Yang Ying-Kui, Chen Min, Clements Ronald H, Abrams Gary A, Aprahamian Charles J, Harmon Carroll M
Department of Surgery, University of Alabama at Birmingham, USA.
Cell Physiol Biochem. 2008;22(5-6):531-8. doi: 10.1159/000185527. Epub 2008 Dec 9.
BACKGROUND/AIMS: Obesity is a common and rapidly growing health problem today. Obesity is characterized by the increase of body fat and an excess of total body fat and, in particular, visceral fat accumulation, is considered to be a risk factor for type 2 diabetes mellitus. To determine whether the malfunction of the mesenteric adipose tissue plays an important role in the diabetic related metabolic syndrome, in this study, lipolysis and gene expression in the subcutaneous, omental and mesenteric adipose tissue of the diabetic subjects were evaluated.
Lipolysis and real time PCR were utilized to determine adipocyte function.
Basal adipose tissue glycerol release is higher in diabetics than that of the non diabetics in all three fat depots. Isoproterenol (ISO) significantly increases glycerol release in subcutaneous, omental and mesenteric adipose tissues of non diabetic subjects but it stimulated glycerol release was significantly impaired in all three fat depots of the diabetic subjects. Gene expression studies indicate that leptin, Peroxisome proliferator-activated receptor-gamma (PPAR-gamma), Fatty acid translocase (FAT/CD36) and 11beta-hydroysteroid dehydrogenase (HSD) gene expression were significantly up regulated in the mesenteric adipose tissue of the diabetic patients.
Human mesenteric adipose tissue in obese diabetic subjects has high basal glycerol release and impaired isoproterenol stimulated glycerol release. The obesity-related gene expressions in the mesenteric adipose tissue are up regulated, suggesting that the alterations of these genes in mesentery adipose depot may play a critical role in insulin resistance of type 2 diabetes and metabolic syndrome.
背景/目的：肥胖是当今常见且迅速增长的健康问题。肥胖的特征是体脂增加以及全身脂肪过多，尤其是内脏脂肪堆积，被认为是2型糖尿病的危险因素。为了确定肠系膜脂肪组织功能障碍是否在糖尿病相关代谢综合征中起重要作用，本研究评估了糖尿病患者皮下、网膜和肠系膜脂肪组织中的脂肪分解及基因表达情况。
采用脂肪分解和实时定量聚合酶链反应来测定脂肪细胞功能。
在所有三个脂肪储存部位，糖尿病患者基础脂肪组织甘油释放量均高于非糖尿病患者。异丙肾上腺素（ISO）可显著增加非糖尿病患者皮下、网膜和肠系膜脂肪组织中的甘油释放，但在糖尿病患者的所有三个脂肪储存部位，其刺激的甘油释放均显著受损。基因表达研究表明，糖尿病患者肠系膜脂肪组织中瘦素、过氧化物酶体增殖物激活受体γ（PPAR-γ）、脂肪酸转运蛋白（FAT/CD36）和11β-羟基类固醇脱氢酶（HSD）基因表达显著上调。
肥胖糖尿病患者的人肠系膜脂肪组织基础甘油释放量高，异丙肾上腺素刺激的甘油释放受损。肠系膜脂肪组织中与肥胖相关的基因表达上调，提示肠系膜脂肪储存部位这些基因的改变可能在2型糖尿病胰岛素抵抗和代谢综合征中起关键作用。
