Overexpression of Alpha2A-Adrenergic Receptors Contributes to Type 2 Diabetes-Reference-Cited by-同舟云学术

Overexpression of Alpha2A-Adrenergic Receptors Contributes to Type 2 Diabetes

Published:2010-01-08 Issue:5962 Volume:327 Page:217-220
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Rosengren Anders H.¹,Jokubka Ramunas¹,Tojjar Damon¹,Granhall Charlotte¹,Hansson Ola¹,Li Dai-Qing²,Nagaraj Vini¹,Reinbothe Thomas M.¹,Tuncel Jonatan³,Eliasson Lena¹,Groop Leif¹,Rorsman Patrik⁴,Salehi Albert¹,Lyssenko Valeriya¹,Luthman Holger¹,Renström Erik¹

Affiliation:

1. Lund University Diabetes Centre, Malmö, SE-20502 Malmö, Sweden.

2. Key Laboratory of Hormones and Development, Ministry of Health, China, Tianjin Metabolic Diseases Hospital, Tianjin Medical University, China.

3. Section for Medical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, SE-17177 Stockholm, Sweden.

4. Oxford Centre for Diabetes Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, UK.

Abstract

Ratting Out a Diabetes Gene Inbred animals with inherited susceptibility to disease can be especially informative regarding pathogenetic mechanisms because they carry naturally occurring genetic variants of the same type that cause disease in humans. This principle is illustrated by Rosengren et al. (p. 217 ; published online 19 November), whose analysis of an inbred strain of rats prone to develop type 2 diabetes led to the discovery of a gene whose aberrant overexpression suppresses pancreatic insulin secretion in both rats and humans. The culprit gene, ADRA2A, encodes the alpha2A adrenergic receptor and is potentially a valuable lead for diabetes therapy because it can be targeted pharmacologically.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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