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Implications of genome wide association studies for the understanding of type 2 diabetes pathophysiology

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Implications of genome wide association studies for the understanding of type 2 diabetes pathophysiology. / Petrie, John R.; Pearson, Ewan R.; Sutherland, Calum.

In: Biochemical Pharmacology, Vol. 81, No. 4, 15.02.2011, p. 471-477.

Research output: Contribution to journalArticle

Harvard

Petrie, JR, Pearson, ER & Sutherland, C 2011, 'Implications of genome wide association studies for the understanding of type 2 diabetes pathophysiology' Biochemical Pharmacology, vol 81, no. 4, pp. 471-477., 10.1016/j.bcp.2010.11.010

APA

Petrie, J. R., Pearson, E. R., & Sutherland, C. (2011). Implications of genome wide association studies for the understanding of type 2 diabetes pathophysiology. Biochemical Pharmacology, 81(4), 471-477. 10.1016/j.bcp.2010.11.010

Vancouver

Petrie JR, Pearson ER, Sutherland C. Implications of genome wide association studies for the understanding of type 2 diabetes pathophysiology. Biochemical Pharmacology. 2011 Feb 15;81(4):471-477. Available from: 10.1016/j.bcp.2010.11.010

Author

Petrie, John R.; Pearson, Ewan R.; Sutherland, Calum / Implications of genome wide association studies for the understanding of type 2 diabetes pathophysiology.

In: Biochemical Pharmacology, Vol. 81, No. 4, 15.02.2011, p. 471-477.

Research output: Contribution to journalArticle

Bibtex - Download

@article{18b6474c6dae40f281222041be3a04fc,
title = "Implications of genome wide association studies for the understanding of type 2 diabetes pathophysiology",
keywords = "Diabetes, Gene, Insulin, Beta cell, Signalling, BETA-CELL FUNCTION, INSULIN-RESISTANCE, CARDIOVASCULAR-DISEASE, NATURAL-HISTORY, RISK, SENSITIVITY, GLUCOSE, MELLITUS, MUTATION, HYPERINSULINEMIA",
author = "Petrie, {John R.} and Pearson, {Ewan R.} and Calum Sutherland",
year = "2011",
doi = "10.1016/j.bcp.2010.11.010",
volume = "81",
number = "4",
pages = "471--477",
journal = "Biochemical Pharmacology",
issn = "0006-2952",

}

RIS (suitable for import to EndNote) - Download

TY - JOUR

T1 - Implications of genome wide association studies for the understanding of type 2 diabetes pathophysiology

A1 - Petrie,John R.

A1 - Pearson,Ewan R.

A1 - Sutherland,Calum

AU - Petrie,John R.

AU - Pearson,Ewan R.

AU - Sutherland,Calum

PY - 2011/2/15

Y1 - 2011/2/15

N2 - <p>The rapid rise in prevalence of type 2 diabetes mellitus (T2DM) has been driven by changes in environmental factors - primarily increased caloric intake and reduced energy expenditure - resulting in reduced whole body insulin sensitivity (often termed insulin resistance). Insulin resistance has been proposed to be a major driver of progression to T2DM. However, of 38 individual susceptibility loci for T2DM recently identified by genome wide association studies, by far the majority code for proteins involved in beta-cell function. In this review, we discuss the possible reasons for the paucity of insulin resistance genes and ask whether the new genetic susceptibility data should focus attention on beta-cell targets in the development of therapies for T2DM. (c) 2010 Elsevier Inc. All rights reserved.</p>

AB - <p>The rapid rise in prevalence of type 2 diabetes mellitus (T2DM) has been driven by changes in environmental factors - primarily increased caloric intake and reduced energy expenditure - resulting in reduced whole body insulin sensitivity (often termed insulin resistance). Insulin resistance has been proposed to be a major driver of progression to T2DM. However, of 38 individual susceptibility loci for T2DM recently identified by genome wide association studies, by far the majority code for proteins involved in beta-cell function. In this review, we discuss the possible reasons for the paucity of insulin resistance genes and ask whether the new genetic susceptibility data should focus attention on beta-cell targets in the development of therapies for T2DM. (c) 2010 Elsevier Inc. All rights reserved.</p>

KW - Diabetes

KW - Gene

KW - Insulin

KW - Beta cell

KW - Signalling

KW - BETA-CELL FUNCTION

KW - INSULIN-RESISTANCE

KW - CARDIOVASCULAR-DISEASE

KW - NATURAL-HISTORY

KW - RISK

KW - SENSITIVITY

KW - GLUCOSE

KW - MELLITUS

KW - MUTATION

KW - HYPERINSULINEMIA

U2 - 10.1016/j.bcp.2010.11.010

DO - 10.1016/j.bcp.2010.11.010

M1 - Article

JO - Biochemical Pharmacology

JF - Biochemical Pharmacology

SN - 0006-2952

IS - 4

VL - 81

SP - 471

EP - 477

ER -

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