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Correspondence to:
Geoffrey F. Gibbons, To whom correspondence should be addressed., geoff.gibbons{at}mrl.ox.ac.uk (E-mail)
Peroxisome proliferator-activated receptor
The results suggest that PPAR
Supplementary key words:
cholesterol, fatty acids, liver, diurnal cycle, plasma, sterol regulatory element-binding protein, peroxisome proliferator-activated receptor
Copyright © 2001 by Lipid Research, Inc.
Original Article
Disturbances in the normal regulation of SREBP-sensitive genes in PPAR
Dilip D. Patela,
Brian L. Knighta,
David Wigginsb,
Sandy M. Humphreysc, and
Geoffrey F. Gibbonsb
-deficient mice
a Lipoprotein Group, MRC Clinical Sciences Centre, Imperial College School of Medicine, Hammersmith Hospital, London W12 ONN, UK
b Metabolic Research Laboratory, Nuffield Department of Clinical Medicine, University of Oxford, Oxford OX2 6HE, UK
c Oxford Lipid Metabolism Group, Nuffield Department of Clinical Medicine, University of Oxford, Oxford OX2 6HE, UK
(PPAR)-null mice were used to investigate the nature of the relationship between the normal circadian rhythm of hepatic PPAR expression and the expression of the lipogenic and cholesterogenic sterol regulatory element-binding protein (SREBP)-regulated genes, acetyl-CoA carboxylase, fatty acid synthase (FAS), and 3-hydroxy-3-methylglutaryl-CoA reductase (HMG-CoAR). The expression of FAS and HMG-CoAR varied rhythmically over the diurnal cycle in the normal mice, with patterns that were the opposite of that of PPAR. The diurnal variation of lipogenic and cholesterogenic gene expression was attenuated or abolished in the PPAR-null mice. This resulted in decreased expression compared with normal mice, but only during the dark phase of the cycle, when food intake was high. The diurnal variation in hepatic fatty acid and cholesterol synthesis was also abolished in the PPAR-null animals and the variations in the concentration of plasma triacylglycerol, nonesterified fatty acids, and cholesterol were all attenuated. The failure of HMG-CoAR expression to increase during the feeding period in the PPAR-null mice was associated with a decrease in hepatic nonesterified cholesterol content and an increase in cholesteryl ester compared with normal mice. There was no defect in the downregulation of hepatic HMG-CoAR mRNA in response to dietary cholesterol in the PPAR-null mice. Under these conditions, hepatic PPAR
expression increased in both the control and PPAR-deficient mice. -deficiency disturbs the normal circadian regulation of certain SREBP-sensitive genes in the liver, but does not affect their response to dietary cholesterol. — Patel, D. D., B. L. Knight, D. Wiggins, S. M. Humphreys, and G. F. Gibbons. Disturbances in the normal regulation of SREBP-sensitive genes in PPAR-deficient mice. J. Lipid Res. 2001. 42: 328;–337. 
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