HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sauvaget, D. Articles by Ribeiro, A. Search for Related Content PubMed PubMed Citation Articles by Sauvaget, D. Articles by Ribeiro, A. Social Bookmarking                What's this?

In Vitro Transcriptional Induction of the Human Apolipoprotein A-II Gene by Glucose

¹ Institut National de la Santé et de la Recherche Médicale (INSERM) U505, Institut Biomédical des Cordeliers, Paris, France
² Institut Fédératif de Recherche 58, Institut Biomédical des Cordeliers, Paris, France
³ INSERM U567, Unité Mixte de Recherche 8104 Centre National de la Recherche Scientifique, Institut Cochin, Paris, France
⁴ INSERM U465, Institut Biomédical des Cordeliers, Paris, France

Type 2 diabetic patients present high triglyceride and low HDL levels, significant determinants for the risk of atherosclerosis. Transgenic mice overproducing human apolipoprotein (apo)A-II, one of the two major apos of HDLs, display the same lipid disorders. Here, we investigated the possible regulation of apoA-II gene expression by glucose. In primary rat hepatocytes and in HepG2 cells, the transcription of the human apoA-II gene was upregulated by glucose. This response was mediated by a hormone-responsive element within the enhancer of the apoA-II promoter and was dependent on hepatocyte nuclear factor-4. Accordingly, in transgenic mice, the human apoA-II gene is stimulated by a high-carbohydrate diet after fasting and at weaning. By contrast, the apoA-II mRNA level is not modified in streptozotocin-induced diabetic rats. In transgenic mice overexpressing the human apoA-II gene, plasma human apoA-II concentration was positively correlated with blood glucose levels. These mice displayed a marked delay in plasma glucose tolerance as compared with control mice. We hypothesize that the following pathogenic pathway might occur in the course of type 2 diabetes: increased apoA-II level causes a rise in plasma triglyceride level and glucose intolerance, resulting in hyperglycemia, which in turn might further increase apoA-II gene transcription.

CiteULike    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				S. Dugue-Pujol, X. Rousset, D. Pastier, N. T. Quang, V. Pautre, J. Chambaz, M. Chabert, and A.-D. Kalopissis Human apolipoprotein A-II associates with triglyceride-rich lipoproteins in plasma and impairs their catabolism J. Lipid Res., December 1, 2006; 47(12): 2631 - 2639. [Abstract] [Full Text] [PDF]