Format

Send to

Choose Destination
See comment in PubMed Commons below
Trends Endocrinol Metab. 2004 Apr;15(3):129-35.

Disregulated glyceroneogenesis: PCK1 as a candidate diabetes and obesity gene.

Author information

1
Department of Cell Biology and Biochemistry, Stop 6540, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA. elmus.beale@ttuhsc.edu

Erratum in

  • Trends Endocrinol Metab. 2004 Jul;15(5):192. ).

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.

PMID:
15046742
DOI:
10.1016/j.tem.2004.02.006
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center