Altomonte Jennifer, Harbaran Sonal, Richter Anja, Dong Hengjiang
Carl C. Icahn Institute for Gene Therapy and Molecular Medicine, Mount Sinai School of Medicine, New York, NY 10029. USA.
Metabolism. 2003 Aug;52(8):958-63. doi: 10.1016/s0026-0495(03)00092-1.
Adiposity, particularly increased intra-abdominal fat, is a predisposing factor for the development of insulin resistance in obesity and type 2 diabetes. Visceral fat seems to differ from subcutaneous adipose tissue in adipocytokine production. This fat depot-related difference has been viewed as an important mechanism by which adipose tissue exerts its paracrine/autocrine effects on peripheral tissue in modulating insulin sensitivity. We have studied the relative expression of adiponectin in visceral versus subcutaneous fat in Zucker fatty versus lean rats. Visceral fat, as opposed to subcutaneous fat, exhibited relatively higher levels of adiponectin production in lean animals. However, in Zucker fatty rats, adiponectin expression in visceral fat was suppressed to basal levels, which correlated with significantly reduced plasma adiponectin concentrations and increased insulin resistance. These results suggest that an impaired depot-specific expression of adiponectin is a contributing factor for the development of insulin resistance in Zucker fatty rats.
肥胖,尤其是腹内脂肪增加,是肥胖症和2型糖尿病发生胰岛素抵抗的一个易感因素。内脏脂肪在脂肪细胞因子产生方面似乎与皮下脂肪组织不同。这种与脂肪储存部位相关的差异被视为脂肪组织在调节胰岛素敏感性时对周围组织发挥旁分泌/自分泌作用的重要机制。我们研究了Zucker肥胖大鼠与瘦大鼠内脏脂肪与皮下脂肪中脂联素的相对表达。与皮下脂肪相反,在瘦动物中,内脏脂肪表现出相对较高水平的脂联素产生。然而,在Zucker肥胖大鼠中,内脏脂肪中脂联素的表达被抑制到基础水平,这与血浆脂联素浓度显著降低和胰岛素抵抗增加相关。这些结果表明,脂联素在特定储存部位的表达受损是Zucker肥胖大鼠发生胰岛素抵抗的一个促成因素。