Food intake is generally assumed to reflect a regulatory tension between homeostatic and hedonic drivers.Information from individuals with memory dysfunction suggests that episodic memory may also play a significant r...Food intake is generally assumed to reflect a regulatory tension between homeostatic and hedonic drivers.Information from individuals with memory dysfunction suggests that episodic memory may also play a significant role.We reasoned that if memory influences food intake,then disrupting a genetic factor that is important in episodic memory formation should affect food intake and energy balance.We performed spatial learning tests on neuronal specific endophilin A1(EENA1)KO mice using the four-arm baited version of the radial arms maze(RAM).Energy regulation has also been evaluated.As anticipated neuronal EENA1 KO mice had impaired spatial memory.However,loss of endophilin A1 did not result in greater food intake,or altered energy absorption efficiency,relative to wild-type(WT)mice,when fed either low or high fat diets.Moreover,loss of EENA1 did not significantly affect other features of energy balance—physical activity and energy expenditure.No statistically significant changes were observed in the expression of hypothalamic neuropeptides related to food intake regulation,or circulating levels of leptin.We conclude that food intake and energy balance are largely governed by homeostatic and hedonic processes,and when these processes are intact memory probably plays a relatively minor role in food intake regulation.展开更多
基金supported by funding from the National Key R&D program of China (2019YFA0801900 to JR Speakman, 2016YFA0500100 to J-J. Liu)the National Natural Science Foundation of China (92057206 to JR Speakman, 31530039 to J-J. Liu and 32070785 to Y. Yang)the Strategic Priority Research Program of Chinese Academy of Science (XDB32020100 to J-J. Liu and XDB13030100 to JR Speakman)
文摘Food intake is generally assumed to reflect a regulatory tension between homeostatic and hedonic drivers.Information from individuals with memory dysfunction suggests that episodic memory may also play a significant role.We reasoned that if memory influences food intake,then disrupting a genetic factor that is important in episodic memory formation should affect food intake and energy balance.We performed spatial learning tests on neuronal specific endophilin A1(EENA1)KO mice using the four-arm baited version of the radial arms maze(RAM).Energy regulation has also been evaluated.As anticipated neuronal EENA1 KO mice had impaired spatial memory.However,loss of endophilin A1 did not result in greater food intake,or altered energy absorption efficiency,relative to wild-type(WT)mice,when fed either low or high fat diets.Moreover,loss of EENA1 did not significantly affect other features of energy balance—physical activity and energy expenditure.No statistically significant changes were observed in the expression of hypothalamic neuropeptides related to food intake regulation,or circulating levels of leptin.We conclude that food intake and energy balance are largely governed by homeostatic and hedonic processes,and when these processes are intact memory probably plays a relatively minor role in food intake regulation.
