Metabolic control of food intake and estrous cycles in Syrian hamsters. I. Plasma insulin and leptin

American Journal of Physiology - Regulatory Integrative and Comparative Physiology - Tập 278 Số 2 - Trang R476-R485 - 2000
Jill E. Schneider1, Robert M. Blum1, George N. Wade2
1Department of Biological Sciences, Lehigh University, Bethlehem, Pennsylvania 18015-4732; and
2Center for Neuroendocrine Studies, Department of Psychology, University of Massachusetts, Amherst, Massachusetts 01003-7720

Tóm tắt

The “adipostat hypothesis” refers to the idea that circulating hormone concentrations reflect levels of body adiposity and act as signals to control food intake and reproduction. Implicit in the adipostatic hypothesis are the following two assumptions: 1) plasma levels of adipostatic hormones accurately reflect body fat content and 2) decreased plasma concentrations of adipostatic hormones necessarily result in increased food intake and inhibited reproductive processes. The present experiments are designed to test these assumptions. Fat and lean Syrian hamsters were either fasted for 12, 24, 36, or 48 h or allowed ad libitum access to food. Contrary to the first assumption, plasma leptin and insulin levels in fat hamsters dropped dramatically by 12 h after the start of a fast, with no significant change in body fat content and no postfast hyperphagia. Lean hamsters showed anestrus after a 48-h fast but not after a 24-h fast. Contrary to the second assumption of the lipostatic hypothesis, lean hamsters fasted for 24 h and then refed for the next 24 h had leptin levels that were not significantly elevated compared with those of 48-h-fasted hamsters. Thus, in adult female Syrian hamsters, plasma leptin concentrations do not accurately reflect body fat content under all conditions; normal estrous cyclicity does not necessarily require plasma leptin concentrations higher than those of fasted hamsters; and decreased plasma leptin levels do not result in increased food intake.

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Tài liệu tham khảo

10.1038/382250a0

10.1152/ajpregu.1997.273.1.R113

10.1159/000126257

10.1210/endo.137.7.8770941

10.1016/0014-5793(95)00943-4

10.1093/ajcn/36.3.450

Boden G., 1996, J. Clin. Endocrinol. Metab., 81, 3419

10.1210/endo-118-6-2483

10.1152/ajpregu.1988.254.4.R616

10.1152/ajpregu.1990.259.1.R25

10.1530/ror.0.0010117

10.1210/endo-128-3-1532

10.1126/science.7624778

10.1172/JCI603

10.1038/ng0396-318

10.1126/science.275.5296.88

10.1210/endo-127-3-1470

Considine R. V., 1996, J. Clin. Invest., 334, 292

10.1038/27376

10.1093/ajcn/62.5.1096S

10.1093/ajcn/67.3.513S

10.1152/ajpregu.1986.251.5.R840

10.1126/science.185.4155.949

10.1126/science.7624777

10.1006/bbrc.1996.0951

10.1152/physrev.1980.60.2.442

10.1093/jn/103.10.1479

10.1093/ajcn/62.5.1123S

10.1098/rspb.1953.0009

10.1113/jphysiol.1963.sp007112

10.2337/diab.45.11.1511

10.1016/0031-9384(72)90251-X

10.1097/00001756-199902050-00042

10.1152/ajpregu.1998.275.4.R1218

10.2337/diab.39.12.1461

10.1038/nm1195-1155

McGarry J. D., 1973, J. Biol. Chem., 248, 270, 10.1016/S0021-9258(19)44471-2

10.1016/S0031-9384(98)00039-0

10.1530/jrf.0.1120347

10.1677/joe.0.1470321

10.1038/43185

10.1095/biolreprod13.1.99

10.1152/ajpregu.1986.251.4.R663

10.1016/0300-9629(82)90435-2

10.1126/science.7624776

10.1093/jn/105.8.1055

10.1006/bbrc.1995.2266

10.1016/0361-9230(85)90111-X

10.1055/s-2007-979869

10.1006/hbeh.1998.1453

10.1016/0031-9384(86)90141-1

10.1152/ajpregu.1987.253.2.R314

10.1126/science.2734610

10.1210/endo.132.5.8477642

Schwartz M. W., 1992, Endocrin. Rev., 13, 387

10.1016/0031-9384(76)90076-7

Simek V., 1974, Physiol. Bohemoslov., 23, 437

10.1038/ng0398-213

10.1042/bst0240565

10.1016/S0149-7634(05)80183-6

10.1152/ajpendo.1996.270.1.E1

10.1038/31474

10.1172/JCI118254

10.1210/endo.137.6.8641210

10.1016/0149-7634(95)00044-F

10.1073/pnas.94.3.1023

10.1038/372425a0

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American Journal of Physiology - Regulatory Integrative and Comparative Physiology

Tập 278 Số 2

R476-R485

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