these aspects (ALBIOS ClinicalTrials.gov Identifier: NCT00707122). [ABSTRACT FROM AUTHOR]

Resistin is a cysteine‐rich adipokine that promotes the release of inflammatory cytokines, particularly interleukin 1 beta (IL‐1β) and tumor necrosis factor alpha (TNF‐α), which are critical pro‐inflammatory mediators in osteoarthritis (OA) pathogenesis. We describe evidence of significantly higher levels of resistin, IL‐1β, and TNF‐α expression in OA knee synovial tissue compared with that from non‐OA knees. Resistin‐induced enhancement of IL‐1β and TNF‐α expression in human OA synovial fibroblasts (OASFs) were attenuated by MEK and ERK inhibitors, as well as their respective siRNAs. Our data reveal that resistin enhances the expression of TNF‐α and IL‐1β in OASFs by inhibiting miR‐149 expression via MEK and ERK signaling. Our findings elucidate the inter‐relationships between resistin and pro‐inflammatory mediators during OA pathogenesis and could help to facilitate the development of synovium‐targeted therapy in OA. [ABSTRACT FROM AUTHOR]

Resistin as an adipokine identified from rodents in 2001 is involved in many biological processes. However, little is known about this gene in fish. We cloned Siberian sturgeon (Acipenser baerii) resistin cDNA of 795 base pairs, encoding 107 amino acids, which showed 38–40% identity to human and rodents. Real‐time quantitative PCR showed that the resistin gene was widely distributed in tissues of Siberian sturgeon, with the highest expression in liver. After fasting for 1, 3, 6 and 10 days, the expression of the resistin gene in the liver of Siberian sturgeon decreased significantly, and after refeeding on the 10 days of fasting the resistin mRNA expression increased rapidly, suggesting that resistin may play an important role in liver in response to starvation. Taken together, these results suggest that resistin may be involved in the regulation of energy homeostasis in liver. [ABSTRACT FROM AUTHOR]

Resistin is a small secretory protein that has a pleiotropic role in rodents and humans. Both rodent resistin and human resistin have an extremely stable and high‐order multimeric structure. Moreover, there is significant variation in the source of secretion and the diversity of functions of resistin. Mouse resistin resists insulin action and contributes to type 2 diabetes mellitus, while human resistin plays a role in inflammation and also functions as a small accessory chaperone. Currently, active research in the area identified a significant role for resistin in stress biology and as a biomarker in diagnostics to evaluate disease status and treatment outcome. This review summarizes recent developments within resistin biology including their association with obesity, inflammation, stress response mechanisms, and its role in clinical diagnostics. [ABSTRACT FROM AUTHOR]

The aim of this work was to clarify whether maternal lithium chloride (LiCl) exposure disrupts the neonatal neuroendocrine‐cytokine axis. Pregnant Wistar rats were orally administrated 50 mg LiCl/kg b.wt. from gestational day (GD) 1 to postpartum day 28. Maternal administration of LiCl induced a hypothyroid state in both dams and their neonates compared to the control dams and neonates at lactation days (LDs) 14, 21 and 28, where the levels of serum free triiodothyronine (FT3) and free thyroxin (FT4) were decreased and the level of serum thyrotropin (TSH) level was increased. A noticeable depression in maternal body weight gain, neonatal body weight and neonatal serum growth hormone (GH) was observed on all examined postnatal days (PNDs; 14, 21 and 28). A single abortion case was recorded at GD 17, and three dead neonates were noted at birth in the LiCl‐treated group. Maternal administration of LiCl disturbed the levels of neonatal serum tumor necrosis factor‐alpha (TNF‐α), transforming growth factor‐beta (TGF‐β), interleukin‐1 beta (IL‐1β), interferon‐gamma (INF‐γ), leptin, adiponectin and resistin at all tested PNDs compared to the control group. This administration produced a stimulatory action on the level of neonatal cerebral serotonin (5‐HT) at PND 14 and on the level of neonatal cerebral norepinephrine (NE) at PNDs 21 and 28. However, this administration produced an inhibitory action on the level of neonatal cerebral dopamine (DA) at all examined PNDs and on the level of neonatal cerebral NE at PND 14 and the level of neonatal cerebral 5‐HT at PNDs 21 and 28 compared to the corresponding control group. Thus, maternal LiCl exposure‐induced hypothyroidism disrupts the neonatal neuroendocrine‐cytokine system, which delay cerebral development. [ABSTRACT FROM AUTHOR]

Aims/Introduction: Resistin is an adipocyte‐derived polypeptide that leads to the progression of insulin resistance and subsequent atherosclerosis. Some studies have reported an association between self‐reported intake of n−3 polyunsaturated fatty acids (PUFAs) and serum resistin levels. However, no studies have investigated the association between the ratio of serum levels of n−3 to serum n−6 PUFAs and the serum resistin concentration in the general population. Materials and Methods: We carried out a cross‐sectional study of 3,200 community‐dwelling Japanese individuals aged ≥40 years in 2002–2003. The ratios of serum eicosapentaenoic acid or docosahexaenoic acid to arachidonic acid (AA) were categorized into quartiles. The associations of serum eicosapentaenoic acid/AA and docosahexaenoic acid/AA with the serum resistin concentration were assessed using linear regression models with adjustment for potential confounding factors. Results: The geometric mean of serum resistin was 10.3 ng/mL. The age‐ and sex‐adjusted geometric mean of serum resistin decreased significantly with increased levels of serum eicosapentaenoic acid/AA (quartile 1: 11.3 ng/mL; quartile 2: 10.6 ng/mL; quartile 3: 10.3 ng/mL; quartile 4: 9.3 ng/mL; P for trend <0.001). A similar association was observed for serum docosahexaenoic acid/AA (quartile 1: 11.1 ng/mL; quartile 2: 10.6 ng/mL; quartile 3: 10.1 ng/mL; quartile 4: 9.7 ng/mL; P for trend <0.001). An adjustment for potential confounding factors did not change these associations. Conclusions: Higher ratios of serum n−3 to n−6 PUFAs were associated with lower serum resistin levels. Consumption of a large amount of n−3 PUFAs might have desirable effects on resistin‐mediated diseases. [ABSTRACT FROM AUTHOR]

Repeated cycles of weight loss and regain, known as weight cycling, is often seen when people try to lose weight. The exact pathophysiological effects and the underlying mechanisms of weight cycling remain largely unclear. Here, we report that weight cycling induced by alternating feeding mice with a low‐fat diet or a high‐fat diet in a 1‐week switch protocol caused further increased epididymal white adipose tissue (eWAT) weight, preadipocyte proliferation, hepatic inflammation, fasting blood glucose level, and glucose intolerance, compared with the continuously HF‐fed mice. Combining the secretory protein database with RNA‐sequencing and quantitative PCR (qPCR) results in eWAT, the mRNA levels of several adipokines, including Retn (encoding resistin), were found altered by weight cycling. A transcriptional co‐factor Lmo4 was found regulated by weight cycling; Lmo4 enhanced preadipocyte proliferation, in vitro adipogenesis, transcription of Retn, and resistin secretion in 3T3‐L1 cells. Primary mouse hepatocytes administrated with recombinant mouse resistin (rm‐resistin), or exposed to media from Lmo4‐overexpressed 3T3‐L1 cells, showed increased inflammatory responses and gluconeogenesis. Furthermore, rm‐resistin‐injected normal chow‐fed mice showed upregulated blood glucose level by increasing gluconeogenesis, and upregulated the hepatic inflammatory responses. Together, our results suggest a regulatory role of Lmo4‐resistin signaling in weight cycling, indicating a crosstalk between the adipose tissue and liver. [ABSTRACT FROM AUTHOR]

Diabetes mellitus is a metabolic and chronic disorder, which is very common all over the world. Many genetic and nongenetic factors are involved in the development of type 2 diabetes mellitus (T2DM). Meanwhile, the resistin gene is an important candidate in the pathogenesis of this complex condition. High levels of transcription of the resistin gene are associated with inflammation, insulin resistance, initiation and development of T2DM and atherosclerosis progression through induction of secretion of bioactive materials from adipocytes. Releasing adipose tissue‐derived inflammatory cytokines is associated with inflammatory processes activation, which causes inhibition of insulin action via interference with insulin signaling, such that these disorders can contribute to insulin resistance. With the direct effect of resistin and other inflammatory mediators on vascular endothelial cells and arterial walls, the expression of cell adhesion molecules is increased. This process can lead to atherosclerosis and will result in coronary artery disease (CAD). In this review, we will explore the effects of resistin on inflammation and insulin resistance that may lead to type 2 diabetes and CAD. [ABSTRACT FROM AUTHOR]

Resistin, secreted by macrophages in tumor microenvironment, has never been investigated in pancreatic cancer models, despite a vibrant tumor microenvironment around pancreatic tumors. We evaluated serum resistin levels in healthy individuals versus pancreatic cancer patients representing different tumor grades. In vitro mechanistic analysis involved MiaPaCa‐2 and SW1990 cells. Resistin signaling depends on binding of resistin to its cognitive receptors. Therefore, we silenced adenylyl cyclase‐associated protein 1 (CAP1) and toll‐like receptor 4 (TLR4), its two known receptors, individually as well as in combination, by short hairpin RNA (shRNA). Effect of resistin on cell proliferation, migration, invasion, cell cycle, and sensitivity to gemcitabine was studied without or with silencing of resistin receptors CAP1 and/or TLR4. The results were also confirmed in vivo in mice xenografted with MiaPaCa‐2 cells without or with receptor silencing. We report high resistin levels in pancreatic cancer patients which correlate positively with tumor grades. We observed a marked reduction in the resistin‐induced proliferation, migration, invasion, and cell cycle of pancreatic cancer cells MiaPaCa‐2 and SW1990 when the receptors were silenced. The results were confirmed in vivo wherein resistin effects were significantly attenuated in MiaPaCa‐2 xenografts with silenced receptors. The combined silencing of CAP1 and TLR4 was found to be most effective in vitro and in vivo. We found activation of STAT3 by resistin in vivo and in vitro which was dependent on the presence of CAP1 and TLR4. Further, resistin was found to induce resistance to gemcitabine through its receptors. Our results describe novel functional roles of resistin with implications toward a better understanding of pancreatic tumor microenvironment. Resistin is secreted by macrophages in tumor microenvironment and, since, tumor microenvironment is particularly of interest in pancreatic cancer, there is need to fully understand resistin and other factors within the tumor microenvironment. Most studies have focused on exogenously added resistin, without consideration for receptors but resistin is not produced by tumor cells and, therefore, the signaling through receptors is critical. In addition to cell line‐based in vitro data, we also present in vivo and clinical data from pancreatic cancer patients, which provides validity and significance to our results. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the effect of quercetin on metabolic and hormonal parameters as well as plasma concentration and gene expression of resistin in overweight or obese women with polycystic ovary syndrome (PCOS). In this randomized, double‐blind, placebo‐controlled trial, 78 overweight or obese women (25 ≤ BMI ≤ 40 kg/m2, 20–40 years) with PCOS were recruited. Patients were randomized to receive 1,000 mg/day quercetin or placebo for 12 weeks. Resistin plasma concentration and gene expression in peripheral blood mononuclear cells, parameters of glucose homeostasis, circulatory testosterone, luteinizing hormone (LH), and sex hormone‐binding globulin, and anthropometries were assessed at baseline and at the end of the study. Following supplementation, quercetin significantly decreased resistin concentration (2.07 ± 0.23 vs. 2.88 ± 0.40 ng/ml, p < 0.001) and mRNA level (0.64 ± 0.58 vs. 1 ± 0.56 fold change, p = 0.008), compared with placebo group. Moreover, testosterone (0.72 ± 0.15 vs. 0.76 ± 0.12 ng/ml, p = 0.001) and LH (8.05 ± 2.88 vs. 8.77 ± 1.99 mIU/ml, p = 0.035) concentrations were significantly lower in quercetin compared with placebo group. Fasting blood glucose (p < 0.001), insulin (p = 0.02), and homeostatic model assessment of insulin resistance (p = 0.009) decreased within the quercetin group; however, no significant differences were observed compared with the placebo group (p = 0.074, p = 0.226, p = 0.22, respectively). Quercetin supplementation decreased resistin plasma levels and gene expression, and testosterone and LH concentration in overweight or obese women with PCOS. [ABSTRACT FROM AUTHOR]

Summary: Background: While adipokines can regulate satiety and energy metabolism, whether they are associated with childhood growth is unclear. Objective: To evaluate whether adipokine levels at birth are associated with growth. Methods: A total of 2264 singletons and 1144 twins from Upstate KIDS (born 2008–2010) had adiponectin, leptin, resistin and complement factor D measured in newborn blood spots. Parents reported anthropometry from paediatric visits via questionnaires every 4–6 months. Generalized linear mixed effects models were used to estimate growth trajectories through 3 years of age. Results: Among singletons, resistin and leptin were associated with greater weight‐for‐age (0.12 z‐score units (95%CI: 0.04, 0.20) [p = 0.003] and 0.15 (0.06, 0.24) [p = 0.001], respectively) and BMI z‐score (0.11; 0.02, 0.20 [p = 0.02] and 0.18; 0.07, 0.28 [p = 0.002], respectively). After adjusting for birthweight, resistin and a ratio of resistin‐to‐adiponectin remained associated with weight through 3 years of age and odds of being overweight at 3 years of age in a subgroup of singletons. Among twins, adiponectin was associated with increased weight‐for‐age and length‐for‐age z‐scores even after adjusting for birthweight (0.18; 0.08, 0.28 [p = 0.0006]; 0.20; 0.07, 0.33 [p = 0.003], respectively). Conclusions: Levels of adipokines were associated with early childhood growth in small magnitudes. Resistin may be relevant for further examination in paediatric obesity. [ABSTRACT FROM AUTHOR]

Background: Experimental data indicate that sepsis influences the mitochondrial function and metabolism. We aim to investigate longitudinal bioenergetic, metabolic, hormonal, amino-acid, and innate immunity changes in children with sepsis.Methods: Sixty-eight children (sepsis, 18; systemic inflammatory response syndrome [SIRS], 23; healthy controls, 27) were enrolled. Plasma amino acids were determined by high-performance liquid chromatography (HPLC); flow-cytometry expressed as mean fluorescence intensity (MFI) of heat shock protein (HSP) levels from monocytes (m) and neutrophils (n); resistin, adiponectin, and extracellular (e) HSPs evaluated by ELISA; ATP levels in white blood cells by luciferase luminescent assay; lipid peroxidation products (TBARS) by colorimetric test; nitrite and nitrate levels by chemiluminescent assay; biliverdin reductase (BVR) activity by enzymatic assay; and energy-expenditure (EE) by E-COVX.Results: Resistin, eHSP72, eHSP90α, and nitrate were longitudinally higher in sepsis compared with SIRS (p<0.05); mHSP72, nHSP72, VO2 , VCO2 , EE, and metabolic pattern were repressed in sepsis compared with SIRS (p<0.05). Septic patients had lower ATP and TBARS compared with controls on day 1, lower ATP compared with SIRS on day 3 (p<0.05), but higher levels of BVR activity. Sepsis exhibited higher phenylalanine levels on day 1, serine on day 3; lower glutamine concentrations on days 3 and 5 (p<0.05). Resistin, inversely related to ATP, was independently associated with sepsis, along with mHSP72 and eHSP90α (p<0.05); TBARS and VO2 were independently associated with organ failure (p<0.05)). Septic nonsurvivors had malnutrition, persistently repressed metabolism, mHSP72, and induced resistin and adiponectin (p<0.05).Conclusions: A pattern of early longitudinal induction of metabolic-hormones and eHSP72/HSP90α, repression of bioenergetics and innate immunity, hypo-metabolism, and amino-acid kinetics changes discriminate sepsis from SIRS; malnutrition, hypo-metabolism, and persistently increased resistin and adiponectin are associated with poor outcome. [ABSTRACT FROM AUTHOR]

Metastasis is the main cause of lung cancer‐related death. The tumor microenvironment greatly contributes to tumor metastasis. Resistin, mainly secreted by tumor‐associated macrophages in tumor tissues, is a 12.5‐kDa cysteine‐rich secretory protein that is found at significantly higher levels in the serum or plasma of cancer patients compared with healthy controls. In this study, we explored the expression and role of resistin in lung adenocarcinoma. Our study showed that resistin was strongly expressed in lung adenocarcinoma tissues and promoted the migration and invasion of lung adenocarcinoma cells in a dose‐dependent manner. Toll‐like receptor 4 (TLR4) was the functional receptor of resistin for migration and invasion in A549 cells. Src/epidermal growth factor receptor (EGFR) was involved in resistin‐induced migration and invasion. Resistin increased the phosphorylation of EGFR through the TLR4/Src pathway. We also found that PI3K/nuclear factor (NF)‐κB were the intracellular downstream effectors mediating resistin‐induced migration and invasion. Taken together, our results suggested that resistin promoted lung adenocarcinoma metastasis through the TLR4/Src/EGFR/PI3K/NF‐κB pathway. [ABSTRACT FROM AUTHOR]

Background: This study aimed to evaluate the levels of resistin and tumor necrosis factor-alpha (TNF-α) in gingival crevicular fluid (GCF) and saliva of obese children with gingivitis.Methods: One-hundred and thirty children (65 obese and 65 normal weight; age range 8 to 12 years) were recruited for the study. The children were classified into four subgroups based on their body mass and periodontal status; 1) obese children with gingivitis (OG, n = 33); 2) obese children with healthy periodontium (OH, n = 32); 3) normal weight children with gingivitis (NWG, n = 32); 4) normal weight children with healthy periodontium (NWH, n = 33). Body mass index (BMI) percentile, probing pocket depth (PPD), gingival index (GI), and plaque index (PI) were recorded. Resistin and TNF-α were analyzed in GCF and saliva samples by ELISA.Results: Obese children had higher BMI percentiles than normal weight children (p < 0.0001). PPD, GI, PI, GCF volume, GCF, and salivary resistin and TNF-α levels were similar between obese and normal weight children (P > 0.05). OG and NWG subgroups had significantly higher GI, PI, GCF volume, GCF resistin total amounts, and salivary resistin concentrations but lower GCF resistin and TNF-α concentrations than OH and NWH (P < 0.0001 for all). GCF resistin total amounts were positively correlated with GI, PI, and GCF TNF-α total amounts (P < 0.05).Conclusions: To our knowledge, this is the first study evaluated the levels of resistin in GCF and saliva of children. Obesity is not associated with GCF and salivary resistin and TNF-α levels in children in the presence of gingival inflammation. [ABSTRACT FROM AUTHOR]

Abstract: Aim: The aim of the present study was to assess the effect of scaling and root planing (SRP) on periodontal parameters and whole salivary resistin and interleukin (IL)‐6 levels in chronic periodontitis (CP) patients with and without obesity. Methods: Participants were divided into two groups; group 1 included obese and non‐obese individuals with CP; and group 2 included obese and non‐obese individuals without CP. In both groups, bleeding on probing (BOP) and probing depth (PD) ≥4 mm and whole salivary resistin and IL‐6 levels were measured using enzyme‐linked immunosorbent assay at baseline and 6 months after SRP. The number of missing teeth was counted, and marginal bone loss was measured on digital panoramic radiographs at baseline and 6 months' postoperatively. Results: BOP was significantly higher among obese patients in group 1 than obese (P < .001) and non‐obese (P < .001) individuals in group 2. At 6 months' follow up, BOP (P < .001) and PD ≥4 mm (P < .001) were significantly lower among obese and non‐obese patients in group 1 than their respective baseline values. At 6 months' follow up, BOP (P < .001) and PD ≥4 mm (P < .001) were significantly higher among obese and non‐obese individuals in group 1 compared with individuals in group 2. Conclusion: SRP is effective in reducing periodontal inflammation in CP patients with and without obesity. CP seems to be the primary factor that influences periodontal status and the expression of resistin and IL‐6 levels in obese and non‐obese patients. [ABSTRACT FROM AUTHOR]

Abstract: Aim: We have shown that some markers of oxidative stress were higher in women with gestational diabetes mellitus (GDM). This study examines the relationship between adipokines and oxidative stress and their potential effects in pregnant women. Methods: Three markers of oxidative stress (malondialdehyde, 8‐isoprostane and xanthine oxidase) and three adipokines (leptin, adiponectin and resistin) were measured in maternal plasma, cord plasma and placenta of 208 pregnant women. Results: Among all these women, 105 were diagnosed with GDM while the other 103 were controls. Leptin, resistin, malondialdehyde, xanthine oxidase and 8‐isoprostane in maternal plasma, cord plasma and placenta were significantly higher while maternal adiponectin significantly lower in women with GDM (P < 0.05). Adipokines in maternal plasma, cord plasma and placenta were positively correlated with markers of oxidative stress. Both markers of oxidative stress and adipokines were correlated inversely with homeostasis model assessment of insulin resistance whereas positively with quantitative insulin sensitivity check index (P < 0.01). Adiponectin is negatively correlated with leptin and resistin. Placental/cord leptin and cord resistin levels were higher in the macrosomia while maternal adiponectin level was lower (P < 0.05) than normal birthweight newborns. Both markers of oxidative stress and adipokines in maternal and cord plasma are negatively correlated with newborn birthweight (P < 0.05). Conclusion: Adipokines interact with markers of oxidative stress, both of which lead to insulin resistance, GDM and macrosomia. It has long been known that placenta involves in the development of GDM. Adipokines might participate in this process and need to be confirmed by further studies. [ABSTRACT FROM AUTHOR]

Our primary aim was to study the effects of 24 weeks of combined aerobic and resistance training performed on the same day or on different days on inflammation markers. Physically active, healthy young men were randomly divided into three groups that performed: aerobic and resistance training consecutively in the same training session (SS) 2‐3 days wk−1 or on alternating days (AD) 4‐6 days wk−1 as well as control (C). The total training volume was matched in the training groups. The control group was asked to maintain their habitual physical activity and exercise level. Maximal leg press strength (1RM) and peak oxygen uptake (VO2peak) were measured. Abdominal fat mass was estimated with dual‐energy absorptiometry (DXA). High‐sensitivity C‐reactive protein (hs‐CRP), interleukin‐6 (IL‐6), monocyte chemoattractant protein 1 (MCP‐1), tumor necrosis factor alpha (TNF‐α), and adipocytokines resistin, adiponectin, and leptin were analyzed from plasma samples. Training significantly reduced circulating hs‐CRP, leptin, and resistin in both training groups (P<.05), whereas MCP‐1 and TNF‐α decreased only in AD (P<.05). Significant correlations were observed between changes in abdominal fat mass and corresponding changes in MCP‐1, leptin, adiponectin, and resistin. Long‐term combined aerobic and resistance training reduced markers of subclinical inflammation in healthy young men. The results indicate that a higher frequency of individual exercise sessions might be more beneficial with respect to the anti‐inflammatory effects of physical activity. The decreases in inflammation markers seem to be related to decreases in abdominal fat mass. [ABSTRACT FROM AUTHOR]

Objective Resistin is secreted by monocytes/macrophages and is associated with insulin resistance, inflammation and cardiovascular diseases. In the Japanese cohort, serum resistin is tightly associated with a single-nucleotide polymorphism ( SNP) at -420 (rs1862513) in the promoter region of the human resistin gene. However, interactions between SNP-420 and environmental factors remain to be elucidated. The aim of this study was to investigate the association between serum resistin levels and nutrient intake, and the effect of SNP-420 on this association. Design, Participants and Measurements The Toon Genome Study is a cohort study of Japanese community-dwelling subjects. A total of 1981 participants were cross-sectionally analysed. Each nutrient intake was assessed using the semiquantitative food frequency questionnaire and categorized into the quartiles (Q1-Q4). Serum resistin was measured by ELISA. Results Serum resistin tended to be inversely associated with fish intake and positively associated with meat intake after adjustment for age, sex, BMI and energy intake. Serum resistin was inversely associated with n-3 polyunsaturated fatty acids ( PUFA) intake after adjustment for age, sex, BMI and energy intake (Q1 12.5, Q2 12.5, Q3 12.2, Q4 11.5 ng/mL; P for trend = .007). This inverse association was strongest in the G/G genotype of SNP-420, followed by C/G and C/C (G/G, Q1 18.9, Q2 19.5, Q3 18.4, Q4 14.5 ng/mL, P = .001; C/G, 14.4, 13.3, 13.1, 12.9, P = .015; C/C, 9.5, 9.5, 9.2, 8.8, P = .020; P for interaction = .004). Conclusions The inverse association between serum resistin and n-3 PUFA intake was strongest in SNP-420 G/G genotype in the Japanese cohort. [ABSTRACT FROM AUTHOR]

Background Oxidative stress and inflammation are assumed as the main pathological triggers for vascular damage in hypersomnolent obstructive sleep apnoea ( OSA) patients, whereas their exact role in less symptomatic population is currently unknown. Aim To determine whether oxidative stress (urinary 8-isoprostane concentration) and inflammation (plasma resistin levels) are associated with vascular damage in non-hypersomnolent (Epworth Sleep Score <11) OSA patients. Methods A total of 325 consecutive patients have undergone standard polysomnography, and 256 of them were diagnosed with OSA. Excessive daytime sleepiness was assessed by the Epworth Sleepiness Scale ( ESS). Only 86 patients with ESS <11 participated in the study. The control group was presented by 45 subjects without OSA. Endothelial function was assessed by ultrasonographic measurement of flow-mediated dilatation ( FMD). Intima-media thickness ( IMT) and ankle-brachial index ( ABI) were determined by ultrasonography. Urinary 8-isoprostanes (Cayman Chemical, USA) were measured, applying mass spectrometry. Resistin (RayBio_ Human ResistinCat#: ELH-Resistin-001) plasma levels were detected by ELISA. Results In patients with OSA, flow-mediated dilatation was significantly lower than in control subjects (4·62% ±1·9) and (7·1% ±2·8), respectively ( P: 0·013). The prevalence of plaques in a.carotis communis was higher in OSA (16% versus 4%). The same is observed regarding a.tibialis posterior (81% vs. 29%). The average IMT and ABI in OSA and in the control group were, respectively, ( IMT − 800 µm versus. 666 µm); ( ABI −1·06 versus 1·20). Urinary isoprostanes were higher in OSA patients (0·091 versus 0·078) and correlated negatively to FMD ( r: −0·825, P: 0·00), IMT ( r: −0·324, P: 0·003) and ABI ( r: −0·226, P: 0·043). No association between resistin and the degree of vascular injury was found. Conclusions In comparison with the control group, increased prevalence of endothelial dysfunction and vascular damage was established in OSA patients without excessive daytime sleepiness. Urinary 8-isoprostanes (oxidative stress markers) are closely associated with FMD (endothelial dysfunction), IMT and ABI (vascular damage). Resistin plasma levels correlated neither to FMD, nor to IMT or ABI. [ABSTRACT FROM AUTHOR]

Background Determining predictive markers for the development of type 2 diabetes (T2D), particularly in young individuals, offers immense potential benefits in preventative medicine. Previous research examining serum fibroblast growth factor 21 ( FGF21) in humans has revealed equivocal relationships with clinical markers of metabolic dysfunction. However, it is unknown to what extent, if any, first-degree family history of T2D (mother or father of the participant diagnosed with T2D) level affects serum FGF21 levels. The aim of this study was to determine whether in healthy individuals with FH+ ( n = 18) and without FH- ( n = 17) a family history of T2D affects serum FGF21. Materials and methods Fasting serum and clinical, metabolic and anthropometric measures were determined using a cross-sectional design. Results Differences between groups for FGF21 were not significant ( FH+ = 266 pg/mL ± 51·4, FH = 180 pg/mL ± 29; Z = 0·97, P = 0·33). Adiponectin values were lower in FH+ (8·81 μg/mL ± 2·14) compared to FH- (10·65 μg/mL ± 1·44; F = 8·83, P = 0·01). Resistin was negatively correlated with FGF21 for all participants ( r = −0·38, P = 0·03), but no other clinical, metabolic, or serum markers were predictive for serum FGF21 in FH+ or FH-. Conclusions Serum FGF21 is not significantly different between FH+ and FH- in young, healthy individuals. Based upon the data of this pilot study, it is unclear whether serum FGF21 can be used as a stand-alone predictive marker for T2D in healthy subjects. [ABSTRACT FROM AUTHOR]

Problem Inflammation is a key process in the establishment and progression of endometriosis. Resistin, an adipocytokine, has biological properties linked to immunologic functions, but its role in endometriosis is unclear. Method of study Resistin gene expression was examined in eutopic and ectopic endometrial tissues from women with (n=25) or without (n=25) endometriosis. Resistin mRNA and protein levels were determined in endometrial tissue using quantitative real-time reverse transcription PCR and Western blotting, following adipokine profiling arrays. Results Resistin protein was detected in human endometrial tissues using an adipokine array test. Resistin mRNA and protein levels were significantly higher in ectopic endometrial tissue of patients with endometriosis than in normal eutopic endometrial tissue. Conclusion Our results indicate that resistin is differentially expressed in endometrial tissues from women with endometriosis and imply a role for resistin in endometriosis-associated pelvic inflammation. [ABSTRACT FROM AUTHOR]

Background Bisphenol A (BPA) exposure has been associated with increased incidence of diabetes and obesity in adults. Objectives To evaluate whether an association between BPA urinary levels and insulin resistance as well as adiponectin and resistin production and serum concentrations may occur in obese children. Methods Clinical and biochemical features of 141 obese children were collected. Serum resistin and adiponectin were evaluated. Insulin resistance and urinary BPA levels were assessed. Moreover, the effect of BPA on adiponectin and resistin gene expression in adipocytes from eight normal weight prepubertal children was investigated by quantitative real-time RT-PCR (qPCR). Results Direct association between BPA and homeostasis model assessment ( r = 0.23; p: 0.0069) and a strong inverse association between BPA and adiponectin have been found ( r = −0.48; p < 0.0001). In adipocytes, resistin expression was detected only after BPA treatment, while adiponectin expression resulted down-regulated after BPA exposure ( p < 0.05 at both 10 and 100 nM BPA concentrations). Conclusions We suggest the involvement of BPA in the development of insulin resistance in childhood obesity highlighting that urinary BPA levels are directly associated with insulin resistance regardless of BMI. This association may be explained, at least partly, by the findings that BPA affects resistin and adiponectin production in adipose tissue cultures. [ABSTRACT FROM AUTHOR]