title: Experimental induction of steatosis in different tissues after the ingestion of a carbohydrate-rich diet: effect on the liver, on the heart and on indicators of oxidation.
abstract: BACKGROUND
  The western dietary pattern is characterized by a high calorie intake with a high proportion of simple sugars. This diet is associated with comorbidities such as hepatic fat deposition and is possibly related to non-alcoholic fatty liver disease.
  
  
  OBJECTIVE
  To evaluate the capacity of a hyperglucidic diet to induce steatosis in adult male Wistar rats. After the administration of a carbohydrate-rich diet, we also evaluated the presence of hepatic and cardiac steatosis and the levels of intrinsic antioxidants in the liver.
  
  
  METHODS
  Forty-six eutrophic adult male Wistar rats were used and 10 of them were chosen, at random, to serve as controls, while the remaining ones formed the experimental group. Control animals received the standard ration offered by the animal house and the experimental group received the hyperglucidic diet. The diets were offered for 21 days and, at the end of this period, tissue samples were collected for analysis of indicators of oxidative stress (malondialdehyde, and reduced glutathione) and of vitamin E. The animals were then sacrificed by decapitation and their viscera were removed for analysis of liver and heart fat.
  
  
  RESULTS
  The hyperglucidic diet used induced hepatic fat deposition, with lipid vacuoles being detected in 83% of the livers analyzed by histology. No lipid vacuoles were observed in the heart. Malondialdehyde and reduced glutathione levels remained unchanged when the animals were submitted to the hyperglucidic diet, probably because there was no liver development of fibrosis or inflammation. In contrast, the levels of vitamin E (antioxidant) were reduced, as confirmed in the literature for steatotic animals.
  
  
  CONCLUSIONS
  The hyperglucidic diet induced hepatic steatosis. In the heart there was an increase in fat content, although no histological changes were observed. These alterations cannot be explained by the presence of malondialdehyde or reduced glutathione (indicators of oxidation), since the values were similar in the groups studied. However, a significant reduction of vitamin E was observed in the experimental group.
authors.affiliation: Departamento de Clínica Médica/Nutrologia, Universidade de São Paulo – SP, Brazil.
authors.forename: Nadia Juliana Beraldo Goulart Borges
authors.initials: NJ
authors.lastname: Haubert
authors.forename: Gilberto João
authors.initials: GJ
authors.lastname: Padovan
authors.forename: Sérgio
authors.initials: S
authors.lastname: Zucoloto
authors.forename: Hélio
authors.initials: H
authors.lastname: Vannucchi
authors.forename: Julio Sergio
authors.initials: JS
authors.lastname: Marchini
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000032:analysis; D004040:Dietary Carbohydrates / Q000009:adverse effects*; D004195:Disease Models, Animal; D005234:Fatty Liver / Q000139:chemically induced* / Q000473:pathology; D005978:Glutathione / Q000032:analysis; D006331:Heart Diseases / Q000139:chemically induced* / Q000473:pathology; D008055:Lipids / Q000097:blood; D008297:Male; D009206:Myocardium / Q000737:chemistry; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar
chemical_list: D000975:Antioxidants; D004040:Dietary Carbohydrates; D008055:Lipids; D005978:Glutathione