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On the role of IRS2 in the regulation of functional beta-cell mass


Niessen, M (2006). On the role of IRS2 in the regulation of functional beta-cell mass. Archives of Physiology and Biochemistry, 112(2):65-73.

Abstract

The proper regulation of blood glucose homeostasis in mammals requires an adequate relation between the capacity to produce insulin and metabolic demand. Insulin receptor substrate proteins (IRS) are signalling intermediates that are required to keep this balance because they are needed for insulin action in target tissues but also for insulin production in pancreatic beta-cells. The total functional beta-cell mass in an individual sets the limit of how much insulin can be produced at a given time. It can change adaptively to meet demand and studies in vivo indicate that the regulation of beta-cell mass involves IRS2, while IRS1 is only required for proper insulin production in beta-cells. Overexpression studies in isolated islets have shown that IRS2, but not IRS1 or Shc, is sufficient to induce proliferation of beta-cells and to protect against d-glucose-induced apoptosis. In light of the finding that many growth factors can regulate Irs2 in islets, this signalling intermediate could balance capacity for insulin production with demand. This review summarizes observations in mouse models and in primary beta-cells and proposes a new hypothetical model of how IRS2 might control beta-cell mass.

Abstract

The proper regulation of blood glucose homeostasis in mammals requires an adequate relation between the capacity to produce insulin and metabolic demand. Insulin receptor substrate proteins (IRS) are signalling intermediates that are required to keep this balance because they are needed for insulin action in target tissues but also for insulin production in pancreatic beta-cells. The total functional beta-cell mass in an individual sets the limit of how much insulin can be produced at a given time. It can change adaptively to meet demand and studies in vivo indicate that the regulation of beta-cell mass involves IRS2, while IRS1 is only required for proper insulin production in beta-cells. Overexpression studies in isolated islets have shown that IRS2, but not IRS1 or Shc, is sufficient to induce proliferation of beta-cells and to protect against d-glucose-induced apoptosis. In light of the finding that many growth factors can regulate Irs2 in islets, this signalling intermediate could balance capacity for insulin production with demand. This review summarizes observations in mouse models and in primary beta-cells and proposes a new hypothetical model of how IRS2 might control beta-cell mass.

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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Endocrinology and Diabetology
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2006
Deposited On:06 Apr 2009 07:19
Last Modified:06 Dec 2017 15:25
Publisher:Informa Healthcare
ISSN:1381-3455
Additional Information:This is an electronic version of an article published in Niessen, M (2006). On the role of IRS2 in the regulation of functional beta-cell mass. Archives of Physiology and Biochemistry, 112(2):65-73. Archives of Physiology and Biochemistry is available online at: www.informaworld.com/smpp/title~content=t713817673
Free access at:PubMed ID. An embargo period may apply.
Publisher DOI:https://doi.org/10.1080/13813450600711409
PubMed ID:16931448

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