Targeting skeletal muscle mitochondrial health in obesity

被引:4
|
作者
Pileggi, Chantal A. [1 ,2 ]
Hooks, Breana G. [1 ,2 ]
McPherson, Ruth [3 ]
Dent, Robert R. M. [4 ]
Harper, Mary-Ellen [1 ,2 ]
机构
[1] Univ Ottawa, Fac Med, Dept Biochem Microbiol & Immunol, 451 Smyth Rd, Ottawa, ON K1H 8M5, Canada
[2] Univ Ottawa, Ottawa Inst Syst Biol, Ottawa, ON K1H 8M5, Canada
[3] Univ Ottawa, Div Cardiol, Heart Inst, Ottawa, ON, Canada
[4] Univ Ottawa, Dept Med, Div Endocrinol, Ottawa, ON, Canada
关键词
BROWN ADIPOSE-TISSUE; GLUCAGON-LIKE PEPTIDE-1; BODY-MASS INDEX; RESTING METABOLIC-RATE; FATTY-ACID OXIDATION; ADENINE-NUCLEOTIDE TRANSLOCASE; ALL-CAUSE MORTALITY; IMPROVES GLUCOSE-HOMEOSTASIS; ENHANCES ENERGY-EXPENDITURE; BETA-ADRENERGIC REGULATION;
D O I
10.1042/CS20210506
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 demands of skeletal muscle are substantial and are characterized normally as highly flexible and with a large dynamic range. Skeletal muscle composition (e.g., fiber type and mitochondrial content) and metabolism (e.g., capacity to switch between fatty acid and glucose substrates) are altered in obesity, with some changes proceeding and some following the development of the disease. Nonetheless, there are marked interindividual differences in skeletal muscle composition and metabolism in obesity, some of which have been associated with obesity risk and weight loss capacity. In this review, we discuss related molecular mechanisms and how current and novel treatment strategies may enhance weight loss capacity, particularly in diet-resistant obesity.
引用
收藏
页码:1081 / 1110
页数:30
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