No acute effect of physiological insulin increase on dehydroepiandrosterone sulfate in women with obesity and/or polycystic ovarian disease**Supported in part by the Clinical Research Center, University of California at Los Angeles United States Public Health Service Grant No. RR00865 and the University of Alabama at Birmingham, Clinical Nutrition Research Unit, National Institute of Health (Bethesda, Maryland) grant no. CA-28103.††Presented at the 38th Annual Meeting of the Society for Gynecologic Investigation, San Antonio, Texas, March 20 to 23, 1991.

Tony Earley was born in San Antonio, Texas, and grew up in North Carolina near the Blue Ridge Mountains. He graduated from Warren Wilson College in 1983 and earned an MFA in creative writing from the University of Alabama. Since 1997 he has taught writing at Vanderbilt University....

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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.

Endocrinology ◽

10.1210/endo.141.12.7815 ◽

2000 ◽

Vol 141 (12) ◽

pp. 4442-4448 ◽

Cited By ~ 69

Author(s):

Julie E. McMinn ◽

Dana K. Sindelar ◽

Peter J. Havel ◽

Michael W. Schwartz

Keyword(s):

Food Intake ◽

Research Unit ◽

Research Fund ◽

Fed State ◽

Satiety Response ◽

Leptin Deficiency ◽

Nutrition Research ◽

Physiological Relevance ◽

The University ◽

Fasted Rats

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< 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 < 0.01), and this effect was prevented by leptin replacement (0.7 ± 0.2 g, P < 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.

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