title: Bromocriptine reduces steatosis in obese rodent models.
abstract: OBJECTIVE
  Obesity is a risk factor for glucose intolerance, steatosis, and oxidative stress, characteristics of nonalcoholic fatty liver disease. Bromocriptine may have anti-obesity, insulin-sensitizing, lipolytic, and antioxidant properties. We, therefore, hypothesized that bromocriptine would improve markers of nonalcoholic fatty liver disease in obese rodent models.
  
  
  METHODS
  We performed a randomized, controlled experiment in genetically obese fatty Zucker rats and diet-induced obese rats to assess for behavioral and peripheral anti-obesity actions of bromocriptine (10mg/kg) that would improve nonalcoholic fatty liver disease.
  
  
  RESULTS
  Behaviorally, food intake decreased and locomotor activity increased in bromocriptine-treated fatty Zucker and dietary-induced obese rats. Peripherally, liver triglycerides were significantly reduced and hepatic manganese superoxide dismutase significantly increased in bromocriptine-treated fatty Zucker and diet-induced obese rats compared to controls. Blood glucose was significantly lower in bromocriptine-treated Zucker rats compared to fatty controls and was no different than that of lean controls.
  
  
  CONCLUSIONS
  Improvements in obesigenic behaviors, glucose tolerance, hepatic lipid accumulation, and mitochondrial oxidative stress observed in genetically obese and diet-induced obese rodents indicate that bromocriptine may be promising as a broad-based therapy for nonalcoholic fatty liver disease.
authors.affiliation: Johns Hopkins Bloomberg School of Public Health, Department of International Health, Center for Human Nutrition, Baltimore, MD 21205-2179, USA. ldavismc@jhsph.edu
authors.forename: Lisa M
authors.initials: LM
authors.lastname: Davis
authors.forename: Zhengtong
authors.initials: Z
authors.lastname: Pei
authors.forename: Michael A
authors.initials: MA
authors.lastname: Trush
authors.forename: Lawrence J
authors.initials: LJ
authors.lastname: Cheskin
authors.forename: Carlo
authors.initials: C
authors.lastname: Contoreggi
authors.forename: Karen
authors.initials: K
authors.lastname: McCullough
authors.forename: Paul A
authors.initials: PA
authors.lastname: Watkins
authors.forename: Timothy H
authors.initials: TH
authors.lastname: Moran
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001823:Body Composition / Q000235:genetics / Q000502:physiology; D001971:Bromocriptine / Q000494:pharmacology*; D004195:Disease Models, Animal; D018491:Dopamine Agonists / Q000494:pharmacology*; D004435:Eating / Q000235:genetics / Q000502:physiology; D005234:Fatty Liver / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D008099:Liver / Q000378:metabolism / Q000473:pathology; D008124:Locomotion / Q000502:physiology; D008297:Male; D009765:Obesity / Q000150:complications / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D011924:Rats, Zucker; D013482:Superoxide Dismutase / Q000378:metabolism; D014280:Triglycerides / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D018491:Dopamine Agonists; D014280:Triglycerides; D001971:Bromocriptine; D013482:Superoxide Dismutase