Gene Expression of LDLR, APOB, APOE, and LPL in Experimentally Induced Diabetes and Dyslipidemia in Rats

Diabetes is the predominant metabolic condition in humans and animals, particularly in pets; it frequently coexists with many other metabolic abnormalities involving carbohydrates, proteins, and lipids. This study was conducted to investigate the correlation between experimentally generated diabetes and dyslipidemia concerning the gene expression of low-density lipoprotein receptor (LDLR), apolipoprotein-B (APOB), apolipoprotein-E (APOE), and lipoprotein lipase (LPL) in adipose tissue. Sixty-four adult male albino rats were divided into four groups: the first group (control group), receiving a standard diet, while the second group became the dyslipidemia group, which was fed accordingly high-fat diet (HFD), the third group was the diabetes and dyslipidemia group or mixed group fed HFD. Taking a single dosage of 50 mg/kg of streptozotocin (STZ) intraperitoneally, the fourth group became the diabetic group. fed a standard diet and using a single-dose of 50 mg/kg STZ. Results demonstrated that diabetes and dyslipidemia cause significant changes in lipid profile, insulin resistance, and body weight parameters. Dyslipidemia exhibited a significant elevation in total cholesterol and triglycerides relative to the control group. STZ caused a notable elevation in glucose levels and a reduction in insulin levels, those changes resulted in upregulation or downregulation in gene expression of LPL, LDLR, APOB, and APOE. LPL gene expression is downregulated except in the diabetes group, which is slightly upregulated. LDLR gene expression significantly increased in dyslipidemia. It could be concluded that the coexistence of diabetes and dyslipidemia worsens most biochemical markers and gene expression, appearing to be more synergistically harmful than either condition alone.