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Type 2 diabetes mellitus and skeletal muscle metabolic function.

Abstract

Type 2 diabetic patients are characterized by a decreased fat oxidative capacity and high levels of circulating free fatty acids (FFAs). The latter is known to cause insulin resistance, in particularly in skeletal muscle, by reducing insulin stimulated glucose uptake, most likely via accumulation of lipid inside the muscle cell. A reduced skeletal muscle oxidative capacity can exaggerate this. Furthermore, type 2 diabetes is associated with impaired metabolic flexibility, i.e. an impaired switching from fatty acid to glucose oxidation in response to insulin. Thus, a reduced fat oxidative capacity and metabolic inflexibility are important components of skeletal muscle insulin resistance. The cause of these derangements in skeletal muscle of type 2 diabetic patients remains to be elucidated. An impaired mitochondrial function is a likely candidate. Evidence from both in vivo and ex vivo studies supports the idea that an impaired skeletal muscle mitochondrial function is related to the development of insulin resistance and type 2 diabetes mellitus. A decreased mitochondrial oxidative capacity in skeletal muscle was revealed in diabetic patients, using in vivo 31-Phosphorus Magnetic Resonance Spectroscopy (31P-MRS). However, quantification of mitochondrial function using ex vivo high-resolution respirometry revealed opposite results. Future (human) studies should challenge this concept of impaired mitochondrial function underlying metabolic defects and prove if mitochondria are truly functional impaired in insulin resistance, or low in number, and whether it represents the primary starting point of pathogenesis of insulin resistance, or is just an other feature of the insulin resistant state.

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  • Authors+Show Affiliations

    ,

    Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Maastricht University, Maastricht, the Netherlands. esther.phielix@hb.unimaas.nl

    Source

    Physiology & behavior 94:2 2008 May 23 pg 252-8

    MeSH

    Animals
    Diabetes Mellitus, Type 2
    Dietary Fats
    Humans
    Insulin Resistance
    Mitochondria, Muscle
    Muscle, Skeletal

    Pub Type(s)

    Journal Article
    Review

    Language

    eng

    PubMed ID

    18342897

    Citation

    Phielix, Esther, and Marco Mensink. "Type 2 Diabetes Mellitus and Skeletal Muscle Metabolic Function." Physiology & Behavior, vol. 94, no. 2, 2008, pp. 252-8.
    Phielix E, Mensink M. Type 2 diabetes mellitus and skeletal muscle metabolic function. Physiol Behav. 2008;94(2):252-8.
    Phielix, E., & Mensink, M. (2008). Type 2 diabetes mellitus and skeletal muscle metabolic function. Physiology & Behavior, 94(2), pp. 252-8. doi:10.1016/j.physbeh.2008.01.020.
    Phielix E, Mensink M. Type 2 Diabetes Mellitus and Skeletal Muscle Metabolic Function. Physiol Behav. 2008 May 23;94(2):252-8. PubMed PMID: 18342897.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Type 2 diabetes mellitus and skeletal muscle metabolic function. AU - Phielix,Esther, AU - Mensink,Marco, Y1 - 2008/01/31/ PY - 2007/08/13/received PY - 2008/01/23/revised PY - 2008/01/25/accepted PY - 2008/3/18/pubmed PY - 2008/7/23/medline PY - 2008/3/18/entrez SP - 252 EP - 8 JF - Physiology & behavior JO - Physiol. Behav. VL - 94 IS - 2 N2 - Type 2 diabetic patients are characterized by a decreased fat oxidative capacity and high levels of circulating free fatty acids (FFAs). The latter is known to cause insulin resistance, in particularly in skeletal muscle, by reducing insulin stimulated glucose uptake, most likely via accumulation of lipid inside the muscle cell. A reduced skeletal muscle oxidative capacity can exaggerate this. Furthermore, type 2 diabetes is associated with impaired metabolic flexibility, i.e. an impaired switching from fatty acid to glucose oxidation in response to insulin. Thus, a reduced fat oxidative capacity and metabolic inflexibility are important components of skeletal muscle insulin resistance. The cause of these derangements in skeletal muscle of type 2 diabetic patients remains to be elucidated. An impaired mitochondrial function is a likely candidate. Evidence from both in vivo and ex vivo studies supports the idea that an impaired skeletal muscle mitochondrial function is related to the development of insulin resistance and type 2 diabetes mellitus. A decreased mitochondrial oxidative capacity in skeletal muscle was revealed in diabetic patients, using in vivo 31-Phosphorus Magnetic Resonance Spectroscopy (31P-MRS). However, quantification of mitochondrial function using ex vivo high-resolution respirometry revealed opposite results. Future (human) studies should challenge this concept of impaired mitochondrial function underlying metabolic defects and prove if mitochondria are truly functional impaired in insulin resistance, or low in number, and whether it represents the primary starting point of pathogenesis of insulin resistance, or is just an other feature of the insulin resistant state. SN - 0031-9384 UR - https://www.unboundmedicine.com/medline/citation/18342897/Type_2_diabetes_mellitus_and_skeletal_muscle_metabolic_function_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0031-9384(08)00023-1 DB - PRIME DP - Unbound Medicine ER -