Skeletal muscle insulin resistance in endocrine disease.

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  • Author(s): Peppa M;Peppa M; Koliaki C; Nikolopoulos P; Raptis SA
  • Source:
    Journal of biomedicine & biotechnology [J Biomed Biotechnol] 2010; Vol. 2010, pp. 527850. Date of Electronic Publication: 2010 Mar 15.
  • Publication Type:
    Journal Article; Review
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Hindawi Pub. Corp Country of Publication: United States NLM ID: 101135740 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1110-7251 (Electronic) Linking ISSN: 11107243 NLM ISO Abbreviation: J Biomed Biotechnol Subsets: MEDLINE
    • Publication Information:
      Publication: 2006- : Cairo : Hindawi Pub. Corp.
      Original Publication: Akron, Ohio : Hindawi Pub. Corp., [2001-
    • Subject Terms:
      Insulin Resistance*; Endocrine System Diseases/*metabolism ; Glucose/*metabolism ; Insulin/*metabolism ; Muscle, Skeletal/*metabolism; Animals ; Humans ; Models, Biological
    • Abstract:
      We summarize the existing literature data concerning the involvement of skeletal muscle (SM) in whole body glucose homeostasis and the contribution of SM insulin resistance (IR) to the metabolic derangements observed in several endocrine disorders, including polycystic ovary syndrome (PCOS), adrenal disorders and thyroid function abnormalities. IR in PCOS is associated with a unique postbinding defect in insulin receptor signaling in general and in SM in particular, due to a complex interaction between genetic and environmental factors. Adrenal hormone excess is also associated with disrupted insulin action in peripheral tissues, such as SM. Furthermore, both hyper- and hypothyroidism are thought to be insulin resistant states, due to insulin receptor and postreceptor defects. Further studies are definitely needed in order to unravel the underlying pathogenetic mechanisms. In summary, the principal mechanisms involved in muscle IR in the endocrine diseases reviewed herein include abnormal phosphorylation of insulin signaling proteins, altered muscle fiber composition, reduced transcapillary insulin delivery, decreased glycogen synthesis, and impaired mitochondrial oxidative metabolism.
    • Number of References:
      116
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    • Accession Number:
      0 (Insulin)
      IY9XDZ35W2 (Glucose)
    • Publication Date:
      Date Created: 20100320 Date Completed: 20100623 Latest Revision: 20211020
    • Publication Date:
      20231215
    • Accession Number:
      PMC2840413
    • Accession Number:
      10.1155/2010/527850
    • Accession Number:
      20300436