title: Hydroxycitric acid ameliorates high-fructose-induced redox imbalance and activation of stress sensitive kinases in male Wistar rats.
abstract: BACKGROUND
  Excess fructose consumption causes dyslipidemia, oxidative stress, and various complications. Hydroxycitric acid (HCA), one of the principal components of the fruit Garcinia cambogia, has been shown to possess antiobesity properties. The objective was to investigate the effects of HCA on redox imbalance and activation of stress sensitive kinases in high fructose-fed rats.
  
  
  METHODS
  Male Wistar rats (n=40) were randomly divided into four groups with 10 rats in each group. The rats were fed with either standard rodent diet or 60% fructose diet and administered with HCA at a dose of 400 mg/kg body wt/day for 10 weeks. Body weight was measured once a week, and food intake was noted daily. At the end of the study, lipid profile and oxidative stress parameters were estimated. Expressions of stress sensitive kinases were analyzed in liver homogenates.
  
  
  RESULTS
  Fructose-fed rats displayed elevated body weight, higher levels of plasma total cholesterol (TC), triacylglycerol (TAG), non-high-density lipoprotein cholesterol (non HDL-C), malondialdehyde (MDA), total oxidant status (TOS), oxidative stress index (OSI), lower levels of HDL-C, glutathione (GSH), glutathione peroxidase (GPx), and total antioxidant status (TAS). Fructose feeding caused higher phosphorylation of stress sensitive kinases ERK ½ and p38. Administration with HCA lowered body weight, food intake, TAG, non-HDL-C, MDA, TOS, and OSI and elevated GSH, GPx, and TAS levels. Reduced phosphorylation of ERK ½ and p38 mitogen-activated protein kinase (MAPK) was observed upon HCA treatment.
  
  
  CONCLUSIONS
  Thus, HCA improved fructose induced redox imbalance and activation of stress sensitive kinases through its hypolipidemic effects.
authors.forename: Ramalingam
authors.initials: R
authors.lastname: Sripradha
authors.forename: Magadi Gopalakrishna
authors.initials: MG
authors.lastname: Sridhar
authors.forename: Nachimuthu
authors.initials: N
authors.lastname: Maithilikarpagaselvi
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001786:Blood Glucose / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002951:Citrates / Q000494:pharmacology*; D004032:Diet; D004435:Eating / Q000187:drug effects; D005632:Fructose / Q000494:pharmacology*; D005951:Glucose Tolerance Test / Q000379:methods; D005978:Glutathione / Q000378:metabolism; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology; D015227:Lipid Peroxidation / Q000187:drug effects; D008055:Lipids / Q000097:blood; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D010084:Oxidation-Reduction / Q000187:drug effects*; D018384:Oxidative Stress / Q000187:drug effects*; D010770:Phosphotransferases / Q000378:metabolism*; D010936:Plant Extracts / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D014280:Triglycerides / Q000097:blood
chemical_list: D000975:Antioxidants; D001786:Blood Glucose; D002951:Citrates; D007328:Insulin; D008055:Lipids; D010936:Plant Extracts; D014280:Triglycerides; D005632:Fructose; D008315:Malondialdehyde; C007999:hydroxycitric acid; D010770:Phosphotransferases; D005978:Glutathione