The small population of DA neurons in the hypothalamus has been known to regulate the secretion of prolactin which also plays a role in regulating food intake and energy balance3738. We, therefore, examined whether deletion of FoxO1 in DA neurons affects prolactin secretion from the pituitary. However, there was no detectable change in prolactin levels in the pituitary and in the serum samples of FoxO1 KODAT mice (Supplementary Fig. 5e and f). Consistent with unaltered DA turnover and hypothalamic TH expression (Supplementary Fig. 5a–d and Supplementary Fig. 6a–c), unchanged prolactin level was in line with the aforementioned observation that FoxO1 KODAT mice showed no difference in homoeostatic feeding and food intake. Although these results could not totally exclude the possibility of an alteration in the hypothalamic-pituitary system caused by FoxO1 deletion in DA neurons of the hypothalamus, unchanged prolactin levels implied that the metabolic phenotypes observed in KO mice might not be the secondary effects of prolactin secretion inhibition.
