Resistin: Insulin resistance to malignancy

被引:124
作者
Codoner-Franch, Pilar [1 ,2 ]
Alonso-Iglesias, Eulalia [3 ]
机构
[1] Dr Peset Univ Hosp, Dept Pediat, Valencia 46017, Spain
[2] Univ Valencia, Dept Pediat Obstet & Gynecol, Valencia 46010, Spain
[3] Univ Valencia, Dept Biochem & Mol Biol, Valencia 46010, Spain
关键词
Adipocytokines; Atherosclerosis; Cancer; Inflammation; Obesity; Resistin; INCREASES LIPID-ACCUMULATION; ENDOPLASMIC-RETICULUM STRESS; LINKED-IMMUNOSORBENT-ASSAY; TYPE-2; DIABETES-MELLITUS; INCREASED SERUM RESISTIN; BODY-MASS INDEX; ADIPOSE-TISSUE; OXIDATIVE STRESS; METABOLIC SYNDROME; LINKING OBESITY;
D O I
10.1016/j.cca.2014.07.043
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Adipose tissue is recognized as an endocrine organ that secretes bioactive substances known as adipokines. Excess adipose tissue and adipose tissue dysfunction lead to dysregulated adipokine production that can contribute to the development of obesity-related co-morbidities. Among the various adipokines, resistin, which was initially considered as a determinant of the emergence of insulin resistance in obesity, has appeared as an important link between obesity and inflammatory processes. Several experimental and clinical studies have suggested an association between increased resistin levels and severe conditions associated with obesity such as cardiovascular disease and malignancies. In this review, we present the growing body of evidence that human resistin is an inflammatory biomarker and potential mediator of obesity-associated diseases. A common pathway seems to involve the combined alteration of immune and inflammatory processes that favor metabolic disturbances, atherosclerosis and carcinogenesis. The mode of action and the signaling pathways utilized by resistin in its interactions with target cells could involve oxidative and nitrosative stress. Therefore, resistin could function as a key molecule in the complications of obesity development and could potentially be used as a diagnostic and prognostic marker. (C) 2014 Elsevier B.V. All rights reserved.
引用
收藏
页码:46 / 54
页数:9
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