Mitochondrial function/dysfunction in white adipose tissue

被引:112
作者
Boudina, Sihem
Graham, Timothy E.
机构
[1] Univ Utah, Sch Med, Div Endocrinol Metab & Diabet, Salt Lake City, UT USA
[2] Univ Utah, Sch Med, Program Mol Med, Salt Lake City, UT USA
关键词
AMINO-ACID-METABOLISM; PHOSPHOENOLPYRUVATE CARBOXYKINASE; INSULIN-RESISTANCE; OXIDATIVE STRESS; ADIPOCYTE DIFFERENTIATION; ADIPONECTIN SYNTHESIS; GLYCERIDE-GLYCEROL; LIPID-METABOLISM; HUMAN OBESITY; 3T3-L1; CELLS;
D O I
10.1113/expphysiol.2014.081414
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The role of mitochondria in white adipocytes has long been neglected due in part to their lower abundance in these cells. However, accumulating evidence suggests that mitochondria are vital for maintaining metabolic homeostasis in white adipocytes because of their involvement in adipogenesis, fatty acid synthesis and esterification, branched-chain amino acid catabolism and lipolysis. It is therefore not surprising that white adipose tissue function can be perturbed by altering mitochondrial components or oxidative capacity. Moreover, studies in humans and animals with significantly altered fat mass, such as in obesity or lipoatrophy, indicate that impaired mitochondrial function in adipocytes may be linked directly to the development of metabolic diseases such as diabetes and insulin resistance. However, recent studies that specifically targeted mitochondrial function in adipocytes indicated dissociation between impaired mitochondrial oxidative capacity and systemic insulin sensitivity.
引用
收藏
页码:1168 / 1178
页数:11
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