Hypercholesterolemia Induces Adipose Dysfunction in Conditions of Obesity and Nonobesity

被引:43
作者
Aguilar, David [1 ]
Fernandez, Maria Luz [1 ]
机构
[1] Univ Connecticut, Dept Nutr Sci, Storrs, CT 06269 USA
关键词
LOW-DENSITY-LIPOPROTEIN; RECEPTOR-RELATED PROTEIN; DIETARY-CHOLESTEROL; FAMILIAL HYPERCHOLESTEROLEMIA; ADIPOCYTE CHOLESTEROL; INSULIN-RESISTANCE; OXIDIZED LDL; MACROPHAGE ACCUMULATION; TRANSCRIPTION FACTOR; METABOLIC SYNDROME;
D O I
10.3945/an.114.005934
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
It is well known that hypercholesterolemia can lead to atherosclerosis and coronary heart disease. Adipose tissue represents an active endocrine and metabolic site, which might be involved in the development of chronic disease. Because adipose tissue is a key site for cholesterol metabolism and the presence of hypercholesterolemia has been shown to induce adipocyte cholesterol overload, it is critical to investigate the role of hypercholesterolemia on normal adipose function. Studies in preadipocytes revealed that cholesterol accumulation can impair adipocyte differentiation and maturation by affecting multiple transcription factors. Hypercholesterolemia has been observed to cause adipocyte hypertrophy, adipose tissue inflammation, and disruption of endocrine function in animal studies. Moreover, these effects can also be observed in obesity-independent conditions as confirmed by clinical trials. In humans, hypercholesterolemia disrupts adipose hormone secretion of visfatin, leptin, and adiponectin, adipokines that play a central role in numerous metabolic pathways and regulate basic physiologic responses such as appetite and satiety. Remarkably, treatment with cholesterol-lowering drugs has been shown to restore adipose tissue endocrine function. In this review the role of hypercholesterolemia on adipose tissue differentiation and maturation, as well as on hormone secretion and physiologic outcomes, in obesity and non-obesity conditions is presented.
引用
收藏
页码:497 / 502
页数:6
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