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Papers In Press, published online ahead of print August 23, 2006
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Pharmacology, Dalhousie University, Halifax, Nova Scotia B3H 1X5
Corresponding Author: csinal{at}dal.ca
Apolipoprotein A-IV (apoA-IV) is a 46-kDa glycoprotein that associates with triglyceride-rich and high density lipoproteins. Blood levels of apoA-IV generally correlate with triglyceride levels and are increased in diabetic patients. The present study investigated the mechanisms regulating in vivo expression of apoA-IV in the liver and intestine of mice in response to changes in nutritional status. Fasting markedly increased liver and ileal apoA-IV mRNA and plasma protein concentrations. This induction was associated with increased serum glucocorticoid levels and was abolished by adrenalectomy. Treatment with dexamethasone increased apoA-IV expression in adrenalectomized mice. Marked increases of apoA-IV expression were also observed in two murine models of diabetes. Reporter gene analysis of the murine and human apoA-IV/CIII promoters revealed a conserved cooperative activation by the hepatic nuclear factor-4alpha (HNF-4alpha) and the peroxisome proliferator activated receptor gamma coactivator-1alpha (PGC-1alpha), but no evidence of a direct regulatory role for the glucocorticoid receptor. Consistent with these in vitro data, induction of apoA-IV in response to fasting was accompanied by increases in HNF-4alpha and PGC-1alpha expression and was abolished in liver-specific HNF-4alpha(-/-) mice. Together these results indicate that induction of apoA-IV expression in fasting and diabetes likely involves PGC-1alpha-mediated coactivation of HNF-4alpha in addition to glucocorticoid-dependent actions.
Revised on August 11, 2006
Accepted on August 23, 2006
Apolipoprotein A-IV is regulated by nutritional and metabolic stress: Involvement of glucocorticoids, HNF-4
and PGC-1
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