Motoshima Hiroyuki, Wu Xiangdong, Sinha Madhur K, Hardy V Elise, Rosato Ernest L, Barbot Donna J, Rosato Francis E, Goldstein Barry J
Dorrance H. Hamilton Research Laboratories, Division of Endocrinology, Diabetes, and Metabolic Diseases, Department of Medicine, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
J Clin Endocrinol Metab. 2002 Dec;87(12):5662-7. doi: 10.1210/jc.2002-020635.
Adiponectin is an adipocyte-derived plasma protein with insulin-sensitizing and antiatherosclerotic properties. Because adipose tissue depots differ in the strength of their association with the adverse metabolic consequences of obesity, we studied the secretion of adiponectin in vitro from paired samples of isolated human omental and sc adipocytes and its regulation by insulin and rosiglitazone. Cells were incubated for 12 or 24 h with and without treatment with 100 nM insulin, 8 micro M rosiglitazone, or both combined; adiponectin secreted into the culture medium was measured by a RIA with a human adiponectin standard and normalized for cellular DNA content. Secretion of adiponectin by omental cells was generally higher than sc cells and showed a strong negative correlation with body mass index (r = -0.78;P = 0.013). In contrast, secretion from the sc cells was unrelated to body mass index. Compared with sc-derived adipocytes, adiponectin secretion from omental cells was increased by insulin or rosiglitazone alone and was up to 2.3-fold higher following combined treatment with insulin and rosiglitazone, whereas secretion from sc adipose cells was unaffected by these treatments. These data suggest that reduced secretion from the omental adipose depot may account for the decline in plasma adiponectin observed in obesity. Furthermore, enhanced adiponectin secretion from fat cells derived from the visceral compartment in response to rosiglitazone alone or in combination with insulin may play a role in some of the systemic insulin-sensitizing and antiinflammatory properties of the thiazolidinediones.
脂联素是一种由脂肪细胞分泌的血浆蛋白,具有胰岛素增敏和抗动脉粥样硬化特性。由于不同脂肪组织库与肥胖不良代谢后果的关联强度不同,我们研究了在体外从分离的人网膜和皮下脂肪细胞的配对样本中脂联素的分泌情况,以及胰岛素和罗格列酮对其的调节作用。将细胞在有或无100 nM胰岛素、8 μM罗格列酮或两者联合处理的情况下孵育12或24小时;通过使用人脂联素标准品的放射免疫分析测定分泌到培养基中的脂联素,并根据细胞DNA含量进行标准化。网膜细胞分泌的脂联素通常高于皮下细胞,且与体重指数呈强烈负相关(r = -0.78;P = 0.013)。相比之下,皮下细胞的分泌与体重指数无关。与皮下来源的脂肪细胞相比,单独使用胰岛素或罗格列酮可增加网膜细胞脂联素的分泌,胰岛素和罗格列酮联合处理后分泌量可高达2.3倍,而皮下脂肪细胞的分泌不受这些处理的影响。这些数据表明,网膜脂肪组织库分泌减少可能是肥胖患者血浆脂联素下降的原因。此外,内脏脂肪组织来源的脂肪细胞对单独使用罗格列酮或与胰岛素联合使用的反应中脂联素分泌增强,可能在噻唑烷二酮类药物的一些全身胰岛素增敏和抗炎特性中发挥作用。