Leptin, the obese (Ob) gene product, is an adipocyte-derived satiety factor
that is involved in the regulation of food intake and body weight. Leptin
signals nutritional status to several other physiological systems and modul
ates their function. As PRL is involved in energy and lipid metabolism, thi
s study was undertaken to investigate the role of PRL on in vivo regulation
of leptin serum concentration and Ob messenger RNA expression in white adi
pose tissue in rats. It was found that increased serum PRL levels, obtained
by pituitary graft or exogenous injected ovine PRL (oPRL, 5 mg/kg), signif
icantly stimulate serum leptin concentration. A significant increase (P < 0
.01) in serum leptin concentration was present in hyperprolactinemic animal
s (4.7 +/- 0.4 mu g/liter) in comparison to controls (1.2 +/- 0.1 mu g/lite
r and 1.09 +/- 0.09 mu g/liter of intact sham operated and ovariectomized r
ats, respectively). Similar results were obtained in oPRL-treated animals w
here leptin levels were 5.4 +/- 0.1 mu g/liter vs. 1.1 +/- 0.1 mu g/liter a
nd 0.8 +/- 0.08 mu g/liter of intact sham operated rats and ovariectomized,
respectively (P < 0.001). This stimulatory effect of PRL on serum leptin l
evels was significantly reduced by food deprivation (P < 0.01) where serum
leptin levels were 12.5 +/- 0.65 mu g/liter in grafted animals vs. 3.2 +/-
0.36 mu g/liter of grafted animals subjected to 48 h of food deprivation. M
oreover, in vivo, PRL was able to induce leptin messenger RNA levels in sev
eral areas of rat white adipose tissue. The data demonstrate that PRL acts
on the adipose tissue increasing leptin synthesis and secretion, suggesting
a new role for this lactogenic hormone in the regulation of food intake.