Moderate long-term modulation of neuropeptide y in hypothalamic arcuate nucleus induces energy balance alterations in adult rats.
Administration of leptin or insulin suppresses the expression of NPY (about 0.5 to 1.5-fold decrease of ARC NPY levels) and reduces food intake in lean rats and in rodent models with elevated NPY expression, such as ob/ob mice, fasted rats or diabetic rats.
NPY production is stimulated by negative energy conditions, such that food deprivation induces a potent up-regulation in the expression of NPY and AGRP (5–10 fold increase as compared to basal).
Furthermore, NPY levels return to initial values within 6 to 24 hours after re-feeding. (well that is good to know,)
In addition, some studies also report elevated levels of hypothalamic NPY (30%, in average) in diet-induced obese mice (DIO). However, other studies show a compensatory down-regulation of NPY expression in the ARC and immunoreactivity in the PVN in rats fed with high-fat diet for variable periods of time which was related to the inhibitor effect of elevated leptin concentrations.
Overall this study shows that a forced increase in basal NPY leads to extreme over-eating and extreme fat gain.
Reducing NPY strangely leads to normal feeding under basal circumstances, BUT, the mice did not increase thier food intake after a period of calorie restriction!
This suggests that the upregulation of NPY after calorie restriction is an essential survival mechanism. This is direct evidence that your body attempts to maintain a "bodyfat set-point", atleast with regards to under-feeding and forced adipose mass depletion.