Okra (Abelmoscus esculentus) Improved Islets Structure, and Down-Regulated PPARs Gene Expression in Pancreas of High-Fat Diet and Streptozotocin-Induced Diabetic Rats

Objective Okra (Abelmoschus esculentus) is a tropical vegetable that is rich in carbohydrates, fibers, proteins and natural antioxidants. The aim of the present study was to evaluate the effects of Okra powder on pancreatic islets and its action on the expression of PPARγ and PPARα genes in pancreas of highfat diet (HFD) and streptozotocin induced diabetic rats. Materials and Methods In this experimental study, diabetes was induced by feeding HFD (60% fat) for 30 days followed by an injection of streptozotocin (STZ, 35 mg/kg). Okra powder (200 mg/kg) was given orally for 30 days after diabetes induction. At the end of the experiment, pancreas tissues were removed and stained by haematoxylin and Eozine and aldehyde fuchsin for determination of the number of βcells in pancreatic islets. Fasting blood sugar (FBS), Triglycerides (TG), cholesterol, high density lipoprotein (HDL), low density lipoprotein (LDL), and insulin levels were measured in serum. Moreover, PPARγ and PPARα mRNAs expression were measured in pancreas using real time polymerase chain reaction (PCR) analysis. Results Okra supplementation significantly decreased the elevated levels of FBS, total cholesterol, and TG and attenuated homeostasis model assessment of basal insulin resistance (HOMAIR) index in diabetic rats. The expression levels of PPARγ and PPARα genes that were elevated in diabetic rats, attenuated in okratreated rats (P 0.05). Furthermore, okra improved the histological damages of pancreas including vacuolization and decreased βcells mass, in diabetic rats. ConclusionOur findings confirmed the potential antihyperglycemic and hypolipidemic effects of Okra. These changes were associated with reduced pancreatic tissue damage. Downregulation of PPARs genes in the pancreas of diabetic rats after treatment with okra, demonstrates that okra may improve glucose homeostasis and βcells impairment in diabetes through a PPARdependent mechanism.