title: Cocoa powder extracts exhibits hypolipidemic potential in cholesterol-fed rats.
abstract: BACKGROUND
  Hypercholesterolemia and oxidative stress are risk factors of cardiovascular diseases.
  
  
  OBJECTIVE
  This study investigated the hypolipidemic effect of cocoa powder extract (CPE) in an experimental model of hypercholesterolemia, using Questran as a reference.
  
  
  METHODS
  Hypercholesterolemia in rats was induced by oral administration of 30 mg/kg cholesterol for eight weeks. Three groups concurrently received Questran (0.26 g/kgb) and CPE (100 mg/kg and 200 mg/kg) respectively. Hypercholesterolemia and dyslipidemia were assessed by lipid profile. Reduced glutathione (GSH), Superoxide dismutase (SOD), Catalase (CAT), Glutathione-S-transferase (GST) and malondialdehyde (MDA) level were also assessed to evaluate the antioxidant status of rats.
  
  
  RESULTS
  There was 56% and 97% increase in total and LDL-cholesterol and 59% decrease in HDL-cholesterol levels on cholesterol administration. Concurrent administration of CPE (100 mg/kg) significantly (p < 0.05) decreased total cholesterol (19%) and LDL-cholesterol (22%) and increased HDL-cholesterol (286%) levels while at 200 mg/kg, 55% and 64% reductions in total and LDL-cholesterol and 250% increase in HDL-cholesterol levels were observed. No significant changes were observed in phospholipid levels. Body weights of rats were not significantly different among groups and CPE (100 mg/kg) ameliorated the cholesterol-induced enlargement of the liver and heart by 14% and 15% respectively and at 200 mg/kg by 21% in the heart. GSH and CAT were significantly depleted, and MDA and SOD significantly elevated in liver and heart of Cholesterol-fed rats. No significant changes in GST, alanine and aspartate aminotransferases occurred among groups. CPE treatment modulated these changes.
  
  
  CONCLUSIONS
  Cocoa powder possesses hypolipidemic potential and may be relevant in treating pathologies with dyslipidemia as an underlying cause.
authors.affiliation: Molecular Drug Metabolism & Toxicology Research Laboratories, Department of Biochemistry, College of Medicine, University of Ibadan, Ibadan, Nigeria.
authors.forename: S O
authors.initials: SO
authors.lastname: Nwichi
authors.forename: E K
authors.initials: EK
authors.lastname: Adewole
authors.forename: A O
authors.initials: AO
authors.lastname: Dada
authors.forename: O
authors.initials: O
authors.lastname: Ogidiama
authors.forename: O E
authors.initials: OE
authors.lastname: Mokobia
authors.forename: E O
authors.initials: EO
authors.lastname: Farombi
mesh_terms: D000818:Animals; D000924:Anticholesteremic Agents / Q000008:administration & dosage / Q000493:pharmacokinetics; D000975:Antioxidants / Q000378:metabolism; D001682:Biological Availability; D002099:Cacao; D002791:Cholesterol, Dietary / Q000008:administration & dosage; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D002792:Cholestyramine Resin / Q000008:administration & dosage / Q000493:pharmacokinetics; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D016903:Drug Monitoring; D006937:Hypercholesterolemia / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism; D050356:Lipid Metabolism / Q000187:drug effects*; D008297:Male; D010936:Plant Extracts / Q000008:administration & dosage / Q000493:pharmacokinetics; D011208:Powders; D051381:Rats; D017208:Rats, Wistar; D016896:Treatment Outcome
chemical_list: D000924:Anticholesteremic Agents; D000975:Antioxidants; D002791:Cholesterol, Dietary; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D010936:Plant Extracts; D011208:Powders; D002792:Cholestyramine Resin