Endocrine Abstracts

Environmental toxins like cadmium chloride (CdCl₂) are implicated in T2D pathogenesis by promoting oxidative stress and impairing insulin signaling. Portulaca oleracea (Purslane), a traditional medicinal plant, is rich in antioxidants and omega-3 fatty acids, suggesting potential antidiabetic properties. However, its efficacy against heavy metal-induced T2D and the comparative potency of its different extracts remain poorly elucidated. This study aimed to investigate and compare the therapeutic effects of purslane aqueous extract (PAE) and purslane hydroalcoholic extract (PHE) on a CdCl₂-induced rat model of T2D, focusing on glycemic control, insulin sensitivity, lipid metabolism, and antioxidant activity.Thirty-five male Sprague-Dawley rats were divided into five groups: a normal control, a CdCl₂-induced diabetic control (1 mg/kg/i.p., daily), a positive control treated with metformin, and two treatment groups receiving either PAE or PHE (400 mg/kg/p.o. each) for four weeks alongside CdCl₂. Fasting blood glucose (FBG) and body weight were monitored weekly. An oral glucose tolerance test (OGTT) was conducted at the end of the study. Serum was analyzed for insulin, adiponectin, leptin, alpha-amylase, alpha-glucosidase, and lipid profile. Homeostatic model assessment for insulin resistance (HOMA-IR) was calculated. Oxidative stress markers were measured in hepatic and pancreatic tissues, followed by histopathological examination.Thirty-five male Sprague-Dawley rats were divided into five groups: a normal control, a CdCl₂-induced diabetic control, a positive control treated with metformin, and two treatment groups receiving either PAE or PHE (400 mg/kg/p.o. each) for four weeks alongside CdCl₂. Fasting blood glucose (FBG) and body weight were monitored weekly. An oral glucose tolerance test (OGTT) was conducted at the end of the study. Serum was analyzed for insulin, adiponectin, leptin, alpha-amylase, alpha-glucosidase, and lipid profile. Homeostatic model assessment for insulin resistance (HOMA-IR) was calculated. Oxidative stress markers were measured in hepatic and pancreatic tissues, followed by histopathological examination.