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 language | English (US) |
|---|---|
| Pages (from-to) | 129-135 |
| Number of pages | 7 |
| Journal | Trends in Endocrinology and Metabolism |
| Volume | 15 |
| Issue number | 3 |
| DOIs | |
| State | Published - Apr 2004 |
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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 journal › Article
}
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 -