Impaired TCA cycle flux in mitochondria in skeletal muscle from type 2 diabetic subjects: Marker or maker of the diabetic phenotype?

被引:48
作者
Gaster, Michael [1 ,2 ]
Nehlin, Jan O. [3 ]
Minet, Ariane D. [1 ]
机构
[1] Odense Univ Hosp, Dept Pathol, Lab Mol Physiol, DK-5000 Odense, Denmark
[2] Odense Univ Hosp, Dept Endocrinol, DK-5000 Odense, Denmark
[3] Odense Univ Hosp, Dept Clin Immunol, Ctr Stem Cell Treatment, DK-5000 Odense, Denmark
基金
英国医学研究理事会;
关键词
TCA cycle; regulation; mitochondria; diabetes; TRICARBOXYLIC-ACID CYCLE; NADP(+)-DEPENDENT ISOCITRATE DEHYDROGENASE; ALPHA-KETOGLUTARATE DEHYDROGENASE; SUCCINYL-COA SYNTHETASES; CYTOSOLIC MALATE-DEHYDROGENASE; FUMARATE HYDRATASE DEFICIENCY; NUCLEAR RESPIRATORY FACTORS; REDUCED LIPID OXIDATION; PRELIMINARY-X-RAY; CITRATE SYNTHASE;
D O I
10.3109/13813455.2012.656653
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The diabetic phenotype is complex, requiring elucidation of key initiating defects. Recent research has shown that diabetic myotubes express a primary reduced tricarboxylic acid (TCA) cycle flux. A reduced TCA cycle flux has also been shown both in insulin resistant offspring of T2D patients and exercising T2D patients in vivo. This review will discuss the latest advances in the understanding of the molecular mechanisms regulating the TCA cycle with focus on possible underlying mechanism which could explain the impaired TCA flux in insulin resistant human skeletal muscle in type 2 diabetes. A reduced TCA is both a marker and a maker of the diabetic phenotype.
引用
收藏
页码:156 / 189
页数:34
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