期刊
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
卷 302, 期 1, 页码 E134-E144出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpendo.00296.2011
关键词
leptin; food intake
资金
- Office of Research and Development, Medical Research Service, Department of Veterans Affairs
- Veterans Affairs Puget Sound Health Care System
- Department of Veterans Affairs
- Department of Veterans Affairs Nebraska Western Iowa Health Care System
- NIH [DK-068304, DK-083042, DK-052989, DK-089056]
- American Heart Association
- Cellular and Molecular Imaging Core of the National Institutes of Health (NIH) Diabetes Endocrinology Research Center (DERC) [P30 DK-17047]
- NIH Nutrition Obesity Research Unit Animal Studies Physiology Core at the University of Washington (NORC) [P30 DK-035816]
- NIH Mouse Metabolic Phenotyping Center Diabetes and Energy Balance Core (MMPC) [U24 DK-076126]
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK017047, R01DK083042, P30DK035816, R01DK052989, R01DK089056, R01DK090320, U24DK076126] Funding Source: NIH RePORTER
Morton GJ, Thatcher BS, Reidelberger RD, Ogimoto K, Wolden-Hanson T, Baskin DG, Schwartz MW, Blevins JE. Peripheral oxytocin suppresses food intake and causes weight loss in diet-induced obese rats. Am J Physiol Endocrinol Metab 302: E134-E144, 2012. First published October 18, 2011; doi:10.1152/ajpendo.00296.2011.-Growing evidence suggests that oxytocin plays an important role in the regulation of energy balance and that central oxytocin administration induces weight loss in diet-induced obese (DIO) animals. To gain a better understanding of how oxytocin mediates these effects, we examined feeding and neuronal responses to oxytocin in animals rendered obese following exposure to either a high-fat (HFD) or low-fat diet (LFD). Our findings demonstrate that peripheral administration of oxytocin dose-dependently reduces food intake and body weight to a similar extent in rats maintained on either diet. Moreover, the effect of oxytocin to induce weight loss remained intact in leptin receptor-deficient Koletsky (fak/fak) rats relative to their lean littermates. To determine whether systemically administered oxytocin activates hindbrain areas that regulate meal size, we measured neuronal c-Fos induction in the nucleus of the solitary tract (NTS) and area postrema (AP). We observed a robust neuronal response to oxytocin in these hindbrain areas that was unexpectedly increased in rats rendered obese on a HFD relative to lean, LFD-fed controls. Finally, we report that repeated daily peripheral administration of oxytocin in DIO animals elicited a sustained reduction of food intake and body weight while preventing the reduction of energy expenditure characteristic of weight-reduced animals. These findings extend recent evidence suggesting that oxytocin circumvents leptin resistance and induces weight-loss in DIO animals through a mechanism involving activation of neurons in the NTS and AP, key hindbrain areas for processing satiety-related inputs.
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