Cellular Physiology Cellular Physiology Cellular Physiology Cellular Physiology Cellular Physiology Human Mesenteric Adipose Tissue Plays Unique Role versus Subcutaneous and Omental Fat in Obesity Related Diabetes
Cellular Physiology Cellular Physiology Cellular Physiology Cellular Physiology Cellular Physiology Human Mesenteric Adipose Tissue Plays Unique Role versus Subcutaneous and Omental Fat in Obesity Related Diabetes
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通讯作者：
Biochemistr;Biochemistr And Biochemistry;Ying-kui Yang;Min Chen;R. Clements;G. Abrams;C. Aprahamian;C. Harmon
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作者：
Biochemistr;Biochemistr And Biochemistry;Ying-kui Yang;Min Chen;R. Clements;G. Abrams;C. Aprahamian;C. Harmon
背景/目标：肥胖是当今一个常见且迅速增长的健康问题。肥胖的特征是体内脂肪增加和全身脂肪过多，特别是内脏脂肪堆积，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的功能障碍是否在糖尿病相关代谢综合征中发挥重要作用，在本研究中，评估了糖尿病受试者的皮下、网膜和肠系膜脂肪组织的脂肪分解和基因表达。方法：利用脂肪分解和实时PCR来测定脂肪细胞功能。结果：在所有三个脂肪库中，糖尿病患者的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) 显着增加非糖尿病受试者皮下、网膜和肠系膜脂肪组织中的甘油释放，但它刺激的糖尿病受试者的所有三个脂肪库中的甘油释放均显着受损。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）、脂肪酸转位酶（FAT/CD36）和11β-氢类固醇脱氢酶（HSD）基因表达显着上调。结论：肥胖糖尿病受试者的人肠系膜脂肪组织具有较高的基础甘油释放和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，表明肠系膜脂肪库中这些基因的改变可能在2型糖尿病和代谢综合征的胰岛素抵抗中发挥关键作用。
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. Methods: Lipolysis and real time PCR were utilized to determine adipocyte function. Results: 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 11β-hydroysteroid dehydrogenase (HSD) gene expression were significantly up regulated in the mesenteric adipose tissue of the diabetic patients. Conclusion: 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.