title: Alteration of the gene and protein levels of insulin-like growth factors in streptozotocin-induced diabetic male rats.
abstract: Insulin-like growth factor (IGFs: IGF-I and IGF-II) systems have been reported to be associated with the onset of diabetic mellitus. Therefore, we investigated the effect of diabetes on regulation of the IGF system in the liver, kidneys and heart, which are important organs in the pathogenesis of diabetes. The experimental groups were subdivided into three groups: 1) controls, 2) streptozotocin (STZ)-induced untreated diabetic group, and 3) an insulin-treated group (plus diabetic rats). In the present study, starting on the second day after STZ treatment, the diabetic group exhibited hyperglycemia, polyuria, and polydipsia, which are characteristic of diabetes melittus. Serum levels of IGF-I were decreased, but those of IGF-II were increased in the diabetic group compared with the controls. The expression levels of IGF-I and IGF-II protein in the livers of the diabetic group had a similar pattern to the serum. In addition, the expression levels of liver IGF-I mRNA and IGF-II mRNA were decreased in the diabetic groups. In the heart, IGF-I levels were decreased, but IGF-II levels were increased in the untreated diabetic groups, which was consistent with the expression levels of their mRNA. However, both the IGF-I and IGF-II levels in the kidneys were increased in the untreated diabetic groups, but the mRNA levels were decreased. Insulin treatment ameliorated the changes of IGF system in the serum, liver, kidneys, and heart. In conclusion, diabetes induced alteration of the IGF system tissue-specifically, and this was blocked by insulin treatment.
authors.affiliation: Department of Veterinary Physiology, College of Veterinary Medicine, Chonnam National University, Gwanju, Korea.
authors.forename: Ho Jae
authors.initials: HJ
authors.lastname: Han
authors.forename: Soo Hyun
authors.initials: SH
authors.lastname: Park
mesh_terms: D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism*; D004195:Disease Models, Animal; D005786:Gene Expression Regulation / Q000187:drug effects; D007004:Hypoglycemic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D007328:Insulin / Q000494:pharmacology* / Q000627:therapeutic use; D007334:Insulin-Like Growth Factor I / Q000235:genetics / Q000378:metabolism; D007335:Insulin-Like Growth Factor II / Q000235:genetics / Q000378:metabolism; D007668:Kidney / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000378:metabolism; D009928:Organ Specificity; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013002:Somatomedins / Q000235:genetics / Q000378:metabolism*; D013311:Streptozocin
chemical_list: D007004:Hypoglycemic Agents; D007328:Insulin; D012333:RNA, Messenger; D013002:Somatomedins; D013311:Streptozocin; D007334:Insulin-Like Growth Factor I; D007335:Insulin-Like Growth Factor II