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Intestinal and hepatic cholesterol transporters in Psammomys Obesus, a model of insulin resistance and type 2 diabetes
Author(s) -
Lalonde Genevieve,
Delvin Edgard,
Elchebly Mounib,
Sane Alain Theophile,
Lambert Marie,
Garofalo Carole,
Ziv Ehud,
Levy Emile
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.948.6
Subject(s) - endocrinology , medicine , insulin resistance , abca1 , cd36 , type 2 diabetes , chylomicron , diabetes mellitus , biology , insulin , cholesterol , chemistry , transporter , lipoprotein , very low density lipoprotein , biochemistry , gene , receptor
Poor glycemic control is associated with hyperlipidemia. Our results have recently shown that the increased transport of chylomicrons from the intestine to the circulation in both conditions could potentially result in circulating lipid abnormalities that likely enhance the risk of atherosclerosis. Although protein transporters have been involved in regulating cholesterol movement into and out of enterocytes, little is known about their status in insulin resistance and diabetes. Our objective was to determine mRNA levels of genes such as ABCA‐1, ABCG5/8, NPC1‐L1, Annexin II, CD36, SCP‐2 and SR‐B1, in intestinal and hepatic tissues in Psammomys Obesus. In diabetic animals, analysis of gene expression by Real‐Time PCR revealed a decrease in intestinal and hepatic levels of ABCG5/8 and ABCA1, which act as efflux pumps favoring cholesterol export out of absorptive cells. Furthermore, a decline was observed in intestinal mRNA levels of NPC1‐L1 that plays a major role in cholesterol absorption, whereas no changes were evidenced in the gene expression of intestinal SR‐BI, annexin 2, CD36 and SCP2. In contrast, raised mRNA concentrations characterized annexin‐2 and SR‐BI in the hepatic tissue. Our results suggest that the expression of cholesterol transporters is differently modulated in the intestine and liver in diabetes type 2. Supported by Diabete Canada.