Disregulated glyceroneogenesis: PCK1 as a candidate diabetes and obesity gene

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

Research output: Contribution to journalArticle

75 Citations (Scopus)

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

Fingerprint

Obesity
Mutation
Type 2 Diabetes Mellitus
Genes
Adipose Tissue
Gluconeogenesis
Fatty Acids
Diet
Phenotype
Glucose
Liver

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Disregulated glyceroneogenesis : PCK1 as a candidate diabetes and obesity gene. / Beale, Elmus G.; Hammer, Robert E; Antoine, Bénédicte; Forest, Claude.

In: Trends in Endocrinology and Metabolism, Vol. 15, No. 3, 04.2004, p. 129-135.

Research output: Contribution to journalArticle

Beale, Elmus G. ; Hammer, Robert E ; Antoine, Bénédicte ; Forest, Claude. / Disregulated glyceroneogenesis : PCK1 as a candidate diabetes and obesity gene. In: Trends in Endocrinology and Metabolism. 2004 ; Vol. 15, No. 3. pp. 129-135.
@article{cbe8e95f7b0d41dda1b71de6b13820b3,
title = "Disregulated glyceroneogenesis: PCK1 as a candidate diabetes and obesity gene",
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.",
author = "Beale, {Elmus G.} and Hammer, {Robert E} and B{\'e}n{\'e}dicte Antoine and Claude Forest",
year = "2004",
month = "4",
doi = "10.1016/j.tem.2004.02.006",
language = "English (US)",
volume = "15",
pages = "129--135",
journal = "Trends in Endocrinology and Metabolism",
issn = "1043-2760",
publisher = "Elsevier Inc.",
number = "3",

}

TY - JOUR

T1 - Disregulated glyceroneogenesis

T2 - PCK1 as a candidate diabetes and obesity gene

AU - Beale, Elmus G.

AU - Hammer, Robert E

AU - Antoine, Bénédicte

AU - Forest, Claude

PY - 2004/4

Y1 - 2004/4

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=1842523229&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=1842523229&partnerID=8YFLogxK

U2 - 10.1016/j.tem.2004.02.006

DO - 10.1016/j.tem.2004.02.006

M3 - Article

C2 - 15046742

AN - SCOPUS:1842523229

VL - 15

SP - 129

EP - 135

JO - Trends in Endocrinology and Metabolism

JF - Trends in Endocrinology and Metabolism

SN - 1043-2760

IS - 3

ER -