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Insulin resistance in skeletal muscle and adipose tissue in polycystic ovary syndrome: are the molecular mechanisms distinct from type 2 diabetes?
Panminerva Med 2008; 50(4):279-94PM

Abstract

The association of polycystic ovary syndrome (PCOS) with insulin resistance was recognized almost three decades ago. Despite the pivotal role of insulin resistance in the pathogenesis of PCOS, the precise cellular and molecular mechanisms of impaired insulin action remain elusive. This review has two aims: 1) to review the mechanisms of insulin resistance, specifically impaired insulin-stimulated glucose transport, in skeletal muscle and adipose tissue in PCOS, and 2) to assess whether mechanisms of insulin resistance in PCOS are distinct from those in type 2 diabetes. As in type 2 diabetes, studies in skeletal muscle in PCOS support the existence of intrinsic defects in insulin signalling but also underscore the importance of in vivo environmental factors for the development of insulin resistance. In PCOS and type 2 diabetes, similar insulin signalling defects in muscle have been described i.e. impaired signalling via IRS-1 and up-regulation of ERK signalling. Similar defects in insulin signalling have also been described in adipose tissue in PCOS and type 2 diabetes, but data are limited. As for type 2 diabetes, PCOS is characterized by chronic inflammation, mitochondrial dysfunction and cellular stress. Androgen excess, a key feature of PCOS, has a genetic component: the relationship of hyperandrogenemia to the development of insulin resistance requires further study. In conclusion, although similar insulin signalling defects have been identified in muscle and adipose tissue in PCOS and type 2 diabetes, these defects probably reflect a common final pathway resulting from genetic and environmental influences on insulin action that are unique to each disorder.

Authors+Show Affiliations

Prince Henry's Institute of Medical Research, Australia. anne.corbould@princehenrys.org

Pub Type(s)

Comparative Study
Journal Article
Review

Language

eng

PubMed ID

19078869

Citation

Corbould, A. "Insulin Resistance in Skeletal Muscle and Adipose Tissue in Polycystic Ovary Syndrome: Are the Molecular Mechanisms Distinct From Type 2 Diabetes?" Panminerva Medica, vol. 50, no. 4, 2008, pp. 279-94.
Corbould A. Insulin resistance in skeletal muscle and adipose tissue in polycystic ovary syndrome: are the molecular mechanisms distinct from type 2 diabetes? Panminerva Med. 2008;50(4):279-94.
Corbould, A. (2008). Insulin resistance in skeletal muscle and adipose tissue in polycystic ovary syndrome: are the molecular mechanisms distinct from type 2 diabetes? Panminerva Medica, 50(4), pp. 279-94.
Corbould A. Insulin Resistance in Skeletal Muscle and Adipose Tissue in Polycystic Ovary Syndrome: Are the Molecular Mechanisms Distinct From Type 2 Diabetes. Panminerva Med. 2008;50(4):279-94. PubMed PMID: 19078869.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Insulin resistance in skeletal muscle and adipose tissue in polycystic ovary syndrome: are the molecular mechanisms distinct from type 2 diabetes? A1 - Corbould,A, PY - 2008/12/17/entrez PY - 2008/12/17/pubmed PY - 2009/4/16/medline SP - 279 EP - 94 JF - Panminerva medica JO - Panminerva Med VL - 50 IS - 4 N2 - The association of polycystic ovary syndrome (PCOS) with insulin resistance was recognized almost three decades ago. Despite the pivotal role of insulin resistance in the pathogenesis of PCOS, the precise cellular and molecular mechanisms of impaired insulin action remain elusive. This review has two aims: 1) to review the mechanisms of insulin resistance, specifically impaired insulin-stimulated glucose transport, in skeletal muscle and adipose tissue in PCOS, and 2) to assess whether mechanisms of insulin resistance in PCOS are distinct from those in type 2 diabetes. As in type 2 diabetes, studies in skeletal muscle in PCOS support the existence of intrinsic defects in insulin signalling but also underscore the importance of in vivo environmental factors for the development of insulin resistance. In PCOS and type 2 diabetes, similar insulin signalling defects in muscle have been described i.e. impaired signalling via IRS-1 and up-regulation of ERK signalling. Similar defects in insulin signalling have also been described in adipose tissue in PCOS and type 2 diabetes, but data are limited. As for type 2 diabetes, PCOS is characterized by chronic inflammation, mitochondrial dysfunction and cellular stress. Androgen excess, a key feature of PCOS, has a genetic component: the relationship of hyperandrogenemia to the development of insulin resistance requires further study. In conclusion, although similar insulin signalling defects have been identified in muscle and adipose tissue in PCOS and type 2 diabetes, these defects probably reflect a common final pathway resulting from genetic and environmental influences on insulin action that are unique to each disorder. SN - 0031-0808 UR - https://www.unboundmedicine.com/medline/citation/19078869/Insulin_resistance_in_skeletal_muscle_and_adipose_tissue_in_polycystic_ovary_syndrome:_are_the_molecular_mechanisms_distinct_from_type_2_diabetes L2 - http://www.diseaseinfosearch.org/result/2243 DB - PRIME DP - Unbound Medicine ER -