β-Cell deterioration during diabetes: what's in the gun?

R. Paul Robertson

doi:10.1016/j.tem.2009.05.004

β-Cell deterioration during diabetes: what's in the gun?

R. Paul Robertson

Research output: Contribution to journal › Review article › peer-review

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Abstract

Clinical management of patients with type 2 diabetes (T2D) successfully prevents extreme hyperglycemia but does not precisely control glucose levels throughout the day. The pathogenesis of T2D is akin to a double-barrel shotgun. The first trigger causes an explosion that sets genetic expression of the disease in motion; the second trigger discharges a host of environmental factors that worsen its clinical course. Candidate shells include glucolipotoxicity, cytokines, oxidative and endoplasmic reticulum stress and insulin resistance. This review considers how each candidate adversely impacts β-cell function to create the downward spiral of glycemic control. Their roles in pathogenesis raise possibilities for new drug therapies designed to protect against adverse effects of residual hyperglycemia in patients treated with conventional drugs.

Original language	English (US)
Pages (from-to)	388-393
Number of pages	6
Journal	Trends in Endocrinology and Metabolism
Volume	20
Issue number	8
DOIs	https://doi.org/10.1016/j.tem.2009.05.004
State	Published - Oct 2009
Externally published	Yes

Bibliographical note

Funding Information:
The author is supported by NIH NIDDK grant R01 85325.

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title = "β-Cell deterioration during diabetes: what's in the gun?",

abstract = "Clinical management of patients with type 2 diabetes (T2D) successfully prevents extreme hyperglycemia but does not precisely control glucose levels throughout the day. The pathogenesis of T2D is akin to a double-barrel shotgun. The first trigger causes an explosion that sets genetic expression of the disease in motion; the second trigger discharges a host of environmental factors that worsen its clinical course. Candidate shells include glucolipotoxicity, cytokines, oxidative and endoplasmic reticulum stress and insulin resistance. This review considers how each candidate adversely impacts β-cell function to create the downward spiral of glycemic control. Their roles in pathogenesis raise possibilities for new drug therapies designed to protect against adverse effects of residual hyperglycemia in patients treated with conventional drugs.",

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AB - Clinical management of patients with type 2 diabetes (T2D) successfully prevents extreme hyperglycemia but does not precisely control glucose levels throughout the day. The pathogenesis of T2D is akin to a double-barrel shotgun. The first trigger causes an explosion that sets genetic expression of the disease in motion; the second trigger discharges a host of environmental factors that worsen its clinical course. Candidate shells include glucolipotoxicity, cytokines, oxidative and endoplasmic reticulum stress and insulin resistance. This review considers how each candidate adversely impacts β-cell function to create the downward spiral of glycemic control. Their roles in pathogenesis raise possibilities for new drug therapies designed to protect against adverse effects of residual hyperglycemia in patients treated with conventional drugs.

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β-Cell deterioration during diabetes: what's in the gun?

Abstract

Bibliographical note

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