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Biochem Cell Biol. 2015 Oct;93(5):452-65. doi: 10.1139/bcb-2015-0012. Epub 2015 May 27.

Targeting skeletal muscle mitochondria to prevent type 2 diabetes in youth.

Author information

1
a Department of Human Anatomy and Cell Science, College of Nursing, Faculty of Health Sciences, University of Manitoba, The Diabetes Research Envisioned and Accomplished in Manitoba (DREAM) Theme of the Children's Hospital Research Institute of Manitoba, John Buhler Research Centre, 715 McDermot Avenue, Winnipeg, MB R3E 3P4, Canada.
2
b Department of Pharmacology and Therapeutics, The Diabetes Research Envisioned and Accomplished in Manitoba (DREAM) Theme of the Children's Hospital Research Institute of Manitoba, John Buhler Research Centre, 715 McDermot Avenue, Winnipeg, MB R3E 3P4, Canada.
3
c Department of Human Anatomy and Cell Science, The Diabetes Research Envisioned and Accomplished in Manitoba (DREAM) Theme of the Children's Hospital Research Institute of Manitoba, John Buhler Research Centre, 715 McDermot Avenue, Winnipeg, MB R3E 3P4, Canada.
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d Hotchkiss Brain Institute, Health Research Innovation Centre, 3330 Hospital Drive NW, Calgary, AB T2N 4N1, Canada.
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e Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary, Calgary, Canada.
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f Department of Pediatrics and Child Health, The Diabetes Research Envisioned and Accomplished in Manitoba (DREAM) Theme of the Children's Hospital Research Institute of Manitoba, John Buhler Research Centre, 715 McDermot Avenue, Winnipeg, MB R3E 3P4, Canada.

Abstract

The prevalence of type 2 diabetes (T2D) has increased dramatically over the past two decades, not only among adults but also among adolescents. T2D is a systemic disorder affecting every organ system and is especially damaging to the cardiovascular system, predisposing individuals to severe cardiac and vascular complications. The precise mechanisms that cause T2D are an area of active research. Most current theories suggest that the process begins with peripheral insulin resistance that precedes failure of the pancreatic β-cells to secrete sufficient insulin to maintain normoglycemia. A growing body of literature has highlighted multiple aspects of mitochondrial function, including oxidative phosphorylation, lipid homeostasis, and mitochondrial quality control in the regulation of peripheral insulin sensitivity. Whether the cellular mechanisms of insulin resistance in adults are comparable to that in adolescents remains unclear. This review will summarize both clinical and basic studies that shed light on how alterations in skeletal muscle mitochondrial function contribute to whole body insulin resistance and will discuss the evidence supporting high-intensity exercise training as a therapy to circumvent skeletal muscle mitochondrial dysfunction to restore insulin sensitivity in both adults and adolescents.

KEYWORDS:

child health; diabète de type 2; exercice; exercise; insulin resistance; mitochondria; mitochondrie; muscle squelettique; résistance à l’insuline; santé de l’enfant; skeletal muscle; type 2 diabetes

PMID:
26151290
DOI:
10.1139/bcb-2015-0012
[Indexed for MEDLINE]

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