Atypical protein kinase C dysfunction and the metabolic syndrome.
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 Clambda, 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 Clambda deficiency might be sufficient to induce metabolic syndrome in mice.
Beguinot
Francesco
F
Dipartimento di Biologia e Patologia Cellulare e Molecolare, Federico II University of Naples Medical School, Via Sergio Pansini 5, Naples, Italy. beguino@unina.it
Formisano
Pietro
P
D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000201:enzymology / Q000235:genetics; D018628:Gene Dosage / Q000502:physiology; D006801:Humans; D007333:Insulin Resistance / Q000235:genetics / Q000502:physiology; D007527:Isoenzymes / Q000235:genetics / Q000502:physiology; D024821:Metabolic Syndrome / Q000201:enzymology* / Q000235:genetics; D051379:Mice; D018345:Mice, Knockout; D008954:Models, Biological; D011493:Protein Kinase C / Q000235:genetics / Q000502:physiology*; D000099293:Protein Kinase C-lambda
D007527:Isoenzymes; D011493:Protein Kinase C; D000099293:Protein Kinase C-lambda; C115015:PKC-3 protein