Interaction of Adiponectin Genotypes and Insulin Resistance on the Occurrence of Taiwanese Metabolic Syndrome

Backgrounds. Adiponectin (apM1) may affect insulin sensitivity, and tumor necrosis factor (TNF-α) can inhibit the binding of insulin and insulin receptors. However, whether apM1 and TNF-α genes influence the development of metabolic syndrome (MetS) preceded by insulin resistance is unclear. The current study examines the interactions between the apM1 +45 genotypes, TNF-α -308 genotypes, and insulin resistance on the occurrence of MetS. Methods. A total of 329 community residents were recruited, and their personal characteristics were collected. Waist circumference and biochemical markers were examined for determining MetS. Genotypes were identified by the polymerase chain reaction. Results. After adjusting for the confounding effects, compared to apM1 +45 GG and GT genotypes carriers with HOMR-IR less than 2.0, those carriers with HOMA-IR greater than 2.0 had an increased MetS risk ( OR = 4.35 , 95% CI 2.14-8.85). Further, apM1 +45 TT carriers with HOMA-IR greater than 2.0 experienced a higher MetS risk ( OR = 5.91 , 95% CI 2.78-12.54). A significant interaction of the apM1 +45 genotype and insulin resistance on the MetS development was observed ( P = 0.04 ). Conclusion. Our data suggested that apM1 +45 genotypes might modify the effect of insulin resistance on the development of Taiwanese MetS.

Serum Levels of Spexin and Kisspeptin Negatively Correlate With Obesity and Insulin Resistance in Women

Spexin (SPX) and kisspeptin (KISS) are novel peptides relevant in the context of regulation of metabolism, food intake, puberty and reproduction. Here, we studied changes of serum SPX and KISS levels in female non-obese volunteers (BMI<25 kg/m2) and obese patients (BMI>35 kg/m2). Correlations between SPX or KISS with BMI, McAuley index, QUICKI, HOMA IR, serum levels of insulin, glucagon, leptin, adiponectin, orexin-A, obestatin, ghrelin and GLP-1 were assessed. Obese patients had lower SPX and KISS levels as compared to non-obese volunteers (SPX: 4.48±0.19 ng/ml vs. 6.63±0.29 ng/ml; p<0.001, KISS: 1.357±0.15 nmol/l vs. 2.165±0.174 nmol/l; p<0.01). SPX negatively correlated with BMI, HOMA-IR, insulin, glucagon, active ghrelin and leptin. Positive correlations were found between SPX and QUICKI index, McAuley index, serum levels of obestatin, GLP-1 and adiponectin and orexin-A Serum KISS negatively correlated with BMI, HOMA-IR, serum levels of insulin, glucagon, active ghrelin and leptin. KISS positively correlated with QUICKI index, McAuley index and adiponectin. In summary, SPX and KISS show negative correlations with obesity, insulin resistance indices, and hormones known to affect insulin sensitivity in females. Both, SPX and KISS could be therefore relevant in the pathophysiology of obesity and insulin resistance.

How much variance in insulin resistance is explained by obesity?

Background: Obesity is believed to be the major cause of insulin resistance, although many other obesity-independent signals are shown to affect insulin sensitivity.Aim: We address the degree to which variation in insulin resistance is explained by morphometric and biochemical measures of obesity.Methods: PubMed and Google Scholar were searched for epidemiological studies published between 1994 and 2015 that report correlations between at least one measure of obesity and that of insulin resistance.Results: A total of 63 studies satisfied inclusion criteria. Frequency distribution of coefficients of determination between morphometric measures of obesity and insulin resistance was skewed with the mode being less than 10%, class and median being 17.3%. Plasma leptin concentration, but not plasma non-esterified fatty acid level, was better correlated with insulin resistance, the median variance explained being 33.29%. Morphometric measures alone had a median variance explained of 16%. Ethnicity explained part of the variance across studies with the correlation being significantly poorer in Asians.Conclusion: The extremely limited predictive power of morphometric and biochemical measures of obesity suggests that more research needs to focus on the obesity-independent signals that affect insulin sensitivity as well as leptin expression.