This review lays out the evidence for the role of E2 in homeostatic and hedonic feeding across several species. While significant effort has been expended on homeostatic feeding research, more studies for hedonic feeding need to be conducted (i.e. are there increases in meal size and enhanced motivation to natural food rewards). By identifying the underlying neural circuitry involved, one can better delineate the mechanisms by which E2 influences feeding behavior. By utilizing more selective neural targeting techniques, such as optogenetics, significant progress can be made toward this goal. Together, behavioral and physiological techniques will help us to better understand neural deficits that can increase the risk for obesity in the absence of E2 (menopause) and aid in developing therapeutic strategies.
Keywords: 17β-estradiol; Food intake; Obesity.
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