Disregulated glyceroneogenesis: PCK1 as a candidate diabetes and obesity gene

Elmus G. Beale, Robert E Hammer, Bénédicte Antoine, Claude Forest

Research output: Contribution to journalReview article

80 Scopus citations

Abstract

Genetics and diet interact to cause type 2 diabetes mellitus and obesity. PCK1 has been implicated as one of many genes associated with type 2 diabetes mellitus. The common assumption is that mutations in PCK1 lead to excessive glucose production through hepatic gluconeogenesis. However, there is an alternative explanation, wherein mutations at the PCK1 locus could selectively affect PCK1 expression in adipose tissue. The result would be changes in glyceroneogenesis that would affect the storage and release of fatty acids. Here, we present the novel hypothesis that a variety of phenotypes could arise from mutations of the various tissue-specific control elements of PCK1. We also suggest specific quantitative metabolic traits that would accompany mutations that selectively affect PCK1 expression in adipose tissue.

Original languageEnglish (US)
Pages (from-to)129-135
Number of pages7
JournalTrends in Endocrinology and Metabolism
Volume15
Issue number3
DOIs
StatePublished - Apr 2004

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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