Loss of Muscle MTCH2 Increases Whole-Body Energy Utilization and Protects from Diet-Induced Obesity

被引：45

作者：

Buzaglo-Azriel, Liat ^{[1
]}

Kuperman, Yael ^{[2
]}

Tsoory, Michael ^{[2
]}

Zaltsman, Yehudit ^{[1
]}

Shachnai, Liat ^{[1
]}

Zaidman, Smadar Levin ^{[3
]}

Bassat, Elad ^{[1
]}

Michailovici, Inbal ^{[1
]}

Sarver, Alona ^{[1
]}

Tzahor, Eldad ^{[1
]}

Haran, Michal ^{[4
]}

Vernochet, Cecile ^{[5
]}

Gross, Atan ^{[1
]}

机构：

[1] Weizmann Inst Sci, Dept Biol Regulat, IL-76100 Rehovot, Israel

[2] Weizmann Inst Sci, Dept Vet Resources, IL-76100 Rehovot, Israel

[3] Weizmann Inst Sci, Dept Chem Res Support, IL-76100 Rehovot, Israel

[4] Kaplan Med Ctr, Inst Hematol, IL-76100 Rehovot, Israel

[5] Pfizer Inc, Cardiovasc Metab & Endocrine Dis CVMED Res Unit, Cambridge, MA 02139 USA

来源：

CELL REPORTS | 2016年 / 14卷 / 07期

基金：

以色列科学基金会;

关键词：

SKELETAL-MUSCLE; OXIDATIVE-PHOSPHORYLATION; METABOLISM; PGC-1-ALPHA; LOCI; METAANALYSIS; ASSOCIATION; EXPRESSION; GENES; CELLS;

D O I：

10.1016/j.celrep.2016.01.046

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

Mitochondrial carrier homolog 2 (MTCH2) is a repressor of mitochondrial oxidative phosphorylation (OXPHOS), and its locus is associated with increased BMI in humans. Here, we demonstrate that mice deficient in muscle MTCH2 are protected from diet-induced obesity and hyperinsulinemia and that they demonstrate increased energy expenditure. Deletion of muscle MTCH2 also increases mitochondrial OXPHOS and mass, triggers conversion from glycolytic to oxidative fibers, increases capacity for endurance exercise, and increases heart function. Moreover, metabolic profiling of mice deficient in muscle MTCH2 reveals a preference for carbohydrate utilization and an increase in mitochondria and glycolytic flux in muscles. Thus, MTCH2 is a critical player in muscle biology, modulating metabolism and mitochondria mass as well as impacting whole-body energy homeostasis.

引用

页码：1602 / 1610

页数：9

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