GONUTS has been updated to MW1.31 Most things seem to be working but be sure to report problems.

Have any questions? Please email us at ecoliwiki@gmail.com

TableEdit

Jump to: navigation, search

PMID:16049329

You don't have sufficient rights on this wiki to edit tables. Perhaps you need to log in. Changes you make in the Table editor will not be saved back to the wiki

See Help for Help on this wiki. See the documentation for how to use the table editor

Citation

Dai, C, Huh, CG, Thorgeirsson, SS and Liu, Y (2005) Beta-cell-specific ablation of the hepatocyte growth factor receptor results in reduced islet size, impaired insulin secretion, and glucose intolerance. Am. J. Pathol. 167:429-36

Abstract

Hepatocyte growth factor (HGF) and its c-met receptor consist of a paired signaling system that has been implicated in the regulation of pancreatic beta-cell survival, proliferation, and function. To define the role of HGF/c-met signaling in beta-cell biology in vivo, we have generated conditional knockout mice in which the c-met receptor gene was specifically inactivated in pancreatic beta cells by the Cre-loxP system. Mice with beta-cell-specific deletion of the c-met receptor (betamet-/-) displayed slight growth retardation, mild hyperglycemia, and decreased serum insulin levels at 6 months of age when compared with their control littermates. Deficiency of the c-met receptor in beta cells resulted in a complete loss of acute-phase insulin secretion in response to glucose and an impaired glucose tolerance. Glucose transporter-2 expression was down-regulated in the beta cells of betamet-/- mice. Compared to controls, betamet-/- mice exhibited reduced islet size and decreased insulin content in the pancreas, but displayed normal islet morphology. Therefore, HGF/c-met signaling plays an imperative role in controlling islet growth, in regulating beta-cell function, and in maintaining glucose homeostasis.

Links

PubMed PMC1603568

Keywords

Animals; Blood Glucose/metabolism; Blotting, Western; Female; Genotype; Glucose Intolerance; Glucose Transporter Type 2; Hyperglycemia/etiology; Insulin/secretion; Integrases; Islets of Langerhans/metabolism; Islets of Langerhans/pathology; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Monosaccharide Transport Proteins/metabolism; Proto-Oncogene Proteins c-met/genetics; Proto-Oncogene Proteins c-met/physiology; Reverse Transcriptase Polymerase Chain Reaction

public



Cancel