title: Inhibitory effects of estrogens on digestive enzymes, insulin deficiency, and pancreas toxicity in diabetic rats.
abstract: Diabetes mellitus, with its attendant disorders and dysfunctional behaviors, constitutes a growing concern to the population of the world. With this concern in mind, the present study investigated the anti-diabetic and hypolipedimic potential of 17β-estradiol (called E2), particularly in terms of its inhibitory effects on maltase, sucrase, lactase, and lipase activities in the intestine of surviving diabetic rats. The findings revealed that this supplement helped protect the β cells of the rats from death and damage. Interestingly, E2 induced considerable decreases of 29%, 46%, 42%, and 84% in the activities of intestinal maltase, lactase, sucrase, and lipase, respectively. The E2 extract also decreased the glucose, triglyceride, and total cholesterol rates in the plasma of diabetic rats by 39%, 27%, and 53%, respectively, and increased the HDL-cholesterol level by 74%, which helped maintain the homeostasis of blood lipid. When compared to those of the untreated diabetic rats, the superoxide dismutase, catalase, and glutathione peroxidase levels in the pancreas of the rats treated with this supplement were also enhanced by 330%, 170%, and 301%, respectively. A significant decrease was also observed in the lipid peroxidation level and lactate dehydrogenase activity in the pancreas of diabetic rats after E2 administration. Overall, the findings presented in this study demonstrate that E2 has both a promising potential with regard to the inhibition of intestinal maltase, sucrase, lactase, and lipase activities, and a valuable hypoglycemic and hypolipidemic function, which make it a potential strong candidate for industrial application as apharmacological agent for the treatment and prevention of hyperlipidemia, obesity, and cardiovascular diseases.
authors.affiliation: Biotechnology High School of Sfax (ISBS), Soukra Km 4.5, P.O. Box 261, Sfax 3052, Tunisia. khaled.hamden@yahoo.fr
authors.forename: Khaled
authors.initials: K
authors.lastname: Hamden
authors.forename: Bassem
authors.initials: B
authors.lastname: Jaouadi
authors.forename: Nedia
authors.initials: N
authors.lastname: Zaraî
authors.forename: Tarek
authors.initials: T
authors.lastname: Rebai
authors.forename: Serge
authors.initials: S
authors.lastname: Carreau
authors.forename: Abdelfattah
authors.initials: A
authors.lastname: Elfeki
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D002374:Catalase / Q000187:drug effects / Q000378:metabolism; D002784:Cholesterol / Q000097:blood / Q000378:metabolism; D008076:Cholesterol, HDL / Q000187:drug effects / Q000378:metabolism; D003920:Diabetes Mellitus / Q000188:drug therapy* / Q000378:metabolism; D004958:Estradiol / Q000494:pharmacology*; D004967:Estrogens / Q000494:pharmacology*; D005979:Glutathione Peroxidase / Q000187:drug effects / Q000378:metabolism; D007328:Insulin / Q000172:deficiency* / Q000378:metabolism*; D007770:L-Lactate Dehydrogenase / Q000187:drug effects / Q000378:metabolism; D043322:Lactase / Q000187:drug effects / Q000378:metabolism; D008049:Lipase / Q000187:drug effects / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D010179:Pancreas / Q000033:anatomy & histology / Q000166:cytology / Q000187:drug effects*; D051381:Rats; D013393:Sucrase / Q000187:drug effects / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism / Q000494:pharmacology / Q000627:therapeutic use; D014280:Triglycerides / Q000097:blood / Q000378:metabolism; D000520:alpha-Glucosidases / Q000187:drug effects / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D008076:Cholesterol, HDL; D004967:Estrogens; D007328:Insulin; D014280:Triglycerides; D004958:Estradiol; D002784:Cholesterol; D007770:L-Lactate Dehydrogenase; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D008049:Lipase; D043322:Lactase; D000520:alpha-Glucosidases; D013393:Sucrase