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Metabolic flexibility in the development of insulin resistance and type 2 diabetes: effects of lifestyle.

Abstract

Lipotoxicity in skeletal muscle plays a critical role in the aetiology of insulin resistance and type 2 diabetes mellitus by interference of lipid metabolites with insulin signalling and action. The dynamics of lipid oxidation and fine tuning with fatty acid uptake and intramyocellular triacylglycerol turnover may be very important to limit the accumulation of lipid intermediates. The use of metabolic inflexibility, defined as the impaired capacity to increase fat oxidation upon increased fatty acid availability and to switch between fat and glucose as the primary fuel source after a meal, does more justice to the complexity of changes in fuel oxidation during the day. Fatty acid availability, uptake and oxidation all play a role in metabolic flexibility and insulin resistance. During high fatty acid availability, fatty acid transporters may limit cellular and mitochondrial fatty acid uptake and thus limit fat oxidation. After a meal, when the demand for fatty acids as fuel is low, an increased fractional extraction of lipids from plasma may promote intramyocellular lipid accumulation and insulin resistance. Furthermore, defects in fuel switching cluster together with impaired mitochondrial content and/or function. Lifestyle changes in dietary fat intake, physical activity and weight loss may improve metabolic flexibility in skeletal muscle, and thereby contribute to the prevention of type 2 diabetes.

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  • Authors+Show Affiliations

    ,

    Department of Human Biology, The Nutrition and Toxicology Research Institute (NUTRIM), Maastricht University, Maastricht, The Netherlands. e.corpeleijn@epi.umcg.nl

    ,

    Source

    MeSH

    Animals
    Diabetes Mellitus, Type 2
    Diet
    Energy Metabolism
    Exercise
    Fatty Acids
    Humans
    Insulin Resistance
    Life Style
    Muscle, Skeletal
    Oxidation-Reduction
    Weight Loss

    Pub Type(s)

    Journal Article
    Review

    Language

    eng

    PubMed ID

    19207879

    Citation

    Corpeleijn, E, et al. "Metabolic Flexibility in the Development of Insulin Resistance and Type 2 Diabetes: Effects of Lifestyle." Obesity Reviews : an Official Journal of the International Association for the Study of Obesity, vol. 10, no. 2, 2009, pp. 178-93.
    Corpeleijn E, Saris WH, Blaak EE. Metabolic flexibility in the development of insulin resistance and type 2 diabetes: effects of lifestyle. Obes Rev. 2009;10(2):178-93.
    Corpeleijn, E., Saris, W. H., & Blaak, E. E. (2009). Metabolic flexibility in the development of insulin resistance and type 2 diabetes: effects of lifestyle. Obesity Reviews : an Official Journal of the International Association for the Study of Obesity, 10(2), pp. 178-93. doi:10.1111/j.1467-789X.2008.00544.x.
    Corpeleijn E, Saris WH, Blaak EE. Metabolic Flexibility in the Development of Insulin Resistance and Type 2 Diabetes: Effects of Lifestyle. Obes Rev. 2009;10(2):178-93. PubMed PMID: 19207879.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Metabolic flexibility in the development of insulin resistance and type 2 diabetes: effects of lifestyle. AU - Corpeleijn,E, AU - Saris,W H M, AU - Blaak,E E, Y1 - 2009/01/15/ PY - 2009/2/12/entrez PY - 2009/2/12/pubmed PY - 2009/6/20/medline SP - 178 EP - 93 JF - Obesity reviews : an official journal of the International Association for the Study of Obesity JO - Obes Rev VL - 10 IS - 2 N2 - Lipotoxicity in skeletal muscle plays a critical role in the aetiology of insulin resistance and type 2 diabetes mellitus by interference of lipid metabolites with insulin signalling and action. The dynamics of lipid oxidation and fine tuning with fatty acid uptake and intramyocellular triacylglycerol turnover may be very important to limit the accumulation of lipid intermediates. The use of metabolic inflexibility, defined as the impaired capacity to increase fat oxidation upon increased fatty acid availability and to switch between fat and glucose as the primary fuel source after a meal, does more justice to the complexity of changes in fuel oxidation during the day. Fatty acid availability, uptake and oxidation all play a role in metabolic flexibility and insulin resistance. During high fatty acid availability, fatty acid transporters may limit cellular and mitochondrial fatty acid uptake and thus limit fat oxidation. After a meal, when the demand for fatty acids as fuel is low, an increased fractional extraction of lipids from plasma may promote intramyocellular lipid accumulation and insulin resistance. Furthermore, defects in fuel switching cluster together with impaired mitochondrial content and/or function. Lifestyle changes in dietary fat intake, physical activity and weight loss may improve metabolic flexibility in skeletal muscle, and thereby contribute to the prevention of type 2 diabetes. SN - 1467-789X UR - https://www.unboundmedicine.com/medline/citation/19207879/Metabolic_flexibility_in_the_development_of_insulin_resistance_and_type_2_diabetes:_effects_of_lifestyle_ L2 - https://doi.org/10.1111/j.1467-789X.2008.00544.x DB - PRIME DP - Unbound Medicine ER -