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2001

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Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/176683

Syntaxin 4 heteozygous knock-out mice develop muscle insulin resistance

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https://doi.org/10.1172/jci12274

Resum

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.

Matèries

Glucosa, Teixit adipós, Resistència a la insulina

Matèries (anglès)

Glucose, Adipose tissues, Insulin resistance

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Articles publicats en revistes (Bioquímica i Biomedicina Molecular)

Citació

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.. Syntaxin 4 heteozygous knock-out mice develop muscle insulin resistance. _Journal of Clinical Investigation_. 2001. Vol. 107, núm. 1311-1318. [consulta: 24 de gener de 2026]. ISSN: 0021-9738. [Disponible a: https://hdl.handle.net/2445/176683]

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