Bromocriptine reduces steatosis in obese rodent models

Lisa M. Davis, Zhengtong Pei, Michael A. Trush, Lawrence J. Cheskin, Carlo Contoreggi, Karen McCullough, Paul A. Watkins, Timothy H. Moran

Research output: Contribution to journalArticlepeer-review

Abstract

Background/Aims: 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 (10 mg/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.

Original languageEnglish (US)
Pages (from-to)439-444
Number of pages6
JournalJournal of Hepatology
Volume45
Issue number3
DOIs
StatePublished - Sep 1 2006

Keywords

  • Bromocriptine
  • Dopamine D2 agonist
  • NAFLD
  • Nonalcoholic fatty liver disease
  • Obesity

ASJC Scopus subject areas

  • Hepatology

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