Deletion of GαZ Protein Protects against Diet-induced Glucose Intolerance via Expansion of β-Cell Mass-Reference-Cited by-同舟云学术

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Deletion of GαZ Protein Protects against Diet-induced Glucose Intolerance via Expansion of β-Cell Mass

Published:2012-06 Issue:24 Volume:287 Page:20344-20355
ISSN:0021-9258
Container-title:Journal of Biological Chemistry
language:en
Short-container-title:Journal of Biological Chemistry

Author:

Kimple Michelle E.,Moss Jennifer B.,Brar Harpreet K.,Rosa Taylor C.,Truchan Nathan A.,Pasker Renee L.,Newgard Christopher B.,Casey Patrick J.

Publisher

Elsevier BV

Subject

Cell Biology,Molecular Biology,Biochemistry

Reference54 articles.

1. The relative contributions of insulin resistance and β-cell dysfunction to the pathophysiology of Type 2 diabetes;Kahn;Diabetologia,2003

2. The evolution of β-cell dysfunction and insulin resistance in type 2 diabetes;Bergman;Eur. J. Clin. Invest.,2002

3. Identifying the links between obesity, insulin resistance and beta-cell function. Potential role of adipocyte-derived cytokines in the pathogenesis of type 2 diabetes;Greenberg;Eur. J. Clin. Invest.,2002

4. Redefining the clinical management of type 2 diabetes. Matching therapy to pathophysiology;Gerich;Eur. J. Clin. Invest.,2002

5. Mechanisms of disease. Molecular and metabolic mechanisms of insulin resistance and β-cell failure in type 2 diabetes;Muoio;Nat. Rev. Mol. Cell Biol.,2008

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2. The prostaglandin E₂ EP3 receptor has disparate effects on islet insulin secretion and content in β-cells in a high-fat diet-induced mouse model of obesity;American Journal of Physiology-Endocrinology and Metabolism;2024-05-01

3. EP3 signaling is decoupled from the regulation of glucose-stimulated insulin secretion in β-cells compensating for obesity and insulin resistance;Islets;2023-07-06

4. Noncanonical Regulation of cAMP‐Dependent Insulin Secretion and Its Implications in Type 2 Diabetes;Comprehensive Physiology;2023-06-26

5. Plasma Prostaglandin E2 Metabolite Levels Predict Type 2 Diabetes Status and One-Year Therapeutic Response Independent of Clinical Markers of Inflammation;Metabolites;2022-12-08

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