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This Article Full Text Full Text (PDF) All Versions of this Article: 291/5/E1038    most recent 00567.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Kok, P. Articles by Pijl, H. Search for Related Content PubMed PubMed Citation Articles by Kok, P. Articles by Pijl, H.

Activation of dopamine D2 receptors simultaneously ameliorates various metabolic features of obese women

¹Department of General Internal Medicine, ²Department of Endocrinology and Metabolic diseases, ³Department of Clinical Chemistry, and ⁴Department of Nuclear Medicine, Leiden University Medical Center, Leiden, The Netherlands

Submitted 20 November 2005 ; accepted in final form 19 June 2006

The metabolic syndrome comprises a cluster of metabolic anomalies including insulin resistance, abdominal obesity, dyslipidemia, and hypertension. Previous studies suggest that impaired dopamine D2 receptor (D2R) signaling is involved in its pathogenesis. We studied the acute effects of bromocriptine (a D2R agonist) on energy metabolism in obese women; body weight and caloric intake remained constant. Eighteen healthy, obese women (BMI 33.2 ± 0.6 kg/m², mean age 37.5 ± 1.7, range 22–51 yr) were studied twice in the follicular phase of their menstrual cycle in a prospective, single-blind, crossover design. Subjects received both placebo (P; always first occasion) and bromocriptine (B; always second occasion) on separate occasions for 8 days. At each occasion blood glucose and insulin were assessed every 10 min for 24 h, and circadian plasma free fatty acid (FFA) and triglyceride (TG) levels were measured hourly. Fuel oxidation was determined by indirect calorimetry. Body weight and composition were not affected by the drug. Mean 24-h blood glucose (P < 0.01) and insulin (P < 0.01) were significantly reduced by bromocriptine, whereas mean 24 h FFA levels were increased (P < 0.01), suggesting that lipolysis was stimulated. Bromocriptine increased oxygen consumption (P = 0.03) and resting energy expenditure (by 50 kcal/day, P = 0.03). Systolic blood pressure was significantly reduced by bromocriptine. Thus these results imply that short-term bromocriptine treatment ameliorates various components of the metabolic syndrome while it shifts energy balance away from lipogenesis in obese humans.

metabolic syndrome; food intake; insulin resistance; d2r agonist; prolactin