title: Neonatally-induced diabetes: lipid profile outcomes and oxidative stress status in adult rats.
abstract: BACKGROUND
  Experimental models are developed for the purpose of enhancing the understanding of the pathophysiological mechanisms involved in diabetes. Experimental findings lead to the development of treatment strategies to maintain metabolic conditions as close to normal as possible. There are several reports about streptozotocin induced mild diabetes to reproduce type 2 diabetes. However, studies about the interaction among glucose levels, lipid profile, and oxidative stress in these animals remain insufficient. Therefore, this study evaluated these parameters in blood samples from adult Wistar rats treated neonatally with streptozotocin.
  
  
  METHODS
  Female newborn Wistar rats received streptozotocin (70 mg/kg, i.p.) on the 5th day of life (n5-STZ). Glycemia was measured in the 3rd and 4th month of life. At the end of the 4th month, blood samples were collected and processed for lipid profile and oxidative stress measurements.
  
  
  RESULTS
  Glycemia of n5-STZ rats were significantly higher compared to those of control rats (p<0.05). There was no alteration in levels of total cholesterol, triglycerides, lipid peroxidation (TBARS), SOD activity and GSH-t determination (p>0.05) in the n5-STZ animals when compared to control group. However n5-STZ animals showed a significant decreased HDL-cholesterol rate (p<0.05).
  
  
  CONCLUSIONS
  This streptozotocin-induced diabetes model in rats caused hyperglycemia (120-360 mg/dL), characterizing mild diabetes. This glycemic level led to HDL-lipoprotein alteration, which was not sufficient to impair antioxidant enzyme activities or determination of lipid peroxidation in adult life of rats. Further this experimental investigation contributed to the understanding of different results found in other models for mild/moderate diabetes induction in laboratory animals as well as to a better comprehension of the pathophysiological mechanisms of mild diabetes or hyperglycemia in humans.
authors.affiliation: Laboratory of Experimental Research in Gynecology and Obstetrics, Botucatu Medical School, Unesp-São Paulo State University, São Paulo, Brasil.
authors.forename: Yuri Karen
authors.initials: YK
authors.lastname: Sinzato
authors.forename: Paula Helena Ortiz
authors.initials: PH
authors.lastname: Lima
authors.forename: Kleber Eduardo de
authors.initials: KE
authors.lastname: Campos
authors.forename: Ana Carolina Inhasz
authors.initials: AC
authors.lastname: Kiss
authors.forename: Marilza Vieira Cunha
authors.initials: MV
authors.lastname: Rudge
authors.forename: Débora Cristina
authors.initials: DC
authors.lastname: Damasceno
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D002784:Cholesterol / Q000097:blood; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000150:complications / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D006943:Hyperglycemia / Q000209:etiology*; D050356:Lipid Metabolism / Q000187:drug effects*; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D017392:Thiobarbituric Acid Reactive Substances; D002784:Cholesterol