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Is insulin resistance caused by defects in insulin's target cells or by a stressed mind?
Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin.
Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin.
2005 (engelsk)Inngår i: Diabetes/Metabolism Research Reviews, ISSN 1520-7552, E-ISSN 1520-7560, Vol. 21, nr 6, s. 487-494Artikkel i tidsskrift (Annet vitenskapelig) Published
Abstract [en]

The importance of understanding insulin action is emphasized by the increasing prevalence of insulin resistance in various populations and by the fact that it plays an important pathophysiological role in many common disorders, for example, diabetes, obesity, hypertension and dyslipidemia. The primary factors responsible for the development of insulin resistance are so far unknown, although both genetic and environmental factors are involved. The genetic defects responsible for the common forms of insulin resistance, for example, in type 2 diabetes, are largely unidentified. Some studies from our group as well as by other investigators suggest that cellular insulin resistance is reversible and that it may be secondary to factors in the in vivo environment. These may include insulin-antagonistic action of hormones like catecholamines, glucocorticoids, sex steroids and adipokines as well as dysregulation of autonomic nervous activity and they could contribute to the early development of insulin resistance. Some of these factors can directly impair glucose uptake capacity and this might be due to alterations in key proteins involved in insulin's intracellular signaling pathways. This article briefly summarizes proposed mechanisms behind cellular and whole-body insulin resistance. In particular, we question the role of intrinsic defects in insulin's target cells as primary mechanisms in the development of insulin resistance in type 2 diabetes and we suggest that metabolic and neurohormonal factors instead are the main culprits.

sted, utgiver, år, opplag, sider
John Wiley & Sons , 2005. Vol. 21, nr 6, s. 487-494
Emneord [en]
adipose tissue/physiology, autonomic nervous system/physiopathology, central nervous system/physiopathology, diabetes mellitus; type 2/physiopathology, humans, hyperglycemia/physiopathology, hyperinsulinism/physiopathology, hypothalamo-hypophyseal system/cytology/physiopathology, insulin antagonists/metabolism, insulin resistance/genetics/*physiology, leptin/physiology, pituitary-adrenal system/cytology/physiopathology, prediabetic state/physiopathology, receptor; insulin/*physiology, stress/*physiopathology, insulin resistance, type 2 diabetes, insulin signaling, insulin-antagonistic hormones, neuroendocrine mechanisms
Identifikatorer
URN: urn:nbn:se:umu:diva-13393DOI: doi:10.1002/dmrr.567PubMedID: 15977304OAI: oai:DiVA.org:umu-13393DiVA, id: diva2:153064
Tilgjengelig fra: 2007-05-08 Laget: 2007-05-08 Sist oppdatert: 2018-06-09bibliografisk kontrollert

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