Please use this identifier to cite or link to this item:
Title: Syntaxin 4 heteozygous knock-out mice develop muscle insulin resistance
Author: Yang, Chunmei
Coker, Kenneth J.
Kim, Jason K.
Mora Fayos, Sílvia
Thurmond, Debbie C.
Davis, Ann C.
Yang, Baoli
Williamson, Roger A.
Shulman, Gerald I.
Pessin, Jeffrey E.
Keywords: Glucosa
Teixit adipós
Resistència a la insulina
Adipose tissues
Insulin resistance
Issue Date: 2001
Publisher: American Society for Clinical Investigation
Abstract: To investigate the physiological function of syntaxin 4 in the regulation of GLUT4 vesicle trafficking, we used homologous recombination to generate syntaxin 4-knockout mice. Homozygotic disruption of the syntaxin 4 gene results in early embryonic lethality, whereas heterozygous knockout mice, Syn4+/-, had normal viability with no significant impairment in growth, development, or reproduction. However, the Syn4+/- mice manifested impaired glucose tolerance with a 50% reduction in whole-body glucose uptake. This defect was attributed to a 50% reduction in skeletal muscle glucose transport determined by 2-deoxyglucose uptake during hyperinsulinemic-euglycemic clamp procedures. In parallel, insulin-stimulated GLUT4 translocation in skeletal muscle was also significantly reduced in these mice. In contrast, Syn4+/- mice displayed normal insulin-stimulated glucose uptake and metabolism in adipose tissue and liver. Together, these data demonstrate that syntaxin 4 plays a critical physiological role in insulin-stimulated glucose uptake in skeletal muscle. Furthermore, reduction in syntaxin 4 protein levels in this tissue can account for the impairment in whole-body insulin-stimulated glucose metabolism in this animal model.
Note: Reproducció del document publicat a:
It is part of: Journal of Clinical Investigation, 2001, vol. 107, p. 1311-1318.
Related resource:
ISSN: 0021-9738
Appears in Collections:Articles publicats en revistes (Bioquímica i Biomedicina Molecular)

Files in This Item:
File Description SizeFormat 
711513.pdf837.7 kBAdobe PDFView/Open

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.