title: The effect of aspirin on atherogenic diet-induced diabetes mellitus.
abstract: Exploration of atherogenic diet-induced diabetes mellitus and the evaluation of antidiabetic potential of aspirin were carried out in this study. Male albino Wistar rats were divided into three groups of seven each (1, 2 and 3). Animals of groups 2 and 3 received CCT diet (normal rat chow supplemented with 4% cholesterol, 1% cholic acid and 0.5%, 2-thiouracil), whereas the animals of group 1 received normal feed and served as control. In addition to CCT, animals of group 3 (CCT + Asp) also received aspirin (8 gm/kg), commencing from day 8 till the end of study (day 15). In another experiment (exp. 2), aspirin-supplemented normal rat chow (Asp) was fed to the animals for 7 days and compared with the normal rat chow-fed control group. In experiment 3, an in vitro nitric oxide radical-scavenging potential of aspirin at three different doses (25, 50 and 100 μg/ml) was evaluated. In response to CCT diet, a decrease in serum insulin, α-amylase activity, hepatic glycogen, pancreatic calcium with a concomitant increase in serum glucose, lipid profile (except high-density lipoprotein cholesterol (HDL-C)), pancreatic nitrite and lipid peroxidation and the size of adipocytes along with macrophages infiltration were observed. Aspirin administration to CCT diet-fed animals (CCT + Asp) reverted all the studied biochemical and histological changes towards normality. In experiment 2, aspirin administration decreased the serum glucose, total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL-C) and VLDL-C with concomitantly increased HDL-C and insulin; however, it increased hepatic glycogen and pancreatic calcium concentration with a decrease in pancreatic and adipose lipid peroxidation. In vitro assay revealed the nitric oxide radical-scavenging potential of aspirin in all the studied doses. It is concluded that CCT diet-induced diabetes mellitus might be the outcome of nitric oxide radical-induced oxidative stress in pancreatic tissue, as well as diminished insulin secretion because of decrease in pancreatic calcium release, obesity and inflammation. However, aspirin treatment reversed all the above-mentioned parameters to normality.
authors.affiliation: School of Biotechnology, Devi Ahilya University, Takshashila Campus, Indore, India.
authors.forename: Apoorva
authors.initials: A
authors.lastname: Sethi
authors.forename: Hamendra S
authors.initials: HS
authors.lastname: Parmar
authors.forename: Anil
authors.initials: A
authors.lastname: Kumar
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000378:metabolism / Q000494:pharmacology*; D001241:Aspirin / Q000378:metabolism / Q000494:pharmacology*; D001786:Blood Glucose / Q000187:drug effects; D002784:Cholesterol / Q000097:blood / Q000378:metabolism; D003920:Diabetes Mellitus / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D004036:Diet, Atherogenic; D016166:Free Radical Scavengers / Q000378:metabolism; D006937:Hypercholesterolemia / Q000097:blood / Q000188:drug therapy / Q000209:etiology; D007004:Hypoglycemic Agents / Q000378:metabolism / Q000494:pharmacology*; D007328:Insulin / Q000097:blood / Q000378:metabolism / Q000502:physiology; D015227:Lipid Peroxidation / Q000187:drug effects; D008055:Lipids / Q000097:blood / Q000502:physiology; D008099:Liver / Q000187:drug effects; D008297:Male; D009569:Nitric Oxide / Q000502:physiology; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D001786:Blood Glucose; D016166:Free Radical Scavengers; D007004:Hypoglycemic Agents; D007328:Insulin; D008055:Lipids; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D002784:Cholesterol; D001241:Aspirin