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胰岛素抵抗大鼠运动时瘦素与肿瘤坏死因子-α的相互变化

Reciprocal changes in leptin and tumor necrosis factor-alpha with exercise in insulin resistant rats.

作者信息

Baba T, Kanda T, Yoshida A, Tsukui S, Nara M, Inukai T, Umeda T, Tamura J, Kobayashi I

机构信息

Department of Laboratory Medicine, Gunma University School of Medicine, Maebashi, Japan.

出版信息

Res Commun Mol Pathol Pharmacol. 2000 Jul-Aug;108(1-2):133-43.

PMID:11758969
Abstract

Leptin and tumor necrosis factor--alpha(TNF-alpha) are important mediators of insulin resistance in obese subjects through their over-expression in adipose tissue. Secretion of leptin into the circulation is a signal for the brain in patients with hyperinsulinemia. Regulation of TNF-alpha affects adipocyte insulin sensitivity and lipid accumulation. Exercise training has been suggested for the prevention and treatment of such disorders. However, how exercise modifies secretion of leptin and TNF-alpha is not known. We investigated leptin and TNF-alpha in a rat model of insulin resistance induced by sucrose. After 4 weeks of sucrose feeding, 4 weeks of voluntary wheel running significantly reduced the concentrations of leptin in mesenteric (MS) and subcutaneous fat (SC) when compared to sedentary sucrose-feeding rats. These results suggest that exercise controls cytokine regulation of leptin and TNF-alpha. The increased TNF-alpha in adipose tissue may activate cytolysis for energy consumption.

摘要

瘦素和肿瘤坏死因子-α(TNF-α)是肥胖个体胰岛素抵抗的重要介质,因为它们在脂肪组织中过度表达。在高胰岛素血症患者中,瘦素分泌入循环是向大脑发出的信号。TNF-α的调节影响脂肪细胞的胰岛素敏感性和脂质蓄积。有人提出运动训练可用于预防和治疗此类疾病。然而,运动如何改变瘦素和TNF-α的分泌尚不清楚。我们在蔗糖诱导的胰岛素抵抗大鼠模型中研究了瘦素和TNF-α。蔗糖喂养4周后,与久坐的蔗糖喂养大鼠相比,4周的自愿轮转跑步显著降低了肠系膜(MS)和皮下脂肪(SC)中瘦素的浓度。这些结果表明,运动可控制瘦素和TNF-α的细胞因子调节。脂肪组织中TNF-α的增加可能激活细胞溶解以消耗能量。

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Reciprocal changes in leptin and tumor necrosis factor-alpha with exercise in insulin resistant rats.胰岛素抵抗大鼠运动时瘦素与肿瘤坏死因子-α的相互变化
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