Differential regulation of hepatic gene expression by starvation versus refeeding following a high-sucrose or high-fat diet.
OBJECTIVE
The objective of this work was to determine the effects of starvation versus refeeding following a high-sucrose diet (HS) or high-fat diet (HF) on fatty acid metabolism in mice.


METHODS
The mice were fed an AIN-76 control diet (CD), a modified HS, or an HF. The three dietary groups were subdivided into three groups each: those fed experimental diets for 12 wk, mice starved for 48 h after 12 wk on an experimental diet, and those with the same starvation treatment but with 72 h of refeeding after starvation, respectively.


RESULTS
Serum total cholesterol levels of CD and HF groups decreased and then increased under starvation and refeeding states, respectively. Refeeding HS and HF increased serum levels of low-density lipoprotein (LDL) cholesterol compared with refeeding of the CD group. Starvation significantly increased hepatic levels of total cholesterol in the HS and HF groups compared with the CD group. Hepatic acyl coenzyme A (CoA) synthetase (ACS) levels in the CD and HS groups but not the HF group increased and then decreased under starved and refed states, respectively; an opposite regulation was observed in the HF group. Levels of hepatic acetyl-CoA carboxylase (ACC) in the HS and HF groups were significantly increased by refeeding. Hepatic levels of carnitine palmitoyltransferase-I mRNA were significantly enhanced by starvation and refeeding in the HS group but decreased in CD and then increased in the HF group.


CONCLUSIONS
Changes in dietary energy nutrients, fasting, and refeeding affect hepatic ACS, CPT-I, and ACC mRNA expression, and these results will serve to enhance our understanding of the molecular mechanisms underlying regulation of fatty acid metabolism.
Ryu
Mi-Hyun
MH
Department of Food Science and Human Nutrition, and Institute for Molecular Biology and Genetics, Chonbuk National University, Chonju, Korea.
Sohn
Hee Sook
HS
Heo
Young Ran
YR
Moustaid-Moussa
Naima
N
Cha
Youn-Soo
YS
D000103:Acetyl-CoA Carboxylase / Q000235:genetics / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000235:genetics / Q000378:metabolism; D015152:Blotting, Northern / Q000379:methods; D001835:Body Weight / Q000502:physiology; D002334:Carnitine O-Palmitoyltransferase / Q000235:genetics / Q000378:metabolism; D002784:Cholesterol / Q000097:blood / Q000235:genetics; D003066:Coenzyme A Ligases / Q000235:genetics / Q000378:metabolism; D004032:Diet; D004041:Dietary Fats / Q000008:administration & dosage*; D004435:Eating / Q000502:physiology*; D002149:Energy Intake / Q000502:physiology; D005227:Fatty Acids / Q000235:genetics / Q000378:metabolism; D015870:Gene Expression / Q000502:physiology*; D007328:Insulin / Q000097:blood / Q000235:genetics; D020738:Leptin / Q000097:blood / Q000235:genetics; D008099:Liver / Q000378:metabolism*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D013217:Starvation / Q000235:genetics / Q000378:metabolism*; D013395:Sucrose / Q000008:administration & dosage*; D013549:Sweetening Agents / Q000008:administration & dosage
D001786:Blood Glucose; D004041:Dietary Fats; D005227:Fatty Acids; D007328:Insulin; D020738:Leptin; D012333:RNA, Messenger; D013549:Sweetening Agents; D013395:Sucrose; D002784:Cholesterol; D002334:Carnitine O-Palmitoyltransferase; D003066:Coenzyme A Ligases; D000103:Acetyl-CoA Carboxylase