title: Myocardial and metabolic dysfunction in type 2 diabetic rats: impact of ghrelin.
abstract: Diabetes mellitus (DM) is commonly associated with metabolic and cardiac dysfunctions. The aim of this study was to examine the effect of ghrelin on metabolic and cardiac dysfunctions in a type-2 diabetes mellitus (T2DM) rat model. For this, 48 male adult Sprague-Dawley rats were divided equally into 4 groups: Group I, fed normal chow, served as normal control group; Groups II-IV, were fed a high-fat diet for 2 weeks followed by injection of streptozotocin (STZ) (35 mg/kg body mass) to create a model of T2DM; Group II, were not treated; Group III, were treated with the vehicle (saline); Group IV, were treated with ghrelin (40 µg/kg body mass) twice daily for 10 days. The untreated diabetic rats showed a significant increase in serum fasting blood glucose, insulin homeostasis model assessment (HOMA) index, triglycerides (TGs), low-density lipoprotein cholesterol (LDL-C), total serum cholesterol (TC), and body mass, with a decrease in high-density lipoprotein cholesterol (HDL-C) (p < 0.05). Hearts isolated from diabetic rats showed a significant increase in myocardial fat content, a significant decrease in GLUT4, and an increase in acyl-CoA oxidase enzyme mRNA (p < 0.05). Ghrelin administration for 10 days caused a significant improvement in lipid profile, HOMA index, and body mass, and significantly corrected the myocardial mass, significantly reduced the fat content of the myocardium, significantly increased GLUT4, and decreased acyl CoA oxidase mRNA (p < 0.05). Thus, ghrelin improves both the metabolic functions and  the disturbed energy metabolism in the cardiac muscle of obese  diabetic rats.
authors.affiliation: Department of Physiology, Mansoura Faculty of Medicine, Mansoura, Egypt. zizomenna@yahoo.com
authors.forename: Abdel-Aziz M
authors.initials: AA
authors.lastname: Hussein
authors.forename: Azza
authors.initials: A
authors.lastname: Abdel-Aziz
authors.forename: Mahmoud
authors.initials: M
authors.lastname: Gabr
authors.forename: Kamel Z
authors.initials: KZ
authors.lastname: Hemmaid
mesh_terms: D042962:Acyl-CoA Oxidase / Q000096:biosynthesis; D000818:Animals; D001786:Blood Glucose / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002334:Carnitine O-Palmitoyltransferase / Q000096:biosynthesis; D002784:Cholesterol / Q000097:blood; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D059305:Diet, High-Fat / Q000009:adverse effects; D054439:Ghrelin / Q000494:pharmacology / Q000627:therapeutic use*; D051275:Glucose Transporter Type 4 / Q000096:biosynthesis; D006321:Heart / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects; D006984:Hypertrophy / Q000150:complications / Q000188:drug therapy; D007004:Hypoglycemic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D007333:Insulin Resistance / Q000502:physiology; D050356:Lipid Metabolism / Q000187:drug effects; D008297:Male; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D054439:Ghrelin; D051275:Glucose Transporter Type 4; D007004:Hypoglycemic Agents; D014280:Triglycerides; D002784:Cholesterol; D042962:Acyl-CoA Oxidase; D002334:Carnitine O-Palmitoyltransferase