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Objective: Increasing evidence revealed the role of adipokines in carbohydrates and fat metabolism. The present study was designed to evaluate the adiponectin, leptin, and resistin levels in prediabetes subjects and evaluate the relationship between these adipokines and insulin resistance. Methods: A hospital-based descriptive study was conducted for one year. 200 individuals who met the inclusion criteria were enrolled in the study. Based on the oral glucose tolerance test, the study subjects were grouped into healthy controls (n = 100), prediabetic non-obese (n = 61), and prediabetic obese (n = 39). Blood glucose estimation was done by the glucose oxidase peroxidase method. Chemiluminescent immunoassay was used for the measurement of insulin level and homeostasis model assessment-estimated insulin resistance was used for the assessment of insulin resistance. Serum adipokines levels were determined by ELISA. Statistical analysis was performed by using SPSS Software. Results: Serum adiponectin levels decreased significantly in obese prediabetes (7.21 ± 2.15 µg/ml) when compared to non-obese prediabetes (7.28 ± 2.41 µg/ml) and healthy control subjects (13.64 ± 2.88 µg/ml, p < 0.001). Serum leptin levels increased significantly in obese prediabetes (13.59 ± 2.59 ng/ml) when compared to non-obese prediabetes (9.84 ± 2.66 ng/ml) and healthy control subjects (12.28 ± 2.65 ng/ml, p < 0.001). Serum resistin levels increased significantly in obese prediabetes (17.67 ± 3.60 ng/ml) when compared to non-obese prediabetes (17.2 ± 3.93 ng/ml) and healthy control subjects (14.46 ± 4.16 ng/ml, p < 0.001). Adiponectin-leptin ratio decreased significantly in obese prediabetes (0.56 ± 0.22) when compared to non-obese prediabetes (0.79 ± 0.4) and healthy control subjects (1.15 ± 0.37; p < 0.001). Fasting insulin resistance was statistically significant (p < 0.001) in all groups. Conclusion: The present study strongly suggests that the adipokine profile is an ideal diagnostic tool to predict prediabetes and metabolic syndrome, especially among those with insulin resistance. [ABSTRACT FROM AUTHOR]

Introduction: Squamous cell carcinoma is the most common epithelial malignancy of the oral cavity. The five years survival rate is approximately 50% and is even lower i.e, 30% in the patients with recurrence of this disease. Since recurrence has a major influence on five years survival, it becomes imperative to identify the molecular elements responsible for recurrence of oral squamous cell carcinoma. Aim: To evaluate the expression of resistin and fascin-1 and their correlation with recurrence in the patients of oral squamous cell carcinoma. Materials and Methods: A cohort study will be conducted in the Department of Oral Pathology, Sharad Pawar Dental College and Hospital, Wardha, Maharashtra, India. The duration of the study will be 24 months. A 4 µm thick section from paraffin embedded blocks of formalin fixed biopsy tissues of 60 cases having primary oral squamous cell carcinoma will be processed and stained for mouse monoclonal resistin (clone C-10) and mouse monoclonal fascin-1 (clone 55k-2) antibodies. Results: The results will be analysed by the correlation tests, Pearson and Spearman correlation coefficient. Conclusion: Local recurrence is influenced by site of tumour, depth of invasion, resection margins and lymphovascular spread. As recurrence is directly related to the poor prognosis and survival rate in the patients of oral squamous cell carcinoma, so it is essential to identify molecular markers indicative of recurrence. Fascin and resistin markers could be used to identify a subset of oral squamous cell carcinoma patients which are prone to recurrence. [ABSTRACT FROM AUTHOR]

Aim: The aim of this study was to find out the association of adiponectin and resistin levels in gingival crevicular fluid (GCF) with the clinical parameters before and after scaling and root planing in periodontitis patients. Methods: A total of 50 patients were recruited from the Outpatient Department of Periodontics, JKK Nattraja Dental College and Hospital, Komarapalayam, Tamil Nadu, India. The protocol was reviewed and approved by the institutional ethical board. Informed consent was obtained from the patients and the study-related procedures were explained. Patients were divided into two groups. Group I (25 patients) consisted of healthy patients. Group II (25 patients) consisted of periodontitis patients. The periodontitis patients after treatment were considered as Group III. GCF samples were collected before treatment and 21 days after treatment. The levels of adiponectin and resistin were evaluated using Immunotag™ Human RETN enzyme-linked immunosorbent assay (ELISA) kit (ITEH0269) and Immunotag™ Human ADP (adiponectin) ELISA kit (ITEH2593). The levels were correlated with the clinical parameters. Results: There were an increase in the mean adiponectin level and a decrease in the mean resistin level at the end of periodontal therapy. Conclusions: Adiponectin which is an anti-inflammatory component was found to increase after periodontal therapy, and resistin which is an inflammatory component has been decreased after periodontal therapy. [ABSTRACT FROM AUTHOR]

Resistin, an adipokine, is involved in obesity and Type 2 Diabetes (T2D). The current study evaluates the association between RETN polymorphisms (−638 G/A, −420C/G & −358 G/A) and the risk towards T2D. Controls and T2D patients were enrolled from Gujarat, India. Polymorphisms of RETN were genotyped by Polymerase Chain Reaction-Restriction Fragment Length Polymorphism. For the genotype-phenotype correlation analysis Fasting Blood Glucose (FBG), Body Mass Index (BMI) and plasma lipid profile were used. Plasma levels of resistin were assayed by ELISA. Our study suggests an association of RETN −420C/G polymorphism with T2D risk. The CC genotype of RETN −420C/G polymorphism was found to be associated with FBG, BMI, and total cholesterol. Plasma resistin levels were found to be significantly increased in diabetic patients as compared to controls. Our findings suggest −420C/G polymorphism of RETN as an important factor which could pose a powerful risk towards T2D susceptibility. • Association between resistin genetic variants and its plasma concentrations with T2D in Gujarat population • RETN -420C/G polymorphism is associated with T2D and altered metabolic profile. • Elevated resistin levels in obese T2D patients. [ABSTRACT FROM AUTHOR]

Objectives: To investigate whether genetic polymorphisms in the resistin and adiponectin genes cause a predisposition towards polycystic ovary syndrome (PCOS) in a South Indian women population.Study Design: This case controlled study included samples from 484 study subjects (282 diagnosed with PCOS and 200 normal controls). The clinical and biochemical parameters of the samples assayed included BMI, LH, FSH, testosterone, fasting glucose, adiponectin and resistin levels. Three single nucleotide polymorphisms of the resistin (RETN) gene 420(C→G) (rs1862513), 299(G→A) (rs3745367), and 62(G→A) (rs3745368), and two single nucleotide polymorphisms of the adiponectin (ADPIOQ) gene 45(T→G) (rs2241766), and 276(G→T) (rs1501299), were analyzed using a PCR-RFLP method. Statistical analysis was carried out to determine the association of the genotypic and allelic variations with the syndrome and also analyze the influence of genotypic variations on adipokine levels.Results: Serum levels of testosterone, LH, fasting glucose and resistin were found to be significantly increased in the PCOS patients when compared to controls, while adiponectin was found to be significantly lower (P<0.05). BMI was found to positively correlate with resistin levels and negatively correlate with adiponectin levels. A positive association was found between the RETN promoter 420 (C→G) SNP and the intron 2 299 (G→A) variant of the resistin gene, while no association was found between the ADPIOQ gene polymorphisms and PCOS. The 'GG' variant of the adiponectin 45 (T→G) variant showed a near-significant tendency towards a decreased concentration of adiponectin in PCOS patients.Conclusions: Polymorphisms of the resistin gene could be assigned to play a role in increasing the risk of PCOS. However, the adiponectin gene does not seem to play a major role in PCOS susceptibility in a South Indian population. Serum adiponectin and resistin levels were more dependent on BMI rather than the presentation of PCOS. Obesity plays a major role in aggravating the hormonal disturbances found associated with PCOS. [ABSTRACT FROM AUTHOR]

Studies on the association of the Pro12Ala and C1431T polymorphisms of PPARγ with diabetes and obesity have revealed extensive population-dependent variations. However, association of these polymorphisms with the metabolic syndrome and its individual components has not been well investigated in the Indian population. The Indian population harbours the maximum number of diabetics in the world who are thus more susceptible to metabolic disorders. We screened a South Indian population (N = 699) for a possible association of these polymorphisms with the metabolic syndrome (MS) and type 2 diabetes. We also investigated the correlation of these two single-nucleotide polymorphisms (SNPs) with plasma resistin levels. The C1431T SNP was associated with higher levels of plasma resistin (P = 0.017). Furthermore, C1431T was associated with resistin in different tertiles. Prevalence of the 'Pro-C' haplotype decreased with increasing tertiles of resistin (84.1% to 75.4%, P = 0.037). Plasma resistin levels were not found to be associated with MS and type 2 diabetes. These results point to a likely association of plasma resistin levels with PPARγ polymorphisms in the Indian population. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Resistin is an adipocyte-derived peptide that might play a role in obesity and insulin resistance (IR); however, its role in humans is largely unknown. The aim of the study was to elucidate the role of serum resistin and explore its relationship with inflammatory marker C-reactive protein (CRP) and adipocytokine (leptin, adiponectin) in Indian diabetic patients. Design and methods: A total of 171 subjects including 41 controls, 41 obese and 89 Type 2 diabetes mellitus (T2DM) patients were recruited in this cross-sectional study. Fasting serum resistin, leptin, adiponectin, insulin and CRP were measured by enzyme immunoassay. The relation between these variables was studied by univariate and multiple regression analysis. Results: Serum resistin levels were significantly reduced in non-obese treated T2DM patients. In the correlation analysis after controlling for age and BMI we found that resistin is significantly associated with leptin (0.687, p <0.002) and CRP (0.549, p <0.018) in only control females and with CRP (0.642, p <0.01) in T2DM female patients. In multiple linear regression analysis resistin was independently predicted by the leptin (p <0.01) and leukocyte (p <0.004) in controls, treated T2DM patients. Conclusion: Reduced resistin and leptin levels in non-obese treated T2DM and significant association between these two in control and treated T2DM suggest interplay between these two adipocytokines. In addition, the weak association of resistin with diabetes indicates that it may be playing an indirect role in the pathogenesis of T2DM. [Copyright &y& Elsevier]

Adipocytokines are the major secretory products of adipose tissue and potential markers of metabolism and inflammation. However, their association in host immune response against tuberculous lymphadenitis (TBL) disease is not known. Thus, we measured the systemic levels of adipocytokines in TBL (n = 44) and compared to pulmonary tuberculosis (PTB, n = 44) and healthy control (HC, n = 44) individuals. We also examined the pre and post-treatment adipocytokine levels in TBL individuals upon completion of standard anti-tuberculosis treatment (ATT). The receiver operating characteristics (ROC) were performed between TBL, PTB and HCs to find the potential discriminatory markers. Finally, principal component (PCA) analysis was performed to reveal the expression patterns of adipocytokines among study groups. Our results demonstrate that TBL is associated with significantly higher systemic levels of adipocytokines (except resistin) when compared with PTB and significantly lower levels when compared with HC (except adiponectin) individuals. Upon completion of ATT, the systemic levels of adiponectin and resistin were significantly decreased when compared to pre-treatment levels. Upon ROC analysis, all the three adipocytokines discriminated TBL from PTB but not with HCs, respectively. Similarly, adipocytokines were differentially clustered in TBL in comparison to PTB in PCA analysis. Therefore, adipocytokines are a distinguishing feature in TBL compared to PTB individuals., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Background: Acute lymphoblastic leukemia survivors are predisposed to obesity. However, the exact underlying mechanisms are not known.Aims: The study was done to assess the role of biomarkers of obesity in acute leukemia survivors.Settings and Designs: This is a cross-sectional study conducted at All India Institute of Medical Sciences in survivors of acute leukemia who had completed treatment at least 1 year before enrollment in this study.Materials and Methods: Obesity was studied by determining the body mass index. Potential biomarkers were studied by assessing serum leptin, resistin, and adiponectin by enzyme-linked immunosorbant assay, and the results were compared in obese versus nonobese survivors.Statistical Analysis: Descriptive analysis for baseline demographic factors and Student's t-test for comparing the mean levels of biomarkers among the obese and nonobese survivors.Results: One hundred and fifty-nine acute leukemia patients were enrolled in this study with a median follow-up of 36.8 months. The median age was 10 (range: 3-18) years, and 123 (77.3%) patients were males. The overall prevalence of overweight/obesity was 26.4%, and this was similar in acute myeloid leukemia and acute lymphoblastic leukemia sub-groups (26.2% vs. 27.3%, P = 0.9). Mean serum leptin and resistin were similar in obese and nonobese leukemia survivors (3.7 vs. 2.85 pg/mL, P = 0.064; 8.01 vs. 9.33 ng/mL, P = 0.36). However, mean serum adiponectin was significantly lower in obese leukemia survivors (7.97 vs. 11.5 μg/mL, P = 0.023).Conclusions: Obese leukemic survivors had lower serum adiponectin levels than nonobese survivors. However, serum resistin and leptin levels were similar in the two groups. [ABSTRACT FROM AUTHOR]

Insulin resistance may become the most powerful predictor of future development of type 2 diabetes mellitus (T2DM) and a therapeutic target for the treatment of the same. Both Resistin, an adipose derived peptide hormone and Urotensin II a potent vasoconstrictor, are reported to be involved in the development of insulin resistance and T2DM but the results remain contradictory. Therefore, investigations were carried out to study the association of T2DM and single nucleotide polymorphism (SNP) in Resistin (RETN) gene at rs3745367 (+ 299 G > A) and Urotensin II (UTS2) gene at rs228648 (+ 143 G > A) and rs2890565 (+ 3836 C > T) in a North Indian population. Method: The present case-control study, conducted from August 2017 to July 2020, involved 168 T2DM patients and 102 healthy controls. SNPs rs3745367, rs228648 and rs2890565 were amplified from genomic DNA in the studied samples by polymerase chain reaction (PCR) using specific primers. The amplified products were genotyped by restriction fragment length polymorphism (RFLP) using particular restriction endonucleases. Clinical parameters viz. glycosylated haemoglobin (HbA1c), fasting blood glucose (FBG), high density lipoprotein cholesterol (HDL-C), triglycerides (TG), total cholesterol (CHL) and fasting insulin were determined by enzymatic methods. Result and conclusion: A statistically significant association between T2DM and RETN gene at SNP rs3745367 (p = 0.001) and UTS2 gene at SNP rs2890565 (p = 0.001) was observed. In RETN gene SNP rs3745367, insulin and homeostasis model assessment of insulin resistance (HOMA-IR) were found to be higher in GA + AA combined genotype than in GG genotype for T2DM subjects. Regression analysis revealed that SNP rs2890565 and HOMA-IR were independently associated with the risk of development of T2DM when three SNPs were taken as independent variable adjusted for clinical variables. Among four haplotypes, A/T was found associated with increased risk of T2DM as determined for rs228648 and rs2890565 of UTS2 gene. It can be concluded from these results that polymorphism at rs3745367 of RETN gene and at rs2890565 of UTS2 gene are associated with risk of T2DM in North Indian population.