Effect of food deprivation and leptin repletion on the plasma levels of estrogen (E2) and NADPH-d reactivity in the ventromedial and arcuate nuclei of the hypothalamus in the female rats
Ee. Otukonyong et al., Effect of food deprivation and leptin repletion on the plasma levels of estrogen (E2) and NADPH-d reactivity in the ventromedial and arcuate nuclei of the hypothalamus in the female rats, BRAIN RES, 887(1), 2000, pp. 70-79
The exact role of leptin in fasting has not been completely elucidated, To
determine whether leptin can act in fasting to influence plasma estrogen le
vels and nitric oxide synthase reactivity in food regulating centers of the
brain, we fasted female rats for 4 days and treated them i.p. with vehicle
or 100 mug of recombinant mouse leptin as 1 mi on the 3rd and 4th day twic
e daily (10.00 and 17.00 h). Proestrus blood was collected at 10.00, 14.00,
18.00 and at 22.00 h, plasma obtained and assayed for estrogen (E2) and le
ptin levels. Verification of ovulation occurrence was by examining the ovid
uct for extruded ovum. The rat brains were removed and processed for nitric
oxide synthase reactivity in the ventromedial hypothalamus (VMH) and arcua
te nucleus (ARC) using NADPH-diaphorase histochemistry, a marker for neuron
s expressing NOS enzyme. Leptin effect on dependable variables such as food
intake, water intake and body weight gain was also investigated. Four days
fasting significantly decreased body weight, estrogen and postfast leptin
levels, nitric oxide reactivity in the VMH and ARC nucleus and stopped ovul
ation in many (4 out of 5) rats fasted and given vehicle. Leptin treatment
significantly increased plasma estrogen and postfast leptin levels, restore
d ovulation in many (4 out of 5) rats and increased nitric oxide reactivity
in the VMH and ARC. Leptin significantly inhibited food intake, water inta
ke and gain in body weight during recommenced feeding. These observations s
uggest that leptin could act in the pituitary-ovarian axis during fasting t
o improve reproductive function by partly stimulating estrogen secretion. (
C) 2000 Elsevier Science B.V. All rights reserved.