Fig. 19.

Schematic summary of the activational effects of gonadal steroid hormones on eating, emphasizing hypothesized neural mechanisms and their integration. The diagram is based on our review of rat, mouse, and anthropoid primate, including human, data. It is superimposed on a schematic midsagittal section of a rat brain, although most named structures are lateral to the midline. Red arrows and text boxes indicate estrogenic mechanisms; question marks and black font identify less well-established mechanisms. Estrogens acting on ERα on neurons in the cmNTS (filled oval) affect the neural processing of peripheral CCK signals (solid red arrow) so as to reduce meal size, food intake, and body weight; the same ERα neurons are hypothesized to be involved in the processing of a variety of other peripheral signals, especially ghrelin and gustatory signals, which are apparently affected by estrogens (dashed red arrows). ERα in the dorsal raphe and several hypothalamic areas are not strongly implicated in the control of eating (open red oval). A number of forebrain signaling molecules, especially 5HT and AgRP, as well as flavor hedonics contribute to the estrogenic control of eating, probably via hypothalamic and telencephalic mechanisms (dashed red arrows). Neural processing in these areas is presumably linked bidirectionally to the cmNTS and other brain stem areas (double-headed dashed red arrow), so that cmNTS ERα may also mediate these effects; non-ERα-expressing AgRP neurons in the Arc are the strongest candidates. Androgens acting on AR in unknown sites increase meal frequency, food intake, and body weight (green arrows and text boxes). In contrast, progestins appear not to have physiological effects on eating (blue, dashed text box). Challenges for future mechanistic studies of sex differences in eating include 1) establishing the physiological and pathophysiological roles of the estrogenic mechanisms shown and 2) identifying the androgenic mechanisms affecting eating.