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Science 6 December 1996:
Vol. 274. no. 5293, pp. 1704 - 1707
DOI: 10.1126/science.274.5293.1704
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Reports

Attenuation of the Obesity Syndrome of ob/ob Mice by the Loss of Neuropeptide Y

Jay C. Erickson, Gunther Hollopeter, Richard D. Palmiter *

The obesity syndrome of ob/ob mice results from lack of leptin, a hormone released by fat cells that acts in the brain to suppress feeding and stimulate metabolism. Neuropeptide Y (NPY) is a neuromodulator implicated in the control of energy balance and is overproduced in the hypothalamus of ob/ob mice. To determine the role of NPY in the response to leptin deficiency, ob/ob mice deficient for NPY were generated. In the absence of NPY, ob/ob mice are less obese because of reduced food intake and increased energy expenditure, and are less severely affected by diabetes, sterility, and somatotropic defects. These results suggest that NPY is a central effector of leptin deficiency.

Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Box 357370, Seattle, WA 98195-7370, USA.
*   To whom correspondence should be addressed.

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Short-Term Fasting Selectively Suppresses Leptin Pulse Mass and 24-Hour Rhythmic Leptin Release in Healthy Midluteal Phase Women without Disturbing Leptin Pulse Frequency or Its Entropy Control (Pattern Orderliness).
M. Bergendahl, A. Iranmanesh, W. S. Evans, and J. D. Veldhuis (2000)
J. Clin. Endocrinol. Metab. 85, 207-213
   Abstract »    Full Text »
The adipoinsular axis: effects of leptin on pancreatic beta -cells.
T. J. Kieffer and J. F. Habener (2000)
Am J Physiol Endocrinol Metab 278, E1-E14
   Abstract »    Full Text »    PDF »
Editorial: The Ups and Downs of Leptin Action.
R. D. Cone (1999)
Endocrinology 140, 4921-4922
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Distinct Physiologic and Neuronal Responses to Decreased Leptin and Mild Hyperleptinemia.
R. S. Ahima, J. Kelly, J. K. Elmquist, and J. S. Flier (1999)
Endocrinology 140, 4923-4931
   Abstract »    Full Text »
Pituitary Hormones as Neurotrophic Signals: Update on Hypothalamic Differentiation in Genetic Models of Altered Feedback.
C. J. Phelps and D. L. Hurley (1999)
Experimental Biology and Medicine 222, 39-58
   Abstract »    Full Text »
Monogenic disorders of obesity and body fat distribution.
D. Chen and A. Garg (1999)
J. Lipid Res. 40, 1735-1746
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Activation of Central Neuropeptide Y Y1 Receptors Potently Stimulates Food Intake in Male Rhesus Monkeys.
P. J. Larsen, M. Tang-Christensen, C. E. Stidsen, K. Madsen, M. S. Smith, and J. L. Cameron (1999)
J. Clin. Endocrinol. Metab. 84, 3781-3791
   Abstract »    Full Text »    PDF »
Physiological Role of Cholecystokinin B/Gastrin Receptor in Leptin Secretion.
S. Attoub, S. Levasseur, M. Buyse, H. Goïot, J.-P. Laigneau, L. Moizo, F. Hervatin, Y. Le Marchand-Brustel, J. M. M. Lewin, and A. Bado (1999)
Endocrinology 140, 4406-4410
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Glucocorticoids reverse leptin effects on food intake and body fat in mice without increasing NPY mRNA.
J. M. Solano and L. Jacobson (1999)
Am J Physiol Endocrinol Metab 277, E708-E716
   Abstract »    Full Text »    PDF »
Evidence That the Inhibition of Luteinizing Hormone Secretion Exerted by Central Administration of Neuropeptide Y (NPY) in the Rat Is Predominantly Mediated by the NPY-Y5 Receptor Subtype.
P. D. Raposinho, P. Broqua, D. D. Pierroz, A. Hayward, Y. Dumont, R. Quirion, J.-L. Junien, and M. L. Aubert (1999)
Endocrinology 140, 4046-4055
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Hypothalamic Obesity: Multiple Routes Mediated by Loss of Function in Medial Cell Groups.
S. Choi and M. F. Dallman (1999)
Endocrinology 140, 4081-4088
   Abstract »    Full Text »


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