Klebanova E M, Balabolkin M I, Kreminskaia V M
Klin Med (Mosk). 2007;85(7):20-7.
The fact that fat issue is an endocrine gland secreting several hormones participating in the pathogenesis of type 2 diabetes mellitus (DM2) is universally recognized. Fat issue secretes leptin, tumor necrosis factor alpha, resistin, adiponectin, interleukin-6, free fatty acids, visfatin, omentin, perilipin, and other substances that influence the condition of insulinoresistance, one of the main factors responsible for DM2. Subcutaneous fat and visceral depot fat tissue differ in the spectrum of hormones they produce; the list of these hormones is presented in the article. The presence of abdominal or visceral obesity is combined with significant insulinoresistance, which, in its turn, increases the risk of vascular complications of diabetes. The article also cover the participation of other mechanisms - insulin secretion defect, oxidation stress, low secretion of glucagon-like peptide 1, apoptosis, an increased quantity of amyloid and the fl-cell pull in the pancreatic island--in DM2 pathogenesis. The authors present data on the secretion of leptin, resistin, adiponectin, and tumor necrosis factor a, as well as the condition of the functional activity of beta-cells and the degree of insulinoresistance in 30 DM2 patients receiving dietotherapy.
脂肪组织是一种分泌多种激素的内分泌腺,参与2型糖尿病(DM2)的发病机制,这一事实已得到普遍认可。脂肪组织分泌瘦素、肿瘤坏死因子α、抵抗素、脂联素、白细胞介素-6、游离脂肪酸、内脏脂肪素、网膜素、脂肪周蛋白等物质,这些物质会影响胰岛素抵抗状况,而胰岛素抵抗是DM2的主要致病因素之一。皮下脂肪和内脏脂肪组织分泌的激素种类不同;本文列出了这些激素。腹部或内脏肥胖与显著的胰岛素抵抗相关,而胰岛素抵抗又会增加糖尿病血管并发症的风险。本文还探讨了其他机制——胰岛素分泌缺陷、氧化应激、胰高血糖素样肽1分泌不足、细胞凋亡、淀粉样蛋白数量增加以及胰岛β细胞功能障碍——在DM2发病机制中的作用。作者展示了30例接受饮食治疗的DM2患者的瘦素、抵抗素、脂联素和肿瘤坏死因子α的分泌数据,以及β细胞功能活性状况和胰岛素抵抗程度。