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[肥胖与炎症]

[Obesity and inflammation].

作者信息

Recasens M, Ricart W, Fernández-Real J M

机构信息

Unidad de Diabetes, Endocrinología y Nutrición, Hospital Universitari de Girona, Doctor Josep Trueta.

出版信息

Rev Med Univ Navarra. 2004 Apr-Jun;48(2):49-54.

Abstract

The adipose tissue produces a vast number of molecules called adipokines such as leptin, tumoral necrosis factor (TNFalpha), interleukins and adiponectin. Many of the metabolic disturbances associated with obesity and the metabolic syndrome may be due to citokine production by adipocytes. The adipose tissue increases the soluble fractions of TNFalpha leading to a rise in its biological activity. The activation of TNFalpha system causes insulin resistance through different mechanisms such as defects in receptor fosforilation and reduction in insulin-sensitive glucose transporters. TNFalpha is also involved in the pathophysiology of hypertension and dyslipidaemia associated with obesity and insulin resistance. More than one third of interleukin-6 (IL-6) concentrations come from the adipocytes. It has been demonstrated a role for IL-6 in the development of hyperlipidemia, diabetes and hypertension. In contrast to the rest of adipokines, adiponectin is reduced in obesity, diabetes or cardiovascular disease. Adiponectin improves insulin resistance, dyslipidaemia and adhesion to endothelial cells protecting from atherosclerosis development. Thus, adipokines have an important role in the pathophysiology of metabolic syndrome by different mechanisms involving metabolic and vascular effects.

摘要

脂肪组织会产生大量被称为脂肪因子的分子,如瘦素、肿瘤坏死因子(TNFα)、白细胞介素和脂联素。许多与肥胖和代谢综合征相关的代谢紊乱可能归因于脂肪细胞产生的细胞因子。脂肪组织会增加TNFα的可溶性部分,导致其生物活性升高。TNFα系统的激活通过不同机制导致胰岛素抵抗,如受体磷酸化缺陷和胰岛素敏感性葡萄糖转运蛋白减少。TNFα还参与与肥胖和胰岛素抵抗相关的高血压和血脂异常的病理生理过程。超过三分之一的白细胞介素-6(IL-6)浓度来自脂肪细胞。已经证实IL-6在高脂血症、糖尿病和高血压的发展中起作用。与其他脂肪因子不同,脂联素在肥胖、糖尿病或心血管疾病中会减少。脂联素可改善胰岛素抵抗、血脂异常以及对内皮细胞的黏附,从而预防动脉粥样硬化的发展。因此,脂肪因子通过涉及代谢和血管效应的不同机制在代谢综合征的病理生理过程中发挥重要作用。

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