News & Updates
Event Calendar
Search Research Content
Resource Finder at Kennedy Krieger Institute
A free resource that provides access to information and support for individuals and families living with developmental disabilities.
Bromocriptine administration reduces hyperphagia and adiposity and differentially affects dopamine D2 receptor and transporter binding in leptin-receptor-deficient Zucker rats and rats with diet-induced obesity.
| Title | Bromocriptine administration reduces hyperphagia and adiposity and differentially affects dopamine D2 receptor and transporter binding in leptin-receptor-deficient Zucker rats and rats with diet-induced obesity. |
| Publication Type | Journal Article |
| Year of Publication | 2009 |
| Authors | Davis LM, Michaelides M, Cheskin LJ, Moran TH, Aja S, Watkins PA, Pei Z, Contoreggi C, McCullough K, Hope B, Wang GJ, Volkow ND, Thanos PK |
| Journal | Neuroendocrinology |
| Volume | 89 |
| Issue | 2 |
| Pagination | 152-62 |
| Date Published | 2009 |
| Abstract | The dopamine (DA) D(2) receptor (D2R) agonist bromocriptine (BC) decreases body fat in animal and human models and increases lean muscle mass, improves glucose intolerance and insulin resistance, and reduces triglycerides and free fatty acids. We have previously shown a negative correlation between D2R and body weight in obese individuals and in rodents, and that chronic food restriction increases D2R binding in genetically obese rats. The purpose of this study was to assess whether the antiobesity and metabolic effects of BC are related to changes in midbrain DA and D2R activity by measuring D2R and DA transporter (DAT) binding in a genetic (leptin-receptor-deficient) and environmental (diet-induced) rodent obesity model. |
| DOI | 10.1002/ddrr.41 |
| Alternate Journal | Neuroendocrinology |

