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AMPK regulation of fatty acid metabolism and mitochondrial biogenesis: implications for obesity.
Mol Cell Endocrinol. 2013 Feb 25; 366(2):135-51.MC

Abstract

Skeletal muscle plays an important role in regulating whole-body energy expenditure given it is a major site for glucose and lipid oxidation. Obesity and type 2 diabetes are causally linked through their association with skeletal muscle insulin resistance, while conversely exercise is known to improve whole body glucose homeostasis simultaneously with muscle insulin sensitivity. Exercise activates skeletal muscle AMP-activated protein kinase (AMPK). AMPK plays a role in regulating exercise capacity, skeletal muscle mitochondrial content and contraction-stimulated glucose uptake. Skeletal muscle AMPK is also thought to be important for regulating fatty acid metabolism; however, direct genetic evidence in this area is currently lacking. This review will discuss the current paradigms regarding the influence of AMPK in regulating skeletal muscle fatty acid metabolism and mitochondrial biogenesis at rest and during exercise, and highlight the potential implications in the development of insulin resistance.

Authors+Show Affiliations

University of Melbourne, Department of Medicine, St. Vincent's Institute of Medical Research, Melbourne, Victoria, Australia. honeill@mcmaster.caNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

22750049

Citation

O'Neill, Hayley M., et al. "AMPK Regulation of Fatty Acid Metabolism and Mitochondrial Biogenesis: Implications for Obesity." Molecular and Cellular Endocrinology, vol. 366, no. 2, 2013, pp. 135-51.
O'Neill HM, Holloway GP, Steinberg GR. AMPK regulation of fatty acid metabolism and mitochondrial biogenesis: implications for obesity. Mol Cell Endocrinol. 2013;366(2):135-51.
O'Neill, H. M., Holloway, G. P., & Steinberg, G. R. (2013). AMPK regulation of fatty acid metabolism and mitochondrial biogenesis: implications for obesity. Molecular and Cellular Endocrinology, 366(2), 135-51. https://doi.org/10.1016/j.mce.2012.06.019
O'Neill HM, Holloway GP, Steinberg GR. AMPK Regulation of Fatty Acid Metabolism and Mitochondrial Biogenesis: Implications for Obesity. Mol Cell Endocrinol. 2013 Feb 25;366(2):135-51. PubMed PMID: 22750049.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - AMPK regulation of fatty acid metabolism and mitochondrial biogenesis: implications for obesity. AU - O'Neill,Hayley M, AU - Holloway,Graham P, AU - Steinberg,Gregory R, Y1 - 2012/06/28/ PY - 2011/12/10/received PY - 2012/03/13/revised PY - 2012/06/21/accepted PY - 2012/7/4/entrez PY - 2012/7/4/pubmed PY - 2013/7/3/medline SP - 135 EP - 51 JF - Molecular and cellular endocrinology JO - Mol Cell Endocrinol VL - 366 IS - 2 N2 - Skeletal muscle plays an important role in regulating whole-body energy expenditure given it is a major site for glucose and lipid oxidation. Obesity and type 2 diabetes are causally linked through their association with skeletal muscle insulin resistance, while conversely exercise is known to improve whole body glucose homeostasis simultaneously with muscle insulin sensitivity. Exercise activates skeletal muscle AMP-activated protein kinase (AMPK). AMPK plays a role in regulating exercise capacity, skeletal muscle mitochondrial content and contraction-stimulated glucose uptake. Skeletal muscle AMPK is also thought to be important for regulating fatty acid metabolism; however, direct genetic evidence in this area is currently lacking. This review will discuss the current paradigms regarding the influence of AMPK in regulating skeletal muscle fatty acid metabolism and mitochondrial biogenesis at rest and during exercise, and highlight the potential implications in the development of insulin resistance. SN - 1872-8057 UR - https://www.unboundmedicine.com/medline/citation/22750049/AMPK_regulation_of_fatty_acid_metabolism_and_mitochondrial_biogenesis:_implications_for_obesity_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0303-7207(12)00333-4 DB - PRIME DP - Unbound Medicine ER -