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Data de publicació

2007-10

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cc-by (c) Llagostera Martín, Esther et al., 2007
Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/43315

Role of Myotonic Dystrophy Protein Kinase [DMPK] in Glucose Homeostasis and Muscle Insulin Action

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Recurs relacionat

http://dx.doi.org/10.1371/journal.pone.0001134

Resum

Myotonic dystrophy 1 (DM1) is caused by a CTG expansion in the 3′-unstranslated region of the DMPK gene, which encodes a serine/threonine protein kinase. One of the common clinical features of DM1 patients is insulin resistance, which has been associated with a pathogenic effect of the repeat expansions. Here we show that DMPK itself is a positive modulator of insulin action. DMPK-deficient (dmpk−/−) mice exhibit impaired insulin signaling in muscle tissues but not in adipocytes and liver, tissues in which DMPK is not expressed. Dmpk−/− mice display metabolic derangements such as abnormal glucose tolerance, reduced glucose uptake and impaired insulin-dependent GLUT4 trafficking in muscle. Using DMPK mutants, we show that DMPK is required for a correct intracellular trafficking of insulin and IGF-1 receptors, providing a mechanism to explain the molecular and metabolic phenotype of dmpk−/− mice. Taken together, these findings indicate that reduced DMPK expression may directly influence the onset of insulin-resistance in DM1 patients and point to dmpk as a new candidate gene for susceptibility to type 2-diabetes.

Matèries

Fisiologia patològica, Proteïnes quinases, Malalties de l'aparell locomotor, Insulina

Matèries (anglès)

Pathological physiology, Protein kinases, Enfermedades del aparato locomotor, Insulin

Citació

Col·leccions

Articles publicats en revistes (Bioquímica i Biomedicina Molecular)
Articles publicats en revistes (Medicina)

Citació

LLAGOSTERA MARTÍN, Esther, et al. Role of Myotonic Dystrophy Protein Kinase [DMPK] in Glucose Homeostasis and Muscle Insulin Action. PLoS One. 2007. Vol. 11, num. e1134. ISSN 1932-6203. [consulted: 19 of August of 2026]. Available at: https://hdl.handle.net/2445/43315

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