Accumulating data has established a tight regulation and coordination between the glucose and lipid homeostasis at cellular and molecular levels. Glucose and fructose are ubiquitous molecules in biology and have been found to be associated with a wide range of fundamental cellular processes to various patho-physiological situations including metabolic syndrome. In the last decade studies from in vitro to in vivo model system have established a pivotal role of ligand activated nuclear receptor Liver X Receptor (LXR) for its ability to regulate two cellular processes i.e. lipid metabolism and inflammation. In addition recent study has identified LXRs as a glucose sensor, where D-glucose has been found to be a direct agonist of LXR and increases its transcriptional activity that integrates hepatic glucose metabolism and fatty acid synthesis. Keeping in view LXRs as a glucose sensor, the present study was designed to explore the synergistic action of glucose and fructose on the regulation of LXR-α transcriptional activity in peripheral blood mononuclear cellular model. For the study we incorporated the LXR-α target genes PPARγ, Low density lipoprotein receptor (LDLR) and Prostate apoptosis response 4 which are positively regulated by LXR-α as well as Interferon γ and Apoptosis antagonizing transcription factor (AATF) which are negatively regulated by LXR-α.

Hyperglycemic-dependent LXR-alpha Gene Regulation within Blood Mononuclear Cells of CHD Patients

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