Hyperglycemia promotes overexpression of SR-BII isoform of the scavenger receptor class B type I in type 2 diabetes mellitus: A study in Juana Koslay City, San Luis, Argentina

GISELA V. MENDOZA, SUSANA SIEWERT, IRMA GONZÁLEZ, MARÍA C. DELLA VEDOVA, GUSTAVO FERNANDEZ, MARTA S. OJEDA*

journal of diabetes mellitus

Scientific Research Publishing

Lugar: Delaware; Año: 2013 vol. 3 p. 172 - 183

2160-5831

Hyperglycemia promotes overexpression of SR-BII isoform of the scavenger receptor class B type I in type 2 diabetes mellitus: A study in Juana Koslay City, San Luis, Argentina Gisela V. Mendoza, Susana Siewert, Irma González, María C. Della Vedova, Gustavo Fernandez, Marta S. Ojeda* The scavenger receptor class B type I (SR-BI) is a high-density lipoprotein (HDL) receptor in- volved in reverse cholesterol transport. Some studies reported the association to be stronger in the presence of diabetes. The full length gene encoding SR-BI is comprised in 13 exons that are alternatively spliced to produce two major transcripts: the full length SR-BI and the splice variant SR-BII, in which exon 12 is skipped. Considering that type 2 diabetes status is char- acterized by changes in the concentration of plasma lipids, modifications in lipoprotein size and composition, which may be important mo- dulators of the SR-BI expression; the aims of the study were to examine the influence of SR-BI polymorphism (rs838895) on lipid profile and SR-BI mRNA expression in a population of dia- betic patients living in Juana Koslay City. Blood samples were drawn from controls (n = 40) and Type 2 diabetic patients (n = 66) and DNA and total RNA were obtained. SR-BI mRNA expres- sion was measured by RT-PCR and SR-BI poly- morphism was detected by Tetra Primer ARMS- PCR. Compared to controls, diabetic patients had higher fasting serum glucose, glycated he- moglobin, triglycerides, total cholesterol, low- density lipoprotein cholesterol, and lower high- density lipoprotein cholesterol. SR-BI mRNA ex- pression was lower in T2DM when compared to controls, suggesting that the hyperglycemia pre- sents in T2DM patients down-regulates SR-BI mRNA expression. Interestingly, we found that decreased SR-BI expression resulted in markedly increased plasma LDL concentrations in T2DM subjects, and the overexpression of SR- BII isoform is responsible for the markedly increased plasma LDL-c concentrations. The polymorphism (rs838895) did not modify the mRNA level of SR-BI in leucocytes from control and diabetic patients. This study provides novel evidence suggesting that hyperglycemia may affect reverse cholesterol transport by controlling SR- BI expression in diabetic patients. LDL cholesterol levels are associated with low SR-BI mRNA expression in T2DM.