title: Activation of dopamine D2 receptors lowers circadian leptin concentrations in obese women.
abstract: BACKGROUND
  Leptin release is regulated by factors other than fat mass alone. Previous observations provide indirect evidence for an inhibitory effect of dopaminergic neurotransmission on leptin secretion. This study was done to establish the effect of bromocriptine treatment on circadian plasma leptin concentrations in obese humans.
  
  
  OBJECTIVE
  The objective of the study was to study the acute effects of bromocriptine (a D2R agonist) on circadian leptin levels in obese women, whereas body weight and caloric intake remained constant.
  
  
  METHODS
  This was a prospective, single-blind, crossover study (2004).
  
  
  METHODS
  The study was conducted at a clinical research center.
  
  
  METHODS
  Eighteen healthy obese women (body mass index 33.2 +/- 0.6 kg/m(2)) were studied twice in the early follicular phase of their menstrual cycle.
  
  
  METHODS
  Treatment consisted of bromocriptine or placebo for 8 d.
  
  
  METHODS
  Blood was collected during 24 h at 20-min intervals for determination of leptin concentrations at the last day of medical treatment (bromocriptine or placebo). Mean 24-h serum concentrations were determined for insulin, glucose, free fatty acids, and triglycerides.
  
  
  RESULTS
  Short-term treatment with bromocriptine reduced leptin concentration (placebo 33.6 +/- 2.5 vs. bromocriptine 30.5 +/- 2.5 ng/liter, P = 0.03). Free fatty acid concentrations were increased by treatment with bromocriptine. The increase of free fatty acids was inversely related with the decline of leptin levels. The decline of glucose, insulin, or prolactin concentrations in response to bromocriptine was not correlated with the reduction of leptin.
  
  
  CONCLUSIONS
  Activation of dopamine D2 receptors by bromocriptine lowers circulating leptin levels in obese women, which suggests that dopaminergic neurotransmission is involved in the control of leptin release in humans.
authors.affiliation: Department of Internal Medicine (C4-83), Leiden University Medical Center, 2300 RC Leiden, The Netherlands.
authors.forename: Petra
authors.initials: P
authors.lastname: Kok
authors.forename: Ferdinand
authors.initials: F
authors.lastname: Roelfsema
authors.forename: Marijke
authors.initials: M
authors.lastname: Frölich
authors.forename: Johannes
authors.initials: J
authors.lastname: van Pelt
authors.forename: A Edo
authors.initials: AE
authors.lastname: Meinders
authors.forename: Hanno
authors.initials: H
authors.lastname: Pijl
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D001971:Bromocriptine / Q000494:pharmacology; D002940:Circadian Rhythm / Q000502:physiology*; D018592:Cross-Over Studies; D018491:Dopamine Agonists / Q000494:pharmacology; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D006801:Humans; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood*; D008875:Middle Aged; D009638:Norepinephrine / Q000652:urine; D009765:Obesity / Q000097:blood*; D017697:Premenopause; D011446:Prospective Studies; D017448:Receptors, Dopamine D2 / Q000187:drug effects / Q000502:physiology*; D054411:Receptors, Leptin; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D018491:Dopamine Agonists; D005230:Fatty Acids, Nonesterified; D007328:Insulin; C515448:LEPR protein, human; D020738:Leptin; D017448:Receptors, Dopamine D2; D054411:Receptors, Leptin; D014280:Triglycerides; D001971:Bromocriptine; D009638:Norepinephrine