Mitochondrial response to nutrient availability and its role in metabolic disease

被引：118

作者：

Gao, Arwen W. ^{[1
]}

Canto, Carles ^{[2
]}

Houtkooper, Riekelt H. ^{[1
]}

机构：

[1] Univ Amsterdam, Acad Med Ctr, Lab Genet Metab Dis, NL-1105 AZ Amsterdam, Netherlands

[2] Nestle Inst Hlth Sci, Lausanne, Switzerland

来源：

EMBO MOLECULAR MEDICINE | 2014年 / 6卷 / 05期

关键词：

caloric restriction; diabetes; high-fat diet; metabolic disease; mitochondrial dynamics; SKELETAL-MUSCLE; CALORIE RESTRICTION; INSULIN-RESISTANCE; RESPIRATORY-CHAIN; OXIDATIVE-PHOSPHORYLATION; TRANSCRIPTION FACTORS; SIRT3; DEACETYLATES; LIPID-METABOLISM; RECEPTOR-ALPHA; MITOFUSIN;

D O I：

10.1002/emmm.201303782

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Metabolic inflexibility is defined as an impaired capacity to switch between different energy substrates and is a hallmark of insulin resistance and type 2 diabetes mellitus (T2DM). Hence, understanding the mechanisms underlying proper metabolic flexibility is key to prevent the development of metabolic disease and physiological deterioration. An important downstream player in the effects of metabolic flexibility is the mitochondrion. The objective of this review was to describe how mitochondrial metabolism adapts to limited nutrient situations or caloric excess by changes in mitochondrial function or biogenesis, as well as to define the mechanisms propelling these changes. Altogether, this should pinpoint key regulatory points by which metabolic flexibility might be ameliorated in situations of metabolic disease.

引用

页码：580 / 589

页数：10

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