The Possible Role of Prolactin in the Circadian Rhythm of Leptin Secretion in Male Rats
- 1 July 2000
- journal article
- Published by Wiley in Proceedings of the Society for Experimental Biology and Medicine
- Vol. 224 (3) , 152-158
- https://doi.org/10.1046/j.1525-1373.2000.22414.x
Abstract
In humans there is a circadian rhythm of leptin concentrations in plasma with a minimum in the early morning and a maximum in the middle of the night. By taking blood samples from adult male rats every 3 hr for 24 hr, we determined that a circadian rhythm of plasma leptin concentrations also occurs in the rat with a peak at 0130h and a minimum at 0730h. To determine if this rhythm is controlled by nocturnally released hormones, we evaluated the effect of hormones known to be released at night in humans, some of which are also known to be released at night in rats. In humans, prolactin (PRL), growth hormone (GH), and melatonin are known to be released at night, and adrenocorticotropic hormone (ACTH) release is inhibited. In these experiments, conscious rats were injected intravenously with 0.5 ml diluent or the substance to be evaluated just after removal of the first blood sample (0.3 ml), and additional blood samples (0.3 ml) were drawn every 10 min thereafter for 2 hr. The injection of highly purified sheep PRL (500 microg) produced a rapid increase in plasma leptin that persisted for the duration of the experiment. Lower doses were ineffective. To determine the effect of blockade of PRL secretion on leptin secretion, alpha bromoergocryptine (1.5 mg), a dopamine-2-receptor agonist that rapidly inhibits PRL release, was injected. It produced a rapid decline in plasma leptin within 10 min, and the decline persisted for 120 min. The minimal effective dose of GH to lower plasma leptin was 1 mg/rat. Insulin-like growth factor (IGF-1) (10 microg), but not IGF-2 (10 microg), also significantly decreased plasma leptin. Melatonin, known to be nocturnally released in humans and rats, was injected at a dose of 1 mg/rat during daytime (1100h) or nighttime (2300h). It did not alter leptin release significantly. Dexamethasone (DEX), a potent glucocorticoid, was ineffective at a 0. 1-mg dose but produced a delayed, significant increase in leptin, manifest 100-120 min after injection of a 1 mg dose. Since glucocorticoids decrease at night in humans at the time of the maximum plasma concentrations of leptin, we hypothesize that this increase in leptin from a relatively high dose of DEX would mimic the response to the release of corticosterone following stress in the rat and that glucocorticoids are not responsible for the circadian rhythm of leptin concentration. Therefore, we conclude that an increase in PRL secretion during the night may be responsible, at least in part, for the nocturnal elevation of leptin concentrations observed in rats and humans.Keywords
This publication has 21 references indexed in Scilit:
- Prolactin (PRL) and Its Receptor: Actions, Signal Transduction Pathways and Phenotypes Observed in PRL Receptor Knockout MiceEndocrine Reviews, 1998
- Synchronicity of frequently sampled, 24-h concentrations of circulating leptin, luteinizing hormone, and estradiol in healthy womenProceedings of the National Academy of Sciences, 1998
- Human leptin levels are pulsatile and inversely related to pituitary–ardenal functionNature Medicine, 1997
- Early Onset of Reproductive Function in Normal Female Mice Treated with LeptinScience, 1997
- Leptin is a metabolic signal to the reproductive systemEndocrinology, 1996
- Specificity of Leptin Action on Elevated Blood Glucose Levels and Hypothalamic Neuropeptide Y Gene Expression in ob/ob MiceDiabetes, 1996
- Correction of the sterility defect in homozygous obese female mice by treatment with the human recombinant leptinNature Genetics, 1996
- Weight-Reducing Effects of the Plasma Protein Encoded by the obese GeneScience, 1995
- Effects of the obese Gene Product on Body Weight Regulation in ob / ob MiceScience, 1995
- A rapid and simple procedure for chronic cannulation of the rat jugular vein.Journal of Applied Physiology, 1974