TY - JOUR
T1 - Increased circadian prolactin release is blunted after body weight loss in obese premenopausal women
AU - Kok, Petra
AU - Roelfsema, Ferdinand
AU - Langendonk, Janneke G.
AU - De Wit, Caroline C.
AU - Frölich, Marijke
AU - Burggraaf, Jacobus
AU - Meinders, A. Edo
AU - Pijl, Hanno
PY - 2006/2
Y1 - 2006/2
N2 - We recently showed that prolactin (PRL) release is considerably enhanced in obese women in proportion to the size of their visceral fat mass. PRL release is inhibited by dopamine 2 receptor (D2R) activation, and dietary restriction/weight loss are associated with increased dopaminergic signaling in animals. Therefore, we hypothesized that enhanced PRL release in obese humans would be reversed by weight loss. To evaluate this postulate, we measured 24-h plasma PRL concentrations at 10-min intervals in 11 obese premenopausal women (BMI 33.3 ± 0.7 kg/m2) before and after weight loss (50% reduction of overweight/ 15% absolute weight loss, using a very low-calorie diet) in the follicular phase of their menstrual cycle. The 24-h PRL concentration profiles were analyzed by a peak detection program (Cluster) and a wave form-independent deconvolution technique (Pulse). Spontaneous 24-h PRL secretion was significantly reduced in obese women [mean daily release, before 128 ± 24 vs. after weight loss 110 ± 17 μg/liter distribution volume (Vdl)-1 x 24 h, P = 0.05]. Body weight loss particularly blunted PRL secretory burst mass (Pulse area, before 230 ± 28 vs. after weight loss 221 ± 31 μg/Vdl-1 x 24 h, P = 0.03), whereas burst frequency was unaffected (no. of pulses, before 11 ± 1 vs. after weight loss 12 ± 1 n/24 h, P = 0.69). Thus elevated PRL secretion rate in obese women is significantly reduced after loss of 50% of overweight. We speculate that amelioration of deficit D2R-mediated neurotransmission and/or diminutions of circulating leptin/ estrogen levels might be involved in the physiology of this phenomenon.
AB - We recently showed that prolactin (PRL) release is considerably enhanced in obese women in proportion to the size of their visceral fat mass. PRL release is inhibited by dopamine 2 receptor (D2R) activation, and dietary restriction/weight loss are associated with increased dopaminergic signaling in animals. Therefore, we hypothesized that enhanced PRL release in obese humans would be reversed by weight loss. To evaluate this postulate, we measured 24-h plasma PRL concentrations at 10-min intervals in 11 obese premenopausal women (BMI 33.3 ± 0.7 kg/m2) before and after weight loss (50% reduction of overweight/ 15% absolute weight loss, using a very low-calorie diet) in the follicular phase of their menstrual cycle. The 24-h PRL concentration profiles were analyzed by a peak detection program (Cluster) and a wave form-independent deconvolution technique (Pulse). Spontaneous 24-h PRL secretion was significantly reduced in obese women [mean daily release, before 128 ± 24 vs. after weight loss 110 ± 17 μg/liter distribution volume (Vdl)-1 x 24 h, P = 0.05]. Body weight loss particularly blunted PRL secretory burst mass (Pulse area, before 230 ± 28 vs. after weight loss 221 ± 31 μg/Vdl-1 x 24 h, P = 0.03), whereas burst frequency was unaffected (no. of pulses, before 11 ± 1 vs. after weight loss 12 ± 1 n/24 h, P = 0.69). Thus elevated PRL secretion rate in obese women is significantly reduced after loss of 50% of overweight. We speculate that amelioration of deficit D2R-mediated neurotransmission and/or diminutions of circulating leptin/ estrogen levels might be involved in the physiology of this phenomenon.
UR - http://www.scopus.com/inward/record.url?scp=33644857285&partnerID=8YFLogxK
U2 - 10.1152/ajpendo.00156.2005
DO - 10.1152/ajpendo.00156.2005
M3 - Article
C2 - 16144819
AN - SCOPUS:33644857285
SN - 0193-1849
VL - 290
SP - E218-E224
JO - American Journal of Physiology - Endocrinology and Metabolism
JF - American Journal of Physiology - Endocrinology and Metabolism
IS - 2
ER -