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

John R. Petrie; Ewan R. Pearson; Calum Sutherland

doi:10.1016/j.bcp.2010.11.010

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

Research output: Contribution to journal › Article › peer-review

Abstract

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.

Original language	English
Pages (from-to)	471-477
Number of pages	7
Journal	Biochemical Pharmacology
Volume	81
Issue number	4
DOIs	https://doi.org/10.1016/j.bcp.2010.11.010
Publication status	Published - 15 Feb 2011

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

Diabetes
Gene
Insulin
Beta cell
Signalling
BETA-CELL FUNCTION
INSULIN-RESISTANCE
CARDIOVASCULAR-DISEASE
NATURAL-HISTORY
RISK
SENSITIVITY
GLUCOSE
MELLITUS
MUTATION
HYPERINSULINEMIA

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10.1016/j.bcp.2010.11.010

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title = "Implications of genome wide association studies for the understanding of type 2 diabetes pathophysiology",

abstract = "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.",

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",

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doi = "10.1016/j.bcp.2010.11.010",

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AU - Petrie, John R.

AU - Pearson, Ewan R.

AU - Sutherland, Calum

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N2 - 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.

AB - 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.

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

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DO - 10.1016/j.bcp.2010.11.010

M3 - Article

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EP - 477

JO - Biochemical Pharmacology

JF - Biochemical Pharmacology

IS - 4

ER -

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

Abstract

UN SDGs

Keywords

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