Abstract
Short-term abstinence from food intake, planned or unplanned, is unavoidable in modern
life, but negatively correlated with appetite control and obesity. This study investigated
the role of estradiol in feeding and body weight (BW) reactions to short-span cessation
of feeding. During acute 1–6-h re-feeding, 12-h food-deprived (FD), estradiol benzoate
(EB)-implanted ovariectomized rats ate less food and gained less weight than FD animals
implanted with oil (O). Full fed (FF)- and FD-EB consumed equal amounts of food over
24 h, but weight gain was greater in the latter; 24-h food intake and BW gain in FD-O
exceeded FD-EB. Caudal fourth ventricular administration of the AMPK activator AICAR
increased dorsal vagal complex AMPK activity in FD-EB and FD-O, but elicited dissimilar
adjustments in hypothalamic metabolic neuropeptide transmitter expression, while respectively
enhancing or reducing acute re-feeding in these animals and reversing FD-O weight
gain. Drug-treated FD-EB and FD-O exhibited respective feeding and weight gain increases
between 6–24 h. AICAR enhanced 24-h consumption in FD-EB vs. FF-EB, but cumulative
intake and BW gain were greater in AICAR-treated FD-O vs. FD-EB. Results show that
estradiol limits acute re-feeding after short-term feeding suspension, but augments
acute re-feeding when energy depletion coincides with suspended feeding. This compound
metabolic stress exerts steroid-dependent effects during later resumption of circadian-induced
feeding, for example, increased consumption vs. weight gain in the presence vs. absence
of estradiol. These studies provide novel evidence that estrogen mitigates acute and
post-acute adverse effects of disrupted fuel acquisition on energy balance.
Key words
ovariectomy - deferred feeding - estradiol benzoate - dorsal vagal complex - AICAR
- body weight
