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Article

Insulin secretory deficiency and glucose intolerance in Rab3A null mice.

The Journal of biological chemistry - 14 Mar 2003

Yaekura Kazuro, Julyan Richard, Wicksteed Barton L, Hays Lori B, Alarcon Cristina, Sommers Scott, Poitout Vincent, Baskin Denis G, Wang Yong, Philipson Louis H, Rhodes Christopher J

Abstract excerpt

Insulin secretory dysfunction of the pancreatic beta-cell in type-2 diabetes is thought to be due to defective nutrient sensing and/or deficiencies in the mechanism of insulin exocytosis. Previous studies have indicated that the GTP-binding protein, Rab3A, plays a mechanistic role in insulin exocytosis. Here, we report that Rab3A(-/-) mice develop fasting hyperglycemia and upon a glucose challenge show...

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Identifiers

PMID: 12510060
DOI: 10.1074/jbc.M211352200

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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