Combining metabolic profiling of plasma and faeces as a fingerprint of insulin resistance in obesity.

Background & Aims: Insulin resistance (IR) is one of the main risk factor for type 2 diabetes mellitus (T2DM). Nevertheless, its underlying pathophysiology is not completely established because IR is triggered by a complex interconnection of numerous factors impairing metabolism, promoting metabolome changes.

Methods: We used a metabolomics approach to identify plasma and faecal metabolites related to IR and obesity.

An Epigenetic Signature in Adipose Tissue Is Linked to Nicotinamide N-Methyltransferase Gene Expression.

Scope: The enzyme nicotinamide N-methyltransferase (NNMT) is a major methyltransferase in adipose tissue. We hypothesized an epigenetic signature in association with NNMT gene expression in adipose tissue.

Methods And Results: The global human methylome was analyzed in visceral adipose tissue (VAT) from morbidly obese patients using the Infinium Human Methylation 450 BeadChip array (discovery cohort: n = 11).

Effect of massive weight loss on inflammatory adipocytokines and the innate immune system in morbidly obese women.

Context: Obesity may be regarded as a low-grade inflammatory state.

Objective: The aim of this study was to evaluate changes in pro-inflammatory adipocytokines and the innate immune system, cardiovascular risk, and insulin sensitivity after massive weight loss.

Design: This was a longitudinal study.

Differential regulation of insulin action and tumor necrosis factor alpha system activity by metformin.

Background: Tumor necrosis factor alpha has a key role in insulin resistance. We study the effects of metformin on glucose tolerance, insulin resistance, beta cell function, and soluble tumor necrosis factor receptor (sTNFR) levels.

Methods: We performed a double-blind, randomized metformin-placebo study.

The interleukin-6 (-174) G/C promoter polymorphism is associated with type-2 diabetes mellitus in Native Americans and Caucasians.

Chronic low-grade activation of the immune system may play a role in the pathogenesis of type-2 diabetes mellitus (T2DM). Interleukin-6 (IL6), a powerful inducer of hepatic acute phase response, has been implicated in the etiology of insulin resistance and T2DM. Recently, an IL6 promoter polymorphism (G/C) at position -174 was found to be associated with measures of insulin sensitivity.