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• W2007800906 abstract "Abstract Leptin administration potentiates the satiety response to signals such as cholecystokinin (CCK), that are released from the gut during a meal. To investigate the physiological relevance of this observation, we hypothesized that leptin deficiency, induced by fasting, attenuates the satiety response to CCK. To test this hypothesis, 48-h-fasted or fed rats were injected with ip saline or CCK. Fasting blunted the satiety response to 3.0 μg/kg CCK, such that 30-min food intake was suppressed by 65.1% (relative to saline-treated controls) in fasted rats vs. 85.9% in the fed state (P&lt; 0.05). In a subsequent experiment, rats were divided into three groups: 1) vehicle/fed; 2) vehicle/fasted; and 3) leptin-replaced/fasted; and each group received 3.0 μg/kg ip CCK. As expected, the satiety response to CCK was attenuated by fasting in vehicle-treated rats (30-min food intake: vehicle/fed, 0.3 ± 0.1 g; vehicle/fasted, 1.7 ± 0.4 g; P &lt; 0.01), and this effect was prevented by leptin replacement (0.7 ± 0.2 g, P &lt; 0.05 vs. vehicle/fasted; P = not significant vs. vehicle/fed). To investigate whether elevated neuropeptide Y (NPY) signaling plays a role in the effect of leptin deficiency to impair the response to CCK, we measured the response to 3.0 μg/kg ip CCK after treatment with 7.5 μg intracerebroventricular NPY. We found that both CCK-induced satiety and its ability to increase c-Fos-like-immunoreactivity in key brainstem-feeding centers were attenuated by NPY pretreatment. We conclude that an attenuated response to meal-related satiety signals is triggered by leptin deficiency and may contribute to increased food intake." @default.
• W2007800906 created "2016-06-24" @default.
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• W2007800906 date "2000-12-01" @default.
• W2007800906 modified "2023-10-16" @default.
• W2007800906 title "Leptin Deficiency Induced by Fasting Impairs the Satiety Response to Cholecystokinin**This work was supported by grants from the NIH (DK-12829, DK-52989, and NS-32272) and by the Royalty Research Fund, the Diabetes Endocrinology Research Center, and the Clinical Nutrition Research Unit of the University of Washington." @default.
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• W2007800906 doi "https://doi.org/10.1210/endo.141.12.7815" @default.
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