Genetic Polymorphisms, Hepatic Steatosis and Lipid Anomalies in Diabetic Patients

• Our research hypothesis is to show that a certain number of genetic polymorphisms of the proteins involved in glucose, lipid and adipocyte metabolism are factors that favour the development of steatosis in patients with Type 2 diabetes.
• We also wish to evaluate more thoroughly lipid anomalies associated with the presence of steatosis, notably with regard to monocyte expression of LDL receptors. We hypothesize that hepatic steatosis is accompanied by activation of transcription factors involved in lipogenesis, notably SREBP factors. The activation of these factors could cause an increase in the expression of LDL receptors, leading to increased LDL catabolism.
• Chronological description of the study During an outpatient consultation at the endocrinology department, diabetic patients, programmed to undergo an examination to assess their diabetes will be invited to participate in the study. Once written informed consent has been provided and clinical data has been recorded, patients with type 1 or type 2 diabetes will have standard biological examination, which is systematically done in such patients (Fasting glycemia, HBA1c, aspartate aminotransferase, alanine amino transferase, Gammaglutamyl-transferases, PAL, bilirubin, blood proteins, albuminemia, Total Cholesterol total, HDL cholesterol, triglycerides, Sedimentation Rate, C-reactive protein, fibrinogen).

As well as the systematic biological tests, 3 additional tubes will be taken to screen for genetic polymorphism in 3 proteins (Microsomal Transfer Protein, Adiponectin receptor - 1, Apolipoprotein A - II).

IN addition, magnetic resonance imaging and magnetic resonance spectroscopy will be done to look for the presence of liver steatosis and to measure carotid intima-media thickness.