| Literature DB >> 3481265 |
M J Holness1, T N Palmer, E B Worrall, M C Sugden.
Abstract
In this study we utilized the phosphorylase b kinase-deficient (gsd/gsd) rat as a model of hepatic substrate utilization where there is a constraint on glycogenesis imposed by the maintenance of high glycogen concentrations. Glucose re-feeding of 48 h-starved gsd/gsd rats led to suppression of hepatic glucose output. In contrast with the situation in normal rats, activation of the pyruvate dehydrogenase complex and lipogenesis was observed. It is suggested that impeding glycogenic flux may divert substrate into lipogenesis, possibly via activation of the pyruvate dehydrogenase complex.Entities:
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Year: 1987 PMID: 3481265 PMCID: PMC1148646 DOI: 10.1042/bj2480969
Source DB: PubMed Journal: Biochem J ISSN: 0264-6021 Impact factor: 3.857