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The hepatic retinyl ester hydrolase activity is depressed at the onset of diabetes in BB rats

Published online by Cambridge University Press:  09 March 2007

Min Chen
Affiliation:
Department of Agricultural, Food & Nutritional Science, Division of Gastroenterology, University of Alberta, Edmonton, Canada
Alan B. R. Thomson
Affiliation:
Department of Medicine, Division of Gastroenterology, University of Alberta, Edmonton, Canada
Andrew T. C. Tsin
Affiliation:
Division of Life Sciences, University of Texas at San Antonio, San Antonio, Texas, USA
Tapan K. Basu*
Affiliation:
Department of Agricultural, Food & Nutritional Science, Division of Gastroenterology, University of Alberta, Edmonton, Canada
*
*Corresponding author: Dr Tapan K. Basu, fax +1 780 492 9130, email [email protected]
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Abstract

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Dietary vitamin A as retinyl ester is hydrolysed and re-esterified with long-chain fatty acids in the small intestine. The esterified vitamin A is subsequently stored in the liver, where it is hydrolysed to free retinol to be transported by carrier proteins to the target tissue. A decreased availability of retinol carrier proteins has been suggested to be responsible for affecting metabolic availability of vitamin A in type 1 diabetes. Using BB Wistar rats, the present study was undertaken to examine whether the presence of a hyperglycaemic state modifies retinyl ester hydrolase (REH) activity in the intestine and the liver. At the onset of diabetes, hepatic REH enzymatic activity was significantly (P<0·05) decreased. However, REH activity remained unaffected in the small intestine, including both ileum and jejunum. Diabetes also resulted in decreased plasma and liver concentrations of retinol. An in vitro study was conducted to examine the effect of diabetes on the intestinal uptake of retinyl palmitate. Jejunum and ileum from diabetic and non-diabetic BB rats were incubated with labelled retinyl palmitate at different concentrations ranging from 32 to 256 nmol/l. The uptake of retinyl palmitate was increased in both diabetic and non-diabetic rats together with the increase of substrate concentration. However, no significant difference was observed in the uptake of retinyl palmitate between diabetic and non-diabetic rats. These present results suggest that the depressed hepatic REH activities may contribute to the diabetes-associated metabolic derangement of vitamin A.

Type
Research Article
Copyright
Copyright © The Nutrition Society 2003

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