Atypical protein kinase C dysfunction and the metabolic syndrome

作者：Beguinot Francesco^*; Formisano Pietro

来源：Trends in Endocrinology and Metabolism, 2008, 19(2): 39-41.

DOI：10.1016/j.tem.2007.11.005

Atypical protein kinase C isoforms are crucial mediators of glucose uptake in insulin-sensitive tissues. In humans, decreased muscular atypical protein kinase C activity has been found in insulin-resistant states. In a recent report by Farese et al., a novel mouse model is described, featuring selective ablation of an atypical protein kinase C, protein kinase C lambda, in muscle. Phenotyping of these mice demonstrated systemic insulin resistance, reduced glucose tolerance, abdominal obesity and dyslipidemia, thus mimicking human metabolic syndrome. Intriguingly, therefore, atypical protein kinase C lambda deficiency might be sufficient to induce metabolic syndrome in mice.

• 出版日期2008-3