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Aronia melanocarpa, a plant rich in anthocyanins, has been studied for its potential to regulate blood sugar and blood lipids, although the specific mechanism is not yet understood. This research aims to identify the differential bacterial flora and elucidate the mechanism by which it improves glucose and lipid metabolism disorders through 16S rDNA gene sequencing. The study reveals the protective effect of Aronia melanocarpa extract (AME) on liver damage in type 2 diabetic rats. Experimental results demonstrate that AME can effectively modulate the abundance of intestinal flora, reduce colon tissue damage, enhance the weight of diabetic rats, and lower levels of fasting blood sugar, low‐density lipoprotein (LDL), and triglycerides (TG). Additionally, liver morphology analysis shows that AME can effectively mitigate liver tissue structural damage in type 2 diabetic rats. In conclusion, AME regulates glucose and lipid metabolism by influencing intestinal flora, ultimately regulating glucose and lipid metabolism in type 2 diabetic rats. [ABSTRACT FROM AUTHOR]

Background: Antiretroviral therapy (ART)‐associated metabolic abnormalities, including impairment of glucose metabolism, are prevalent in adults living with HIV. However, the prevalence and pathogenesis of impaired glucose metabolism in children and adolescents living with HIV, particularly in sub‐Saharan Africa, are not well characterized. We investigated the prevalence of impaired glucose metabolism among children and adolescents living with perinatally infected HIV in Ghana. Methods: In this multicentre, cross‐sectional study, we recruited participants from 10 paediatric antiretroviral treatment clinics from January to June 2022 in 10 facilities in Greater Accra and Eastern regions of Ghana. We determined impaired glucose metabolism in the study sample by assessing fasting blood sugar (FBS), insulin resistance as defined by the homeostatic model assessment for insulin resistance (HOMA‐IR) index and glycated haemoglobin (HbA1c) levels. The prevalence of impaired glucose metabolism using each criterion was stratified by age and sex. The phenotypic correlates of glucose metabolism markers were also assessed among age, sex, body mass index (BMI) and waist‐to‐hip ratio (WHR). Results: We analysed data from 393 children and adolescents living with HIV aged 6–18 years. A little over half (205/393 or 52.25%) of the children were female. The mean age of the participants was 11.60 years (SD = 3.50), with 122/393 (31.00%) aged 6–9 years, 207/393 (52.67%) aged 10–15 years, and 62/393 (15.78%) aged 16–18 years. The prevalence rates of glucose impairment in the study population were 15.52% [95% confidence interval (CI): 12.26–19.45], 22.39% (95% CI: 18.54–26.78), and 26.21% (95% CI: 22.10–30.78) using HbA1c, HOMA‐IR, and FBS criteria, respectively. Impaired glucose metabolism detected by FBS and HOMA‐IR was higher in the older age group, whereas the prevalence of abnormal HbA1c levels was highest among the youngest age group. Age and BMI were positively associated with FBS and HOMA‐IR (p < 0.001). However, there was negative correlation of WHR with HOMA‐IR (p < 0.01) and HbA1c (p = 0.01). Conclusion: The high prevalence of impaired glucose metabolism observed among the children and adolescents living with HIV in sub‐Saharan Africa is of concern as this could contribute to the development of metabolic syndrome in adulthood. [ABSTRACT FROM AUTHOR]

The circadian timing system controls glucose metabolism in a time‐of‐day dependent manner. In mammals, the circadian timing system consists of the main central clock in the bilateral suprachiasmatic nucleus (SCN) of the anterior hypothalamus and subordinate clocks in peripheral tissues. The oscillations produced by these different clocks with a period of approximately 24‐h are generated by the transcriptional‐translational feedback loops of a set of core clock genes. Glucose homeostasis is one of the daily rhythms controlled by this circadian timing system. The central pacemaker in the SCN controls glucose homeostasis through its neural projections to hypothalamic hubs that are in control of feeding behavior and energy metabolism. Using hormones such as adrenal glucocorticoids and melatonin and the autonomic nervous system, the SCN modulates critical processes such as glucose production and insulin sensitivity. Peripheral clocks in tissues, such as the liver, muscle, and adipose tissue serve to enhance and sustain these SCN signals. In the optimal situation all these clocks are synchronized and aligned with behavior and the environmental light/dark cycle. A negative impact on glucose metabolism becomes apparent when the internal timing system becomes disturbed, also known as circadian desynchrony or circadian misalignment. Circadian desynchrony may occur at several levels, as the mistiming of light exposure or sleep will especially affect the central clock, whereas mistiming of food intake or physical activity will especially involve the peripheral clocks. In this review, we will summarize the literature investigating the impact of circadian desynchrony on glucose metabolism and how it may result in the development of insulin resistance. In addition, we will discuss potential strategies aimed at reinstating circadian synchrony to improve insulin sensitivity and contribute to the prevention of type 2 diabetes. [ABSTRACT FROM AUTHOR]

BACKGROUND: Lead (Pb) is an ancient toxic metal and is still a major public health issue. Our previous study found that Pb exposure promotes metabolic disorders in obese mice, but the molecular mechanisms remain unclear. The present study explored the effects of Pb exposure on glucose homeostasis in mice fed a normal diet (ND) and high-fat diet (HFD) from the perspective of gut microbiota. RESULTS: Pb exposure had little effect on glucose metabolism in ND mice, but exacerbated hyperglycemia and insulin resistance, and impaired glucose tolerance in HFD mice. Pb exposure impaired intestinal tight junctions and mucin expression in HFD mice, increasing intestinal permeability and inflammation. Moreover, Pb exposure altered the composition and structure of the gut microbiota and decreased short-chain fatty acids (SCFAs) levels in HFD mice. Correlation analysis revealed that the gut microbiota and SCFAs were significantly correlated with the gut barrier and glucose homeostasis. Furthermore, the fecal microbiota transplantation from Pb-exposed HFD mice resulted in glucose homeostasis imbalance, intestinal mucosal structural damage and inflammation in recipient mice. However, Pb did not exacerbate the metabolic toxicity in HFD mice under depleted gut microbiota. CONCLUSION: The findings of the present study suggest that Pb induces impairment of glucose metabolism in HFD mice by perturbing the gut microbiota. Our study offers new perspectives on the mechanisms of metabolic toxicity of heavy metals and demonstrates that the gut microbiota may be a target of action for heavy metal exposure. [ABSTRACT FROM AUTHOR]

Background: Alisol A can ameliorate glucose metabolism disorders, however, there is no data regarding its role in diabetic nephropathy (DN). The present work evaluates the role of Alisol A in DN and the underlying mechanism. Methods: RNA expression of circ_0001831, miR‐346, and lin‐28 homolog B (LIN28B) was detected by qRT‐PCR. Cell viability and proliferation were investigated by MTT assay and EdU assay, respectively. The inflammatory cytokines were examined by ELISAs. Oxidative stress was evaluated by the commercial kits. Protein expression was detected by western blotting. The interactions among circ_0001831, miR‐346, and LIN28B were identified by dual‐luciferase reporter assay and RIP assay. DN mouse model assay was used to analyse the effect of Alisol A on renal injury of diabetic mice. Results: HG treatment promoted HRMC proliferation, fibrosis, inflammation, and oxidative stress; however, these effects were reversed after Alisol A treatment. Alisol A treatment ameliorated STZ‐induced renal injury of diabetic mice. Additionally, circ_0001831 or LIN28B overexpression or miR‐346 downregulation relieved Alisol A‐induced effects under HG conditions. Mechanistically, circ_0001831 acted as a miR‐346 sponge, and LIN28B was identified as a target gene of miR‐346. Further, the regulation of circ_0001831 in HG‐induced HRMC dysfunction involved LIN28B. Conclusion: Alisol A ameliorated HG‐induced HRMC fibrosis, inflammation, and oxidative stress and STZ‐induced renal injury of diabetic mice by regulating the circ_0001831/miR‐346/LIN28B pathway. [ABSTRACT FROM AUTHOR]

Diabetes mellitus (DM) is a metabolic inflammatory disease with a high incidence worldwide. Patients with DM are at a high risk for all types of infections. Type 1 DM is characterised with immune destruction of pancreatic β cells, while type 2 diabetes is characterised with insulin resistance and β cell dysfunction, both of which result in disorders of glucose and lipid metabolism. This metabolic disorder causes functional defects of immune cells, aberrant production of inflammatory cytokines, dysregulated immune responses, advanced pathophysiological injury of the body, and increased mortality in populations with DM upon infections. Starting with the change of natural immune system in patients with DM, this paper focused on the enhanced severity of infections in DM and the underlying innate immune alterations in preclinical and clinical studies, aiming to better understand the influence of DM on the susceptibility, pathophysiology, and clinical outcomes in infections. [ABSTRACT FROM AUTHOR]

Introduction: Treatment strategies for depression based on interventions for glucose and lipid metabolism disorders are receiving increasing attention. Investigating the mechanism of their antidepressant effect and exploring new diagnostic and therapeutic biomarkers have attracted increasing attention. Dulaglutide, a long‐acting GLP‐1 receptor agonist, has been reported to alleviate cognitive deficits and neuronal damage. However, the antidepressant effect of dulaglutide and, especially, the underlying mechanism are still poorly understood. In this study, we aimed to explore the underlying biomarkers of depression and potential modulatory targets of dulaglutide in chronic mild stress (CMS) mice. Methods: Sixty mice were randomly divided into a control group (CON group), a CMS+Vehicle group (CMS+Veh group), a CMS+0.3 mg/kg dulaglutide group (Low Dula group), and a CMS+0.6 mg/kg dulaglutide group (High Dula group). Numerous behavioral tests, mainly the open field test, forced swimming test, and tail suspension test, were applied to evaluate the potential effect of dulaglutide treatment on anxiety‐ and depression‐like behaviors in mice exposed to chronic stress. Furthermore, a liquid chromatography–tandem mass spectrometry‐based metabolomics approach was utilized to investigate the associated mechanisms of dulaglutide treatment. Results: Three weeks of dulaglutide treatment significantly reversed depressive‐like but not anxiety‐like behaviors in mice exposed to chronic stress for 4 weeks. The results from the metabolomics analysis showed that a total of 20 differentially expressed metabolites were identified between the CON and CMS+Veh groups, and 46 metabolites were selected between the CMS+Veh and High Dula groups in the hippocampus of the mice. Comprehensive analysis indicated that lipid metabolism, amino acid metabolism, energy metabolism, and tryptophan metabolism were disrupted in model mice that experienced depression and underwent dulaglutide therapy. Conclusion: The antidepressant effects of dulaglutide in a CMS depression model were confirmed. We identified 64 different metabolites and four major pathways associated with metabolic pathophysiological processes. These primary data provide a new perspective for understanding the antidepressant‐like effects of dulaglutide and may facilitate the use of dulaglutide as a potential therapeutic strategy for depression. [ABSTRACT FROM AUTHOR]

The pathogenesis of diabetes is accompanied by increased levels of inflammatory factors, also known as "metabolic inflammation", which runs through the whole process of the occurrence and development of the disease. Mitochondria, as the key site of glucose and lipid metabolism, is often accompanied by mitochondrial function damage in type 2 diabetes mellitus (T2DM). Damaged mitochondria release pro‐inflammatory factors through damage‐related molecular patterns that activate inflammation pathways and reactions to oxidative stress, further aggravate metabolic disorders, and form a vicious circle. Currently, the pathogenesis of diabetes is still unclear, and clinical treatment focuses primarily on symptomatic intervention of the internal environment of disorders of glucose and lipid metabolism with limited clinical efficacy. The proinflammatory effect of mitochondrial damage‐associated molecular pattern (mtDAMP) in T2DM provides a new research direction for exploring the pathogenesis and intervention targets of T2DM. Therefore, this review covers the most recent findings on the molecular mechanism and related signalling cascades of inflammation caused by mtDAMP in T2DM and discusses its pathogenic role of it in the pathological process of T2DM to search potential intervention targets. [ABSTRACT FROM AUTHOR]

BACKGROUND: Foxtail millet (Setaria italica) is a whole millet grain that has been considered for improving the disorder of glucose and lipid metabolism. The purpose of the work is to explore the extraction and enrichment of polyphenols from foxtail millets which can regulate the disorder of glucose and lipid metabolism by increasing endogenous GLP‐1 (glucagon‐like peptide‐1). RESULTS: The optimum ultrasound‐assisted extraction (UAE) of foxtail millet polyphenols (FMPs) was as follows: 70 °C and 400 W and 70% ethanol concentration, further purification using macroporous resin. In vitro, the FMP eluent of 60% ethanol (FMP‐60) has the best effect in promoting GLP‐1 secretion from L cells among the different active components of FMP. Millet polyphenols (MPs) were obtained from finishing foxtail millet with the bran removed by the same extraction and purification method. Compared with MP‐60, FMP‐60 mainly included eight active phenolic constituents and contained more ferulic acid, p‐coumaric acid, 2‐hydroxycinnamic acid, and coniferaldehyde. After gavage treatment of diet‐induced obese (DIO) mice with FMP‐60, FMP‐60 promoted endogenous GLP‐1 secretion in mice and ameliorated disorders of glucolipid metabolism in DIO mice. CONCLUSION: FMP‐60 could improve glucose homeostasis and ameliorates metabolic disease by promoting the endogenous GLP‐1 level and preventing weight gain in DIO mice. © 2023 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

Introduction: Current use of combined hormonal contraceptives worsens glucose tolerance and increases the risk of type 2 diabetes mellitus at late fertile age, but the impact of their former use on the risk of glucose metabolism disorders is still controversial. Material and methods: This was a prospective, longitudinal birth cohort study with long‐term follow‐up consisting of 5889 women. The cohort population has been followed at birth, and at ages of 1, 14, 31 and 46. In total, 3280 (55.7%) women were clinically examined and 2780 also underwent a 2‐h oral glucose tolerance test at age 46. Glucose metabolism indices were analyzed in former combined hormonal contraceptive users (n = 1371) and former progestin‐only contraceptive users (n = 52) and in women with no history of hormonal contraceptive use (n = 253). Results: Compared with women with no history of hormonal contraceptive use, those who formerly used combined hormonal contraceptives for over 10 years had an increased risk of prediabetes (odds ratio [OR] 3.9, 95% confidence interval [CI]: 1.6–9.2) but not of type 2 diabetes mellitus. Former progestin‐only contraceptive use was not associated with any glucose metabolism disorders. The results persisted after adjusting for socioeconomic status, smoking, alcohol consumption, parity, body mass index and use of cholesterol‐lowering medication. Conclusions: Former long‐term use of combined hormonal contraceptives was associated with a significantly increased risk of prediabetes in perimenopausal women, which potentially indicates a need of screening for glucose metabolism disorders in these women. [ABSTRACT FROM AUTHOR]

Identifying non‐diabetic hyperglycaemia (NDH) and intervening to halt the progression to type 2 diabetes has become an essential component of cardiovascular and cerebrovascular risk reduction. Diabetes prevention programs have been instigated to address the increasing prevalence of NDH and type 2 diabetes by targeting lifestyle modifications. Evidence suggests that the risk of progression from NDH to type 2 diabetes declines with age, and that a diagnosis of type 2 diabetes in older adults is not associated with the same risk of adverse consequences as it is in younger age groups. The current definition of NDH is not adjusted based on a person's age. Therefore, there is debate about the emphasis that should be placed upon a diagnosis of NDH in older adults. This article will explore the evidence and current clinical practice surrounding dysglycaemia through the spectrum of different age ranges, and the potential implications this has for older adults. [ABSTRACT FROM AUTHOR]

Background: Early diagnosis of hospitalized elderly patients with infectious stress hyperglycaemia (ISH) is clinically important, especially under the global coronavirus disease 2019 (COVID-19) pandemic, as without timely prevention and effective treatment, it is likely to deteriorate into septic shock, thus worsening patient survival and complications. Moreover, cumulative studies have showed that patients with COVID-19 are reported to have a greater prevalence of hyperglycaemia. However, the underlying mechanism remained unknown. Aim and method: Systematic screening of specific biomarkers of serum exosome-derived microRNAs (sE-miRNAs) from ISH patient has not yet been reported. In this study, sE-miRNAs were derived from 10 elderly patients with ISH and 5 control patients with disease-match without hyperglycaemia (non-ISH). RNA sequencing identified that a total number of 49 sE-miRNAs with differential expression between ISH and control group.Ofwhich, top 22miRNAs ranked by sensitivity x specificity were chosen for further research. Moreover, 7 out of 22 miRNAs that related to glucose metabolism or immune disorder were picked up for further validation in an independent cohort consisting of 52 participants (31 ISH and 21 non-ISH). Result: A validation analysis revealed that three miRNAs (hsa-miR-21-5p, hsamiR- 335-5p and hsa-miR-28-3p) were statistically up-regulated in exosomes from ISH patients. In the validation cohort and discovery cohort, the AUC of three individual miRNAs ranged from 0.73 to 0.88. A logistic model combining three miRNAs achieved an AUC of 0.96. Besides, sE-miRNAs-based signatures effectively characterized patients' poor clinical outcome. Survival curve analysis showed that hsa-miR-335-5p, hsa-miR-28-3p but not hsa-miR-21-5p, were significantly closely related to mortality, and the combination of these three miRNAs could also predict patients outcome (p < .05). Conclusion: This study depicted the circulating exosomal miRNAs change in ISH patient, which could be used as a promising biomarker to detect ISH at an early stage and predict patients clinical outcome. [ABSTRACT FROM AUTHOR]

Background: Changes in vascular function are closely associated with the development of cardiovascular disease (CVD). Pulse wave velocity (PWV) is a potential indicator of vascular dysfunction; it allows noninvasive assessment of arterial stiffness. Currently, evidence for the effects of different classes of antidiabetic drugs on arterial stiffness remains limited. In this study, a network meta‐analysis (NMA) was performed to explore the associations between changes in arterial stiffness and first‐line antidiabetic drugs by evaluating PWV in patients with different metabolic abnormalities. Methods: We systematically searched several electronic databases for randomized controlled trials (RCTs) published from inception until 25 August 2022, without language restrictions. The primary outcome was the change in PWV (ΔPWV) in all included studies; subgroup analysis was performed for patients with abnormal glucose metabolism, including prediabetes and diabetes mellitus. NMA was performed to calculate the mean differences (MDs) with 95% confidence intervals (CIs) as effect sizes to evaluate the ΔPWV. Results: Among the 2257 candidate articles identified in the initial search, 18 RCTs were eventually included in the analysis. In all studies, two classes of new antidiabetic drugs, glucagon‐like peptide‐1 receptor (GLP‐1R) agonists and sSodium‐glucose co‐transporter 2 (SGLT‐2) inhibitors, improved arterial stiffness by decreasing PWV compared with placebo (MD = −1.11, 95% CI: −1.94 to 0.28) and (MD = −0.76, 95% CI: −1.45 to −0.08). A conventional antidiabetic drug, metformin, also showed similar efficacy compared with placebo (MD = −0.73, 95% CI: −1.33 to −0.12). Finally, in subgroup studies of patients with abnormal glucose metabolism diseases, GLP‐1R agonists (MD = −1.06, 95% CI: −2.05 to −0.10) significantly decreased PWV compared with placebo. Conclusion: Three classes of antidiabetic drugs—GLP‐1R agonists, SGLT‐2 inhibitors, and metformin—have the potential to improve arterial stiffness. Among the six classes of antidiabetic drugs analyzed, GLP‐1R agonists constitute the only class of drugs that improves arterial stiffness in patients with abnormal glucose metabolism diseases. [ABSTRACT FROM AUTHOR]

Glycosylphosphatidylinositol‐specific phospholipase D (GPLD1) is a specific enzyme for glycosylphosphatidylinositol (GPI) anchors, thereby exerting its biological functions by cleaving membrane‐associated GPI molecules. GPLD1 is abundant in serum, with a concentration of approximately 5−10 µg/mL. Previous studies have demonstrated that GPLD1 plays a crucial role in the pathogenesis of numerous chronic diseases including disorders of lipid and glucose metabolism, cancer, and neurological disorders. In the present study, we reviewed the structure, functions, and localization of GPLD1 in chronic diseases, as well as exercise‐mediated regulation of GPLD1, thus providing a theoretical support to develop GPLD1 as a new therapeutic target for chronic diseases. [ABSTRACT FROM AUTHOR]

Older patients are prone to multimorbidity or related polypharmacy, which may cause various adverse drug reactions (ADRs) and a high incidence of drug‐related health problems. Although not often noted, ADRs include nutrition‐related adverse reactions. Aging, multiple illnesses, mental and psychological problems, declining physical function, and environmental factors can lead to decreased food intake and increased metabolic stress in older people, resulting in energy imbalances that cause malnutrition. ADRs can lead to appetite loss, followed by decreased food intake, which in turn causes malnutrition and deficiencies of various nutrients. However, these nutrition‐related ADRs have received less attention. This review article describes drug–nutrition interactions, with a particular focus on older patients. Geriatr Gerontol Int 2023; 23: 465–477. Pharmacotherapy is a very important means of disease prevention and treatment for older patients. However, adverse drug reactions can have a significant negative impact on the health of older people. In this paper, the impact of drug therapy on nutritional status, dietary intake, the absorption and excretion of nutrients, and metabolism, with a focus on older people, is reviewed. [ABSTRACT FROM AUTHOR]

Aims: Diabetes mellitus is a common chronic disease of glucose metabolism. Endothelial dysfunction is an early event in diabetes complicated by cardiovascular disease. This study aimed to reveal the expression of BASP1 and its biological roles in endothelial cell dysfunction in diabetes complicated by cardiovascular disease. Materials and Methods: By analyzing the databases related to diabetes complicated with coronary heart disease, BASP1 was screened out as an upregulated gene. Human umbilical vein endothelial cells (HUVECs) and primary mouse aortic endothelial cells were treated with high glucose to establish cell models of diabetes‐related endothelial dysfunction, and the expression changes of BASP1 were verified by RT‐qPCR, western blot, and immunofluorescence. BASP1 was silenced or overexpressed by siRNA or overexpression plasmid, and its effects on cell migration, apoptosis, tube formation, inflammatory response, and ROS were detected. The possible signaling pathway of BASP1 was found and the mechanism of BASP1 on promoting the progression of endothelial dysfunction was explored using the EGFR inhibitor, gefitinib. Results: Bioinformatics analysis indicated that the expression of BASP1 in patients with diabetes mellitus and concomitant coronary heart disease was increased. High glucose induced the upregulation of BASP1 expression in endothelial cells, and showed a time‐dependent relationship. Silencing of BASP1 alleviated the damage of high glucose to endothelial cells. BASP1 regulated EGFR positively. The promoting effect of BASP1 on endothelial cell apoptosis may be achieved by regulating the EGFR pathway. Conclusion: BASP1 promotes endothelial cell injury induced by high glucose in patients with diabetes, which may be activated by activating the EGFR pathway. [ABSTRACT FROM AUTHOR]

Background: To investigate the relation of established glucose and lipid metabolism indexes and blood inflammatory biomarkers with severe periodontitis in systemically healthy patients.Methods: Systemically healthy stage III/IV periodontitis patients (case group) (n = 397), stage II periodontitis patients (n = 36), and periodontally healthy subjects (control group) (n = 285) were recruited. A periodontal examination, complete blood cell examination, and blood biochemical examination were conducted for all participants. Full-mouth apical films were taken for the case group. Both the case and control groups were divided by age into younger (≤35 years) and elder subjects. Multiple logistic regression analysis and Pearson correlation analysis were conducted. A logistic least absolute shrinkage and selection operator (LASSO) model was constructed for the younger subgroups.Results: Various glucose and lipid metabolism indexes and blood inflammatory biomarkers significantly differed between severe periodontitis patients and healthy controls, and the younger subgroups presented a greater degree of statistical differences than the elder ones. More pairs of periodontal parameters and blood indexes with significantly fair linear correlations were found in the younger patient subgroup. A logistic LASSO regression model containing eight blood indexes to assess a severe periodontitis outcome in younger subgroups showed satisfactory predictive ability.Conclusion: The present study revealed various glucose and lipid metabolism indexes and blood inflammatory biomarkers significantly differ between severe periodontitis patients and healthy controls, especially in the younger subgroups. A LASSO regression model could be a viable option to assess severe periodontitis risk for younger patients.Summary: The present study revealed significant differences in glucose and lipid metabolism indexes and blood inflammatory biomarkers between patients with severe periodontitis and periodontally healthy individuals, especially in younger subjects. This article is protected by copyright. All rights reserved. [ABSTRACT FROM AUTHOR]

Background and Objectives: Periodontitis is a highly prevalent disease in psychiatric patients, including those undergoing symptomatic treatment with second-generation antipsychotics. Some of these drugs, such as clozapine (CLO) and olanzapine (OLA), have prominent metabolic effects such as weight gain, hyperglycemia, and dyslipidemia, which are risk factors for periodontitis. In addition to the metabolic effects, there are reports of changes in salivary flow, gingival bleeding, and caries. In this context, we aimed to evaluate if the metabolic effects of OLA and CLO alter periodontal parameters in an animal model of periodontitis without the environmental and psychosocial biases inherent to human diseases. Methods: In the first set of experiments, male and female adult Wistar rats received oral administration of CLO, OLA, or vehicle for 45 days. They were evaluated for body mass composition and weight gain, blood glucose parameters (fasting and glucose tolerance and insulin resistance tests), and lipid profile (HDL, total cholesterol, and triglycerides). In a second set of experiments, the same measurements were performed in female rats exposed to the antipsychotics for 45 days and ligature-induced periodontitis on the 30th day of treatment. Macroscopic measurements of exposed roots, microtomography in the furcation region of the first molar, and histological evaluation of the region between the first and second molars were evaluated to assess bone loss. Additionally, gingival measurements of myeloperoxidase activity and pro-inflammatory cytokine TNF-α were made. Results: Only females exposed to OLA had more significant weight gain than controls. They also exhibited differences in glucose metabolism. Ligature-induced periodontitis produced intense bone retraction without changing the density of the remaining structures. The bone loss was even higher in rats with periodontitis treated with OLA or CLO and was accompanied by a local increase in TNF-α caused by CLO. These animals, however, did not exhibit the same metabolic impairments observed for animals without periodontitis. Conclusion: The use of clozapine and olanzapine may be a risk factor for periodontal disease, independent of systemic metabolic alterations. [ABSTRACT FROM AUTHOR]

Hyperglycemia is the most important factor leading to the complications of type 2 diabetes mellitus (T2DM). The primary condition for the treatment of T2DM is to change the glucose and lipid metabolism disorders in the liver and other insulin‐sensitive tissues. The current study aims to unearth the potential molecular mechanism of inhibiting liver gluconeogenesis to provide a new theoretical basis for the treatment of T2DM. High glucose (HG) induction of HepG2 cells followed by treatment with sequence‐similar family 3 member D (FAM3D). Dual specificity phosphatases 1 (DUSP1), zinc finger protein 36 (ZFP36), salt‐induced kinase 1 (SIK1), p‐SIK1, posphoenolpyruvate carboxykinase (PEPCK) and glucose‐6‐phosphatase (G6Pase) gene and protein expression level were detected by quantitative real‐time polymerase chain reaction and western blot. The PEPCK and G6Pase activities were detected by enzyme linked immunosorbent assay. Glucose production assay to determine glucose content. The RNA binding protein immunoprecipitation assay was used to detect the binding of ZFP36 to SIK1. FAM3D facilitated the expression of DUSP1 but suppressed the expression of gluconeogenesis‐related factors in an HG environment. The expression of ZFP36 was up‐regulated in an HG environment. ZFP36 could reverse the inhibition of gluconeogenesis caused by FAM3D. HG‐induced upregulation of ZFP36 was downregulated by overexpression of DUSP1. ZFP36 bound to SIK1, and downregulation of ZFP36 promoted SIK1 expression and inhibits gluconeogenesis. Our study demonstrated FAM3D inhibited gluconeogenesis through the DUSP1/ZFP36/SIK1 axis in an HG environment, which provided a new theoretical basis for exploring the pathogenesis and treatment strategy of T2DM. [ABSTRACT FROM AUTHOR]

Perceived discrimination is a significant risk factor for worse ageing health outcomes. Yet, the specific individual and relational stress pathways linking discrimination to disease are less understood, especially in the context of cardiometabolic health. We tested family stress and psychophysiological distress (negative affect and high‐risk lipid/fat metabolism) as mediators linking perceived discrimination to cardiometabolic morbidity and health appraisal over 20 years for midlife adults. Using data from participants who completed the Biomarker Project (2004–2009) of the Midlife in the U.S. project, and examining data over the study's three waves (1995–1996, 2004–2006, and 2013–2014), we used structural equation modelling to test pathways for participants who reported zero cardiometabolic conditions at baseline (n = 799). Greater Time 1 discrimination was associated with greater Time 2 family strain, which was in turn associated with worse negative affect; worse Time 2 negative affect was associated with worse Time 3 health appraisal; metabolic lipids risk did not serve as an indirect pathway to Time 3 cardiometabolic morbidity (χ2 = 147.74, p < 0.001; RMSEA = 0.056; CFI = 0.902; SRMR = 0.047). The inclusion of family in interventions to mitigate the impact of discrimination may be indicated for promoting cardiometabolic wellness. [ABSTRACT FROM AUTHOR]

Background: The objectives of this study were to determine the longer‐term trends in childhood obesity and glucose metabolism abnormalities among residents of Fukushima Prefecture 5 years after the Great East Japan Earthquake. Methods: We evaluated the changes in height, weight, body mass index (BMI), BMI SD score, fasting plasma glucose (FPG) concentration, and hemoglobin A1c (HbA1c) among elementary and junior high school residents who had lived in the evacuation zone between 2011 and 2015. Results: Of the residents, 11,112 received health checks in 2011, while in 2012, 2013, 2014, and 2015, 5,737, 4522, 4297 and 3405 received health checks, respectively. The mean BMI SD score for all participants in 2011 was 0.149, and this score gradually decreased from 2011 to 2015. FPG levels and HbA1c levels for all participants with a BMI value +2SD or more in 2011 were higher than those in residents with a BMI value of less than +2SD. The frequency of participants with a FPG level of 126 mg/dl or more and the frequency of participants with a HbA1c level of 6.5% or more in 2011 were higher than those in 2012, 2013, and 2015. Conclusions: These results suggest that a number of pediatric residents suffered from obesity and glucose metabolism abnormalities. However, the longer‐term observations indicated an improvement in obesity and glucose metabolism abnormalities. There was a strong association observed between obesity and glucose metabolism, thus, it is important to continue with health checks for children with obesity and strive to improve their health. [ABSTRACT FROM AUTHOR]

The article focuses on the concept of the stress hyperglycaemia ratio (SHR) as a measure of relative hyperglycaemia in hospitalized patients, exploring its association with mortality and its potential implications for clinical management. Topics discussed include the performance of SHR in identifying patients at risk of deterioration, discrepancies in SHR measurement across different pathologies, and the need for further research to elucidate the relationship between SHR and clinical outcomes.

Insulin degludec/insulin aspart Low fasting glucose-to-estimated average glucose ratio was associated with superior response to insulin degludec/aspart compared with basal insulin in patients with type 2 diabetes, Jang 85-93. Type 1 diabetes mellitus Impact of flash glucose monitoring on glycemic control varies with the age and residual -cell function of patients with type 1 diabetes mellitus, Zhang 552-559. Diabetes mellitus type 2 Current status of oral antidiabetic drug prescribing patterns based on the body mass index for Japanese type 2 diabetes mellitus patients and yearly changes in diabetologists' prescribing patterns from 2002 to 2019 (JDDM61), Yagi 65-73. 2A protease Immunohistochemical detection of enteroviruses in pancreatic tissues of patients with type 1 diabetes using a polyclonal antibody against 2A protease of Coxsackievirus, Jimbo 435-442. Type 2 diabetes mellitus Bariatric surgery versus medical treatment in mildly obese patients with type 2 diabetes mellitus in Japan: Propensity score-matched analysis on real-world data, Seki 74-84. [Extracted from the article]

Exposure to fine particulate matter (PM2.5) was associated with an increased incidence of liver metabolic disease. Melatonin has been shown to prevent liver glucolipid metabolism disorders. However, whether melatonin could rescue PM2.5‐induced liver metabolic abnormalities remains uncertain. This study was to evaluate the mitigating effect of melatonin on PM2.5‐accelerated hepatic glucose metabolism imbalance in vivo and in vitro. Schiff periodic acid shiff staining and other results showed that PM2.5 led to a decrease in hepatic glycogen reserve and an increase in glucose content, which was effectively alleviated by melatonin. Targeted lipidomics is used to identify lipid biomarkers associated with this process, including glycerolipids, glycerophospholipids, and sphingolipids. In addition, gene microarray and quantitative polymerase chain reaction analysis of ApoE−/− mice liver suggested that PM2.5 activated the miR‐200a‐3p and inhibited DNAJB9, and the targeting relationship was verified by luciferase reports for the first time. Further investigation demonstrated that DNAJB9 might motivate endoplasmic reticulum (ER) stress by regulating Ca2+ homeostasis, thus altering the protein expression of GSK3B, FOXO1, and PCK2. Meanwhile, melatonin effectively inhibited miR‐200a‐3p and glucose metabolism disorder. Knockout of miR‐200a‐3p in L02 cells revealed that miR‐200a‐3p is indispensable in the damage of PM2.5 and the therapeutic effect of melatonin. In summary, melatonin alleviated PM2.5‐induced liver metabolic dysregulation by regulating ER stress via miR‐200a‐3p/DNAJB9 signaling pathway. Our data provide a prospective targeted therapy for air pollution‐related liver metabolism disorders. [ABSTRACT FROM AUTHOR]

Previous studies have indicated that indolepropionic acid (IPA), derived from dietary tryptophan via gut microbiota conversion, is negatively correlated with type 2 diabetes mellitus and systemic low‐grade inflammation. However, the effects of IPA administration on obesity, as well as the underlying mechanisms, remain unclear. In the present study, we observed that obesity leads to a dramatic reduction in IPA levels in both the serum and colonic mucosa, and IPA supplementation exerted beneficial effects on weight, as well as on glucose and lipid metabolism disorders. In adipose tissue, IPA treatment had no direct effect on adipocyte differentiation, but it significantly ameliorated adipose inflammation, thus preventing adipocyte enlargement. Moreover, IPA administration promoted gut integrity, increased the expression of tight junction proteins, and downregulated colonic inflammation; these effects were demonstrated to have a poor relationship with gut microbiota composition. Mechanistically, IPA significantly promoted the expansion of the tuft cell lineage in the gut and increased the secretion of interleukin‐25 both in vivo and ex vivo, which contributes to the integrity of the gut barrier. This may partly depend on the free fatty acid receptor 3 pathway in tuft cells. Overall, our results demonstrate that IPA supplementation prevents the development of high‐fat diet‐induced obesity and metabolic disorders by restoring tuft cell‐interleukin‐25‐mediated colonic barrier integrity; hence, IPA could be a potential agent for treatment of obesity. [ABSTRACT FROM AUTHOR]

Summary: Increased intestinal permeability has an important role in metabolic dysregulation. In this cross‐sectional study, we examined whether serum intestinal permeability marker zonulin and related pro‐inflammatory molecules were associated with the oral disposition index, a predictor for the development of type 2 diabetes, in a cohort of children and adolescents with overweight and obesity. Ninety‐two children and adolescents were recruited [Male: 43; 12.7 (2.35) years; BMI SDS: 2.7 (0.96)]. Anthropometric and clinical parameters, lipid profile, glucose metabolism and plasma levels of zonulin, lipopolysaccharide‐binding protein and Interleukin‐6 were measured. We found an association between oral disposition index and zonulin (β = −0.243; p = 0.019) and age (β = −0.307; p = 0.004), independent of sex and BMI SDS [R2 = 0.16; p = 0.005]. Our results show an association between serum zonulin concentration and oral disposition index supporting the hypothesis of increased intestinal permeability as a possible risk factor for glucose metabolism dysregulation in children and adolescents with obesity. [ABSTRACT FROM AUTHOR]

Aim: Studies using oral glucose tolerance tests (OGTT) have shown that impaired glucose metabolism presents in the early stages of schizophrenia (SCZ). However, there is a lack of studies on changes in glucose metabolism with the stage of the disease. We first explored the features of glucose metabolic pattern at different phases of male SCZ. Methods: We recruited 83 male first episode drug‐naïve patients with SCZ (FEDN‐SCZ) and 64 male chronic patients with SCZ (CH‐SCZ), as well as 14 male healthy controls. The Positive and Negative Syndrome Scale (PANSS) was used to assess the psychopathology of patients. OGTT, fasting plasma glucose and lipid profiles of all participants were examined. Results: While the impaired glucose tolerance (IGT) rate of male SCZ patients was higher than that of HC (P <.05), there was no difference in IGT prevalence between FEDN‐SCZ and CH‐SCZ. In male FEDN‐SCZ, LDL (OR = 2.64, 95% CI = 1.11–6.29, P =.028) and PANSS total score (OR = 1.03, 95% CI = 1.00–1.06, P =.046) were positively correlated with IGT; in male CH‐SCZ, BMI (OR = 1.7, 95% CI = 1.08–2.67, P =.023), PANSS total score (OR = 0.82, 95% CI = 0.70–0.96, P =.015) and positive symptoms (OR = 0.45, 95% CI = 0.20–0.99, P =.046) were significantly correlated with IGT. Conclusions: Our findings reflect different glucose metabolism patterns in different stages of SCZ. [ABSTRACT FROM AUTHOR]

Background: Increased production of reactive oxygen species (ROS) and oxidative stress are known to play a key role in the pathogenesis of type 2 diabetes (T2D); however, the relationship between genes encoding a multi‐subunit ROS‐generated enzyme NADPH oxidase and disease susceptibility remains unexplored. Aims: The present pilot study investigated whether single‐nucleotide polymorphisms (SNP) at the RAC1 gene (Rac family small GTPase 1), a molecular switcher of NADPH oxidase, are associated with the risk of T2D, glucose metabolism and redox homeostasis. Materials & Methods: DNA samples from 3206 unrelated Russian subjects (1579 T2D patients and 1627 controls) were genotyped for six common SNPs rs4724800, rs7784465, rs10951982, rs10238136, rs836478 and rs9374 of RAC1 using the MassArray‐4 system. Results: SNP rs7784465 was associated with an increased risk of T2D (p =.0003), and significant differences in the RAC1 haplotypes occurred between the cases and controls (p =.005). Seventeen combinations of RAC1 genotypes showed significant associations with T2D risk (FDR <0.05). Associations of RAC1 polymorphisms with T2D were modified by environmental factors such as sedentary lifestyle, psychological stresses, a dietary deficit of fresh fruits/vegetables and increased carbohydrate intake. RAC1 polymorphisms were associated with biochemical parameters in diabetics: rs7784465 (p =.015) and rs836478 (p =.028) with increased glycated haemoglobin, rs836478 (p =.005) with increased fasting blood glucose, oxidized glutathione (p =.012) and uric acid (p =.034). Haplotype rs4724800A–rs7784465C–rs10951982G–rs10238136A–rs836478C–rs9374G was strongly associated with increased levels of hydrogen peroxide (p <.0001). Conclusion: Thus, polymorphisms in the RAC1 gene represent novel genetic markers of type 2 diabetes, and their link with glucose metabolism and disease pathogenesis is associated with the changes in redox homeostasis. [ABSTRACT FROM AUTHOR]

Prolonged excess of glucocorticoids (GCs) has adverse systemic effects leading to significant morbidities and an increase in mortality. Metabolic alterations associated with the high level of the GCs are key risk factors for the poor outcome. These include GCs causing excess gluconeogenesis via upregulation of key enzymes in the liver, a reduction of insulin sensitivity in skeletal muscle, liver and adipose tissue by inhibiting the insulin receptor signalling pathway, and inhibition of insulin secretion in beta cells leading to dysregulated glucose metabolism. In addition, chronic GC exposure leads to an increase in visceral adipose tissue, as well as an increase in lipolysis resulting in higher circulating free fatty acid levels and in ectopic fat deposition. Remission of hypercortisolism improves these metabolic changes, but very often does not result in full resolution of the abnormalities. Therefore, long‐term monitoring of metabolic variables is needed even after the resolution of the excess GC levels. [ABSTRACT FROM AUTHOR]

Prolactin, a hormone that has been studied for almost a century, has evolved from a reproductive regulator to a key player in metabolic health. Initially identified for its lactogenic role, the impact of prolactin on glucose and lipid metabolism became evident in the 1970s, leading to a paradigm shift in our understanding. Deviations in prolactin levels, including hyperprolactinaemia and hypoprolactinaemia, have been associated with adverse effects on glucose and lipid metabolism. Mechanistically, prolactin regulates metabolic homoeostasis by maintaining islet abundance, regulating the hypothalamic energy regulatory centre, balancing adipose tissue expansion, and regulating hepatic metabolism. Given the widespread use of pharmaceutical agents that affect prolactin levels, it is important to examine prolactin-related metabolic effects. Recently, a profound exploration of the intricate metabolic role of prolactin has been conducted, encompassing its rhythm-dependent regulatory influence on metabolism and its correlation with cognitive impairment associated with metabolic diseases. In this review, we highlight the role of prolactin as a metabolic regulator, summarise its metabolic effects, and discuss topics related to the association between prolactin and metabolic comorbidities., (© 2024 John Wiley & Sons Ltd.)

Angiopoietin‐like protein (ANGPTL) 4 is a key factor in the regulation of lipid and glucose metabolism in metabolic diseases. ANGPTL4 is highly expressed in various cancers, but the regulation of energy metabolism in tumours remains to be determined. This study explored the role of ANGPTL4 in aerobic glycolysis, glutamine consumption and fatty acid oxidation in nonsmall cell lung cancer (NSCLC) cells. Two NSCLC cell lines (A549 and H1299) were used to investigate the role of ANGPTL4 in energy metabolism by tracer techniques and with Seahorse XF technology in ANGPTLs4 knockdown cells. RNA microarrays and specific inhibitors were used to identify targets in ANGPTLs4‐overexpressing cells. The results showed that knockdown of ANGPTLs4 could inhibit energy metabolism and proliferation in NSCLC. ANGPTLs4 had no significant effect on glycolysis but affected glutamine consumption and fatty acid oxidation. Knockdown of ANGPTLs4 also significantly inhibited tumour metastasis and energy metabolism in mice and had a weak effect on glycolysis. RNA microarray analysis showed that ANGPTLs4 significantly affected glutaminase (GLS) and carnitine palmitoyl transferase 1 (CPT1). ANGPTLs4‐overexpressing cells were exposed to a glutamine deprivation environment, and cell proliferation and energy metabolism were significantly decreased but still differed from normal NSCLC cells. Treatment of ANGPTLs4‐overexpressing cells with GLS and CPT1 inhibitors simultaneously prevented the regulatory effects on cell proliferation and energy metabolism. ANGPTLs4 could promote glutamine consumption and fatty acid oxidation but not glycolysis or accelerate energy metabolism in NSCLC. [ABSTRACT FROM AUTHOR]

Aims: Liver cirrhosis increases the risk of developing dysglycaemia (pre-diabetes and diabetes), thus people with cirrhosis should undergo regular screening for dysglycaemia. The utility of screening using the laboratory glycated haemoglobin (HbA1c) test has been questioned in this setting. This study examines the relationship between different potential screening modalities: 75 g oral glucose tolerance test (OGTT) and HbA1c, using continuous glucose monitoring (CGM) as a comparator. Methods: Participants ≥18 years with no known diabetes, were recruited from a gastroenterology cirrhosis surveillance register. Study measurements included a 75 g OGTT, laboratory HbA1c and two weeks of 'blinded' CGM (Freestyle Libre Pro). The possibility of intravascular haemolysis affecting HbA1c interpretation was also assessed. Results: All 20 participants had compensated cirrhosis. OGTT tended to diagnose more dysglycaemia (N = 7) than did HbA1c (N = 4). Bland-Altman analysis showed laboratory and CGM-estimated HbA1c were broadly comparable, with a difference of 4mmol/mol (95% CI -3 to 12), or 0.4% (95% CI -0.3 to 1.1). Laboratory HbA1c tended to be higher than the CGM-estimated HbA1c, perhaps reflecting positive lifestyle changes in participants during their two weeks of wearing 'blinded' CGM (Hawthorne effect). In the population studied, there was no evidence that haemolysis affected interpretation of HbA1c results. Conclusions: In the setting of compensated cirrhosis, the OGTT and HbA1c remain standard screening test for diabetes, but multiple studies show the OGTT diagnoses more people with dysglycaemia than does the HbA1c. Blinded CGM in an ambulatory, real world setting provides additional insights into glycaemic excursions but cannot be used to diagnose dysglycaemia. [ABSTRACT FROM AUTHOR]

Aims/Introduction: Glucose metabolic disorder is the main cause for type 2 diabetes progression. Exploring the molecular mechanisms of metabolic disorder are crucial for type 2 diabetes treatment. Materials and Methods: Micro ribonucleic acid (miR)‐363, NOTCH1 and forkhead box C2 (FOXC2) expressions in high glucose (HG)‐treated HepG2 cells and the livers of type 2 diabetes mellitus rats were assessed using quantitative polymerase chain reaction. Protein levels of NOTCH1, FOXC2 and phosphatidylinositol 3‐kinase (PI3K)/serine/threonine protein kinase (Akt)‐related proteins were evaluated using western blot. Lipid accumulation was determined using Oil Red O staining. Then glucose consumption, blood glucose level and glycogen content were detected using kits. Finally, dual luciferase reporter assay was used to verify the binding relationship between miR‐363 and NOTCH1, and the binding relationship between miR‐363 and FOXC2. Results: MiR‐363 was significantly upregulated in the livers of diabetic rats and HG‐induced HepG2 cells, whereas NOTCH1 and FOXC2 were downregulated. In HG‐induced HepG2 cells, miR‐363 inhibitor markedly increased glucose consumption and uptake, and reduced accumulation of lipid droplets. Then NOTCH1 and FOXC2 were identified as downstream targets of miR‐363. NOTCH1 overexpression or FOXC2 overexpression could ameliorate glucose and lipids metabolism disorder in type 2 diabetes model cells. In addition, we found that FOXC2 inhibition abolished the effect of NOTCH1 overexpression on HG‐induced HepG2 cells. Finally, we proved that the PI3K/Akt pathway was the downstream pathway of FOXC2. Conclusion: MiR‐363 was considered as a key regulator of glucose and lipids metabolism in type 2 diabetes mellitus, which regulated PI3K/Akt axis by targeting NOTCH1 and FOXC2, thus leading to hepatic glucose and lipids metabolism disorder in type 2 diabetes. [ABSTRACT FROM AUTHOR]

Aims To evaluate the performance of the WATCH-DM risk score, a clinical risk score for heart failure (HF), in patients with dysglycaemia and in combination with natriuretic peptides (NPs). Methods and results Adults with diabetes/pre-diabetes free of HF at baseline from four cohort studies (ARIC, CHS, FHS, and MESA) were included. The machine learning-[WATCH-DM(ml)] and integer-based [WATCH-DM(i)] scores were used to estimate the 5-year risk of incident HF. Discrimination was assessed by Harrell's concordance index (C-index) and calibration by the Greenwood-Nam-D'Agostino (GND) statistic. Improvement in model performance with the addition of NP levels was assessed by C-index and continuous net reclassification improvement (NRI). Of the 8938 participants included, 3554 (39.8%) had diabetes and 432 (4.8%) developed HF within 5 years. The WATCH-DM(ml) and WATCH-DM(i) scores demonstrated high discrimination for predicting HF risk among individuals with dysglycaemia (C-indices = 0.80 and 0.71, respectively), with no evidence of miscalibration (GND P =0.10). The C-index of elevated NP levels alone for predicting incident HF among individuals with dysglycaemia was significantly higher among participants with low/intermediate (<13) vs. high (=13)WATCH-DM(i) scores [0.71 (95% confidence interval 0.68-0.74) vs. 0.64 (95% confidence interval 0.61-0.66)]. When NP levels were combined with the WATCH-DM(i) score, HF risk discrimination improvement and NRI varied across the spectrum of risk with greater improvement observed at low/intermediate risk [WATCH-DM(i)<13] vs. high risk [WATCH-DM(i) =13] (C-index = 0.73 vs. 0.71; NRI = 0.45 vs. 0.17). Conclusion TheWATCH-DM risk score can accurately predict incident HF risk in community-based individuals with dysglycaemia. The addition of NP levels is associated with greater improvement in the HF risk prediction performance among individuals with low/intermediate risk than those with high risk. [ABSTRACT FROM AUTHOR]

Maternal lipopolysaccharide (LPS) exposure during pregnancy induces metabolic abnormalities in male offspring, but the underlying mechanisms remain unclear. The purpose of this study was to investigate the effects of maternal LPS exposure during pregnancy on metabolic profiling of maternal serum and male fetal liver using Liquid Chromatograph Mass Spectrometer techniques. From day 15 to day 17 of gestation, pregnant mice were administered intraperitoneal LPS (experimental group) (50 μg/kg/d) or saline (control group). On day 18 of gestation, maternal serum and male fetal liver were collected. After LPS exposure, levels of 38 and 75 metabolites, mainly glycerophospholipid and fatty acid metabolites, were altered in maternal serum and male fetal liver, respectively. It was found that in maternal serum and male fetal livers, the glycerophospholipids containing saturated fatty acids (SFAs) and the SFAs were upregulated, while the glycerophospholipids containing polyunsaturated fatty acids (PUFAs) and the PUFAs were downregulated. This concordance between maternal and fetal alterations in glycerophospholipid and fatty acid metabolites may be a metabolomic signature of the early intrauterine period and may provide insight into the mechanisms by which maternal LPS exposure induces disorders of glucose metabolism in male offspring. [ABSTRACT FROM AUTHOR]

Conclusion: Even in patients with T2D with HbA1c >9%, IDegLira treatment achieved glycaemic control with a high proportion of patients achieving HbA1c <7% and clinically important composite endpoints of HbA1c <7% without hypoglycaemia and/or weight gain. PE029 Effect of Dexamethasone treatment in patients with COVID - 19: A survey of Mongolian patients Bilguun Erdenechuluun SP * sp and Altaisaikhan Khasag Central Hospital of the Mongolian National University of Medical Sciences, Department of Endocrinology Objective: To study effect of dexamethasone treatment in patients with COVID-19 who are admitted to the university hospital. October 7(Thu)-9(Sat), 2021 Clinical Diabetes and Therapeutics PE002 Effect of SGLT2 inhibitors on weight reduction in overweight and obese population without dia... Yun Kyung Cho SP 1,* sp , Ye-Jee Kim SP 2 sp and Chang Hee Jung SP 3,4 sp SP 1 sp Hallym University Sacred Heart Hospital, Hallym University College of Medicine, Department of Internal Medicine, SP 2 sp Asan Medical Center, University of Ulsan College of Medicine, Department of Clinical Epidemiology and Biostatistics, SP 3 sp Asan Medical Center, University of Ulsan College of Medicine, Department of Internal Medicine, SP 4 sp Asan Medical Center, Asan Diabetes Center Objective: We aimed to evaluate the efficacy of sodium-glucose cotransporter 2 (SGLT2) inhibitors to manage obesity in non-diabetic overweight or obese patients. [Extracted from the article]

Background: In recent years, studies have revealed that cognition may be impaired by glucose metabolism disorder. Meanwhile, physical activity has been demonstrated to maintain blood glucose. This meta‐analysis was conducted to assess the effect of physical activity on cognition in patients with diabetes and provide evidence for the treatment of cognition impairment among them. Methods: We searched studies published in five databases from 1 January 1984 to 29 August 2020. A random‐effect or fixed‐effect meta‐analysis was used to estimate the pooled effect of physical activity on the change of cognition throughout intervention duration and post‐intervention cognition scores by standardized mean difference (SMD) and its 95% confidence interval (CI). We used funnel plots to evaluate the publication bias, I2 statistic to evaluate the heterogeneity and did subgroup analysis stratified by sample size and follow‐up time. Results: Five eligible studies involving 2581 patients with diabetes were included. The pooled effect of physical activity on cognition improvement in patients with diabetes was significant (SMD = 0.98, 95% CI: 0.34–1.62), while the effect on post‐intervention cognition scores was not significant (SMD = 0.35, 95% CI: −0.04–0.73). In the subgroup analysis, the pooled effect was significantly higher in studies of follow‐up time less than 1 year (SMD = 2.14, 95% CI: 1.63–2.64), while observing no significant effect in studies of follow‐up time over 1 year (SMD = 0.10, 95% CI: −0.11–0.32). Conclusions: Physical activity is beneficial to improving cognition in patients with diabetes. However, the long‐term effect needs to be explored in future studies. [ABSTRACT FROM AUTHOR]

The high plasma glucose induced in glucose metabolism disorders leads to the non‐enzymatic glucose‐dependent modification (glycation) of type 1 collagen, which is an essential component of bone tissue. The glycation of proteins induces the formation of advanced glycation end‐products, such as carboxymethyl arginine, which is preferentially generated in glycated collagen. However, the effect of advanced glycation end‐product formation on the characteristics of type 1 collagen remains unclear due to the lack of suitable in vitro experimental systems analyzing type 1 collagen. Here, we show that the glycation of type 1 collagen can be analyzed in vitro using a goldfish‐scale bone model. Our study using these scales provides evidence that the advanced glycation end‐product formation in type 1 collagen induced by glyoxal, the carboxymethyl arginine inducer, facilitates the crosslinking of type 1 collagen, decreasing both its strength and flexibility. [ABSTRACT FROM AUTHOR]

Cognitive dysfunction is one of the complications of diabetes. Unfortunately, there is no effective methods to block its progression currently. One of the pathophysiological mechanisms is synaptic protein damage and neuronal signal disruption because of glucose metabolism disorder. Dystroglycan protein, located in the post‐synaptic membrane of neurons, links the intracellular cytoskeleton with extracellular matrix. Abnormal expression of dystroglycan protein affects neuronal biological functions and leads to cognitive impairment. However, there are no relevant studies to observe the changes of β‐dystroglycan protein in diabetes rat brain and in primary neurons under high glucose exposure. Our data demonstrated the alterations of cognitive abilities in the diabetic rats; β‐dystroglycan protein degradation occurred in hippocampal and cortical tissues in diabetic rat brain. We further explored the mechanisms underlying of this phenomenon. When neurons are exposed to high glucose environment in long‐term period, microRNA‐132 (miR‐132) would be down‐regulated in neurons. Matrix Metalloproteinases‐9 (MMP‐9) mRNA, as a target of miR‐132, could be up‐regulated; higher expression and overlay activity of MMP‐9 protein could increase β‐DG protein degradation. In this way, β‐DG degradation may affect structure and functions among the synapses, which related to cognition decline. It may provide some theoretical basis for elucidating the molecular mechanism of diabetes‐induced cognitive dysfunction. [ABSTRACT FROM AUTHOR]

Background: Iron status has been linked with impaired glucose metabolism (IGM), type 2 diabetes mellitus (T2DM) and the metabolic syndrome (MetS), but the role of hepatic steatosis or iron overload on these associations remains uncertain. Methods: We analysed data from 2310 participants without known T2DM of the population‐based Study of Health in Pomerania (SHIP‐TREND, Germany) through logistic regression models. We tested additive and multiplicative interactions between ferritin and hepatic steatosis or iron overload. Results: Serum ferritin was positively associated with IGM (OR per 100 µg/L: 1.11 [1.01, 1.23]), T2DM (OR per 100 µg/L: 1.20 [1.06, 1.36]) and MetS (OR per 100 µg/L: 1.11 [1.02, 1.20]) in the total population as well as in participants without hepatic iron overload. However, the synergistic effect of higher ferritin concentrations and hepatic iron overload showed stronger associations with IGM and T2DM. Similarly, while ferritin was positively associated with T2DM and MetS even in the absence of hepatic steatosis, the synergistic effect of higher ferritin concentrations and hepatic steatosis showed stronger associations with IGM, T2DM and MetS. Transferrin was associated with isolated impaired glucose tolerance but not with T2DM and MetS. Conclusions: Our study suggests that ferritin may be associated with glucose metabolism disorders and MetS even in people without hepatic steatosis or iron overload. However, in individuals with higher ferritin concentrations, the presence of hepatic steatosis may indicate stronger risk for glucose metabolism disorders and MetS, while the presence of hepatic iron overload may indicate stronger risk only for glucose metabolism disorders. [ABSTRACT FROM AUTHOR]

This work focused on the separation of the active ingredients of maca (Lepidium meyenii Walpers) and evaluated the antioxidative capability of these components with effects on improving glucose and lipid metabolism in insulin‐resistant HepG2 cells. DPPH free radical scavenging and reducing power assays were used to evaluate the antioxidant activity of maca extracts. An insulin‐resistant HepG2 cell model induced by glucose, fructose, oleic acid, and palmitic acid was adopted to investigate the effects of maca extracts on regulating glucose and lipid metabolism in this study. LC‐MS/MS was then used for determination of the maca n‐butanol (NBT) subfraction. The results showed that maca ethanol extract and subfractions of this extract exhibited certain antioxidant capacity. Furthermore, the NBT subfraction reversed the disorders in glucose and lipid metabolism in insulin‐resistant HepG2 cells and significantly increased the mRNA expression of phosphoinositide 3‐kinases (PI3K) and AKT in insulin‐resistant HepG2 cells in a dose‐dependent manner. In addition, the LC‐MS/MS results showed that the NBT subfraction contained many active ingredients. Overall, this study suggests that the NBT subfraction of the ethanol extract rich in glucosinolates modulates insulin resistance via PI3K/AKT activation in insulin‐resistant HepG2 cells and might exert potentially beneficial effects in improving or treating glucose and lipid metabolic disorders. [ABSTRACT FROM AUTHOR]

Alcoholic injury can alter the hormonal signaling pathway and lead to glucose and lipid metabolism disorders. In this study, we investigated whether the strength training could exert protective effects against the alterations caused by ethanol consumption on prostatic metabolism. A UChB, ethanol‐preferring rats were used in this study. Strength training was conducted for 3 days per week for 13 weeks, rats performed jumps in water carrying a weight load strapped to their chests as part of a strength training protocol. The reduced alcohol consumption by strength training was accompanied by increased glucose, serum lipid profile, total protein levels, and reduced hormonal levels. The results of protein expression of prostatic tissues in the ethanol‐ and strength training‐treated groups indicated that "steroidal hormone receptors," "fatty acid translocation," and "cell regulation" were significantly different between ethanol‐ and strength training‐treated groups. Taken together, these findings show that strength training effectively ameliorated prostatic injuries in alcoholic rats at least partially by acting on lipids receptors and steroidal hormone receptors pathway, suggesting the strength training as a potential novel therapeutic strategy for treating prostate injuries caused by ethanol. [ABSTRACT FROM AUTHOR]

Background: Previous positron emission tomography studies have reported the changes of cerebral glucose metabolism in bipolar disorder. However, the findings across studies remain controversial, containing differing results. Methods: A systematic literature search of the PubMed, Embase, Cochrane Library, and Web of Science databases was conducted. We conducted a voxel‐wide meta‐analysis of cerebral glucose metabolism studies, using the seed‐based mapping approach, in patients with bipolar disorder (BD). Results: We identified 7 studies suitable for inclusion, which included a total of 126 individuals with BD and 160 healthy controls. The most consistent and robust findings were an increase in cerebral glucose metabolism in the right precentral gyrus and a decrease in the left superior temporal gyrus, left middle temporal gyrus, and cerebellum. Additionally, the sex distribution and illness duration had significant moderating effects on cerebral glucose metabolism alterations. Conclusions: Cerebral glucose metabolism alterations in these brain regions are likely to reflect the disease‐related functional abnormalities such as emotion and cognition. These findings contribute to a better understanding of the neurobiological underpinnings of bipolar disorder. Limitations. This study was done at a study level and cannot be addressed at the patient level. Subgroup analysis of BD I and BD II is not possible due to limited literature data. [ABSTRACT FROM AUTHOR]

Objectives: Comparative data on glucose disorders using fasting blood samples between people living with HIV (PLWH) and the general population are lacking. The objective of this study was to compare the prevalence and risk factors of obesity and disturbances in glucose homeostasis between PLWH treated with modern antiretroviral therapy and the general population. Methods: Adjusted prevalence of obesity, features of insulin resistance (triglyceride:high‐density lipoprotein cholesterol ratio and alanine aminotransferase), impaired fasting glucose (IFG), diabetes mellitus (DM) and combined dysglycaemia (presence of IFG or DM) were determined using fasting blood samples among 1041 PLWH and 7047 subjects representing the general population. Results: People living with HIV had a lower prevalence of obesity [18.2%, 95% confidence interval (CI): 15.1–21.2 vs. 23.9%, 95% CI: 22.4–25.4], but a higher prevalence of insulin resistance and IFG (20.0%, 95% CI: 16.6–23.4 vs. 9.8%, 95% CI: 8.7–10.8) than the general population. Fasting glucose concentration was higher, but glycated haemoglobin (HbA1c) was lower, among PLWH. Prevalence of dysglycaemia for a given body mass index (BMI) was higher in PLWH than in the general population. The prevalence of DM did not differ between PLWH (13.2%, 95% CI: 10.2–15.9) and the general population (14.5%, 95% CI: 13.6–15.4). Conclusions: The prevalence of obesity was lower, but the risk of dysglycaemia for a given BMI was significantly higher, among PLWH, highlighting the importance of prevention and treatment of obesity among HIV‐infected subjects. Regardless of the increased prevalence of insulin resistance and IFG, DM was surprisingly not more common among PLWH, raising concern about the under‐diagnosis of DM, possibly due to low sensitivity of HbA1c in this patient population. [ABSTRACT FROM AUTHOR]

Aims/Introduction: To investigate the differential effects of maternal versus paternal history of diabetes on the risks for diabetes and prediabetes, as well as on insulin secretion and resistance in Chinese individuals. Materials and Methods: From the 2007 to 2008 China National Diabetes and Metabolism Disorders Study, 39,244 participants were included and divided into four categories: negative parental history, paternal history only (PH), maternal history only (MH), and both paternal and maternal history. Results: The age‐ and sex‐standardized prevalence rates of diabetes in the negative parental history, PH, MH, and both paternal and maternal history groups were 8.59, 12.56, 15.86 and 29.81%, respectively. The prevalence rates of impaired glucose metabolism were 24.13, 25.41, 31.13 and 50.80%, with the prevalence in the MH group being significantly higher than that in the PH group. Compared with that in the FH0 group, the risks of diabetes in the PH, MH, and both paternal and maternal history groups were 2.01‐, 2.67‐ and 6.37‐fold greater, and the risks of impaired glucose metabolism were 1.28‐, 1.65‐ and 3.45‐fold greater. In addition, MH had a significantly greater impact on impaired glucose metabolism than PH (PMHvsPH = 0.0292). Regression analyses suggested MH was associated with homeostatic model assessment for β‐cell function (β[SE] = −0.0910[0.0334], P = 0.0065), insulinogenic index (−0.1866[0.0550], P = 0.0007), homeostatic model assessment for insulin resistance (0.0662[0.0227], P = 0.0036) and Matsuda Index [−0.0716(0.0203), P = 0.0004]. PH was specifically associated with homeostatic model assessment for insulin resistance (0.1343[0.0267], P < 0.0001) and Matsuda Index (−0.1566[0.0243], P < 0.0001), but the effects were stronger than those of MH (PMHvsPH = 0.0431, 0.0054). Conclusions: MH and PH differentially influence the risks for diabetes, insulin secretion, and insulin resistance in the Chinese population, suggesting they participate in the pathogenesis of diabetes through different mechanisms. [ABSTRACT FROM AUTHOR]

Diabetes is associated with a plethora of metabolic changes which may underlie the propensity to development of stroke (Figure 1).1 Insulin resistance has multiple drivers, is inextricably linked to type 2 diabetes, and is associated with coronary artery2 and cerebrovascular3 atherosclerosis. The long-term degree of hyperglycemia correlates with stroke likelihood, although there is no evidence that intensive glycemic treatment reduces stroke. Similarly, it appears that acute hyperglycemia at the time of stroke is associated with worse outcome, although there is no evidence that intensive glycemic treatment at the time of stroke improves outcome. Diabetes treatment approaches with evidence of pre-stroke prevention might play roles in post-stroke protection. [Extracted from the article]

Aims: To evaluate the prevalence of diabetes and impaired fasting glucose in Poland in 2013–2014 and to determine the temporal trends between 2003–2005 and 2013–2014. Methods: A questionnaire survey was conducted in a representative sample of Polish adults, complemented by anthropometric and fasting plasma glucose measurements. The research was part of the national cross‐sectional WOBASZ study. Diabetes was assessed as self‐reported or screened (fasting plasma glucose level ≥ 7 mmol/l, based on one blood sample). Results: In the years 2013–2014 among 5694 participants aged 20–74 years, 6.0% (95% CI 5.4–6.6) reported a previous diagnosis of diabetes (5.8% in women and 6.2% in men). In addition, 2.4% of the participants (95% CI 2.0–2.8) without a previous diagnosis of diabetes (1.8% of women and 3.1% of men) had a fasting blood glucose level ≥7.0 mmol/l in a single measurement. In a single measurement, 18.4% of the participants (95% CI 17.4–19.4; 13.2% of women and 23.8% of men) had impaired fasting glucose. The prevalence of dysglycaemia in the WOBASZ II study was significantly higher compared to the WOBASZ I study findings from 2003–2005, increased from 6.6% to 8.4% for diabetes and from 9.3% to 18.4% for impaired fasting glucose (after age and sex standardization to the 2013 Polish population). Conclusions: The prevalence of diabetes in Poland is similar to that observed in other European populations and has increased significantly over the last decade. What's new?: The prevalence of diabetes (for type 1 and type 2) in Poland in 2014 is 8.4% and is similar to that in other European countries.More than every fourth person with diabetes is unaware of their disease.The prevalence of diabetes has increased significantly over the last decade (2004–2014), from 6.6% to 8.4%. [ABSTRACT FROM AUTHOR]

Keywords: Diabetes; Diagnosis; Guideline; Treatment EN Diabetes Diagnosis Guideline Treatment 1020 1076 57 07/27/20 20200701 NES 200701 PREFACE Objectives of the current guideline for the management of diabetes The current guideline represents the 6th edition of the "Japanese Clinical Practice Guideline for Diabetes" which has been revised every three years since its first appearance in 2004 to promote evidence-based, rational, efficient and consistent clinical practice in diabetes. b Intensive insulin therapy has been shown to be effective in preventing the onset of macroangiopathy in type 2 diabetes 9,31,32. 7 DIABETES SELF-MANAGEMENT EDUCATION AND SUPPORT FOR THE SELF-MANAGEMENT OF DIABETES B [CQ7-1] Are organized support and education for the self-management of diabetes useful for the management of diabetes? MNT for elderly patients with diabetes B [VIII-CQ-1] Is MNT as effective for elderly patients with diabetes as for non-elderly patients? Glycemic control and cancer risk in patients with diabetes The "Report of the Committee on Diabetes and Cancer II" addressed this issue and examined the impact of glycemic control on the subsequent risk of cancer in patients with diabetes[443], demonstrating that there is no high-quality evidence available, at present, to clarify the association between glycemic control and cancer risk in patients with diabetes. Management and prognosis of patients with cancer and diabetes It is reported that patients with cancer and diabetes are associated with poorer short-term and long-term life prognosis than patients with cancer without diabetes[[446]]. [Extracted from the article]

Charcot‐Marie‐Tooth disease type 1A (CMT1A) is the most common type of hereditary neuropathy worldwide and diabetes mellitus (DM) is the most frequent cause of peripheral neuropathy in the Western world. CMT1A typically manifest as a predominant motor neuropathy, while, DM‐related neuropathy often manifests as a predominant sensory disorder. There are some evidences that CMT1A patients that also had DM had a more severe neuropathy. Although the real frequency and the underlying mechanisms related to this association has not yet been addressed in the literature. We sought to characterize the phenotypic variability of CMT1A patients with persistent high glucose levels (DM or impaired glucose tolerance [IGT]). Nineteen patients with CMT1A and DM (CMTdiab), seven with CMT1A and IGT (CMTintol) and 27 with CMT1A without comorbidities were analyzed. They were evaluated through clinical assessment, application of the following scales: visual analogue scale, McGill, CMTNS, SF‐36 and COMPASS 31 and electrophysiological studies. Patients CMTdiab had a more severe motor and sensory neuropathy, more intense autonomic symptoms and worse quality of life. Surprisingly, proximal weakness and temporal dispersion on nerve conduction studies are frequently observed in this group. Patients CMTintol also had a more severe neuropathy. Curiously, we observed that the association of CMT1A and glucose metabolism disorders (CMTglic) clustered in some families. Patients CMTglic develop a more severe neuropathy. As there is yet no cure to CMT1A, a strict blood sugar control may be a useful measure. [ABSTRACT FROM AUTHOR]