Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:6.4.1.2 (
acetyl-CoA carboxylase
)
2,876
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Multiple adult morbidities are associated with intrauterine growth retardation (IUGR) including dyslipidemia. We hypothesized that uteroplacental insufficiency and subsequent IUGR in the rat would lead to altered hepatic fatty acid metabolism. To test this hypothesis, we quantified hepatic mRNA levels of
acetyl-CoA carboxylase
(
ACC
), carnitine palmitoyltransferase (CPTI), the beta-oxidation-trifunctional protein (
HADH
), fasting serum triglycerides, and hepatic malonyl-CoA levels at different ages in control and IUGR rats. Fetal gene expression of all three enzymes was decreased. Juvenile gene expression of CPTI and
HADH
continued to be decreased, whereas gene expression of
ACC
was increased. Serum triglycerides were unchanged. A sex-specific response was noted in the adult rats. In males, serum triglycerides, hepatic malonyl-CoA levels, and
ACC
mRNA levels were significantly increased, and CPTI and
HADH
mRNA levels were significantly decreased. In contrast, the female rats demonstrated no significant changes in these variables. These results suggest that uteroplacental insufficiency leads to altered hepatic fatty acid metabolism that may contribute to the adult dyslipidemia associated with low birth weight.
...
PMID:Uteroplacental insufficiency alters hepatic fatty acid-metabolizing enzymes in juvenile and adult rats. 1112 50
