NPYergic neurons in the hypothalamic arcuate nucleus (ARC) that projec
t to the paraventricular nucleus (PVN) are postulated to regulate food
intake and energy balance. This projection is overactive in lactation
and is thought to drive hyperphagia in this condition. We have explor
ed further the relationship between hypothalamic NPY and food intake i
n lactation and tested the hypothesis that hypoinsulinemia is the stim
ulus to NPY neuronal activity. Compared with nonlactating controls (n
= 10), freely fed lactating rats (n = 9) showed significantly increase
d (p < 0.05) NPY levels in the ARC and medial preoptic area (MPO), but
there was no significant increase in whole hypothalamic NPY mRNA leve
ls. Lactating rats (n = 8) that were restricted to control rats' food
intake for 3 days showed generally higher hypothalamic NPY levels, wit
h significantly higher concentrations than controls (p < 0.05) in the
ARC, MPO, PVN, and lateral hypothalamic area(LHA);NPY mRNA levels were
also significantly increased (p < 0.05). Across all three experimenta
l groups, there was a significant inverse correlation between plasma i
nsulin concentration and hypothalamic NPY mRNA levels (r = -0.39, p <
0.01). We conclude that the ARC-PVN projection is overactive in lactat
ion and that this is not a consequence of hyperphagia. Hypoinsulinemia
may stimulate these neurons, as it thought to do in other conditions
of energy deficit.