Human WAT STAMP2 associates with obesity and insulin resistance independently of adiponectin, but the role of STAMP2 in obesity and its complications seems different from that in mice.
Follistatin is a new adipokine important for adipogenesis. Down-regulated WAT expression of follistatin in obesity may counteract adiposity but could, by inhibiting adipogenesis, contribute to hypertrophic obesity (large fat cells) and insulin resistance.
A healthy Nordic diet reduces inflammatory gene expression in SAT compared with a control diet independently of body weight change in individuals with features of the metabolic syndrome.
MTCH2 is highly expressed in human WAT and adipocytes with increased levels in obese women. These results suggest that MTCH2 may play a role in cellular processes underlying obesity.
The alpha 2 Heremans-Schmid glycoprotein (AHSG) gene is implicated in the regulation of body fat and insulin sensitivity. The Met/Met genotype of the common singlenucleotide polymorphism (SNP), rs4917 , in the AHSG gene has been shown to be associated with reduced plasma levels as well as lower body fat. Here, we studied the association of this variation with subcutaneous adipocyte lipolysis. Ninetythree obese and nonobese healthy men were genotyped for Thr230Met, and subcutaneous adipose tissue biopsies were analyzed for lipolysis characteristics. The Met/Met genotype was associated with a marked increase of 1.5 log units in the lipolytic sensitivity to the  2-adrenoceptor agonist terbutaline ( P ؍ 0.0008) as compared with the Thr/Thr and Thr/Met genotypes. This corresponds to an approximately 35-fold increase in  2-adrenoceptor function. The genotype effect was independent of body mass index and waist circumference. In contrast, lipolytic sensitivity to both the  1-adrenoceptor agonist dobutamine ( P ؍ 0.25) and the ␣ 2A-adrenoceptor agonist clonidine ( P ؍ 0.54) was unaffected by the Thr230Met variation. Moreover, no difference in either maximal stimulation or inhibition of lipolysis was found between genotypes.We conclude that a common variation (Thr230Met) in the AHSG gene is associated with a marked increase in  2-adrenoceptor sensitivity in subcutaneous fat cells, which may be of importance in body weight regulation. -Lavebratt, C., E. Dungner, and J. Hoffstedt. Obesity with associated metabolic complications constitutes a well-known risk factor for both cardiovascular morbidity and mortality. Although lifestyle factors including eating behavior and physical activity are crucial, family studies have provided evidence also for a strong genetic influence on obesity development. In searching for genes that may affect body fat content and metabolism, the alpha 2 Heremans-Schmid glycoprotein (AHSG), also known as fetuin-A, is an attractive candidate. AHSG is a glycoprotein synthesized in the liver and circulating in plasma at high concentrations (1). Mice null for the AHSG gene are insulin sensitive, resistant to weight gain, and have decreased body fat content, which in turn may be due to altered lipid metabolism or higher energy expenditure (2). A double-single nonsynonymous nucleotide substitution [single-nucleotide polymorphism (SNP)] at amino acid positions 230 (rs4917 , Thr230Met) and 238 ( rs4918 , Thr238Ser) has been described (3) and was recently found to be associated with decreased plasma concentrations of AHSG (4). In agreement with these findings, we have shown that homozygosity for the rs2593813 :G-rs4917 :Met-rs4918 : Ser haplotype of the AHSG gene conferred an increased risk for leanness in men (5), which in turn suggests a protective role of AHSG gene variation in body fat accumulation in man.
Polymorphism of the AHSG gene is associated with in-A fundamental aspect of adipose tissue metabolism is the process of triglyceride breakdown, lipolysis. In subcutaneous fat cells, ca...
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