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Retinyl Ester Storage Is Normal in Transgenic Mice with Enhanced Expression of Cellular Retinol-Binding Protein Type I¹

Gunhild Trøen, Winnie Eskild^*, Sigurd H. Fromm, Sjur Reppe, Astrid Nilsson, Kaare R. Norum and Rune Blomhoff²

Institute for Nutrition Research ^* Institute of Medical Biochemistry Laboratory of Molecular Embryology, University of Oslo Oslo, Norway

This report describes the production and characterization of transgenic mice with high expression of human cellular retinol-binding protein type I [hCRBP(I)]. In initial experiments, overexpression of hCRBP(I) was driven by the strong promoter SR, but no transgenic offspring were produced. When we used the less efficient mouse metallothionein I promoter fused to the hCRBP(I) cDNA for microinjection, we obtained 12% transgenic offspring. Two of these transgenic mice (409/1 and 401/2) expressed mRNA and immunoreactive hCRBP(I) in several organs. Both lines had relatively high contents of hCRBP(I) in intestine, testis and epididymis. On the other hand, only 401/2 transgenic mice had high contents of hCRBP(I) in kidney. Effects on storage of vitamin A were studied by measuring the concentration of retinyl esters in different organs. The concentrations of retinyl esters in liver, lung and kidney did not significantly differ between transgenic and control mice, and the concentration of total retinol in plasma was within the normal range in transgenic mice. Furthermore, feeding mice a diet with high or low concentrations of vitamin A for 2 wks resulted in no marked differences in the concentrations of retinyl esters in liver, kidney, lung, intestine and testis in transgenic mice compared with control mice. Therefore, in spite of high expression of hCRBP(I) in several organs, the transgenic mice had normal storage of retinyl esters in all organs studied. The present in vivo study indicates that the CRBP(I) content alone does not control retinyl ester storage.

KEY WORDS: • vitamin A • cellular retinol-binding protein I • transgenic mice • metallothinein promoter

¹ The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

² To whom correspondence and reprint requests should be addressed: Institute for Nutrition Research, University of Oslo, P.O. Box 1046, 0316 Oslo, Norway.

Manuscript received 8 February 1996. Revision accepted 1 July 1996.