The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
PVN infusion of GLP-1-(7—36) amide suppresses feeding but does not induce aversion or alter locomotion in rats
Abstract
Intracerebroventricular infusion of glucagon-like peptide-1-(7—36) amide (GLP-1) reduces feeding in rats, an effect that could be localized to the hypothalamic paraventricular nucleus (PVN). Intracerebroventricular GLP-1, however, may also induce conditioned taste aversion (CTA), thereby putting into question the specificity of the action of GLP-1 on feeding. The present experiments evaluated the action of PVN GLP-1 (0, 100, or 200 ng) on induction of CTA, on locomotion, and finally, on feeding and drinking in rats. PVN infusion of GLP-1 (100 or 200 ng) did not support the induction of CTA and did not reliably alter locomotion, but did suppress feeding and drinking. The present study suggests that GLP-1 infusions into the PVN reduce food and water intake without producing illness or disrupting locomotor behavior. These data, in conjunction with reports of increased feeding following antagonism of central GLP-1 receptors, support the notion that endogenous GLP-1, perhaps within the PVN, functions to suppress feeding in the rat.
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Cites
A role for glucagon-like peptide-1 in the central regulation of feeding
Turton, M. D., O'Shea, D., Gunn, I., Beak, S. A., Edwards, C. M. B., Meeran, K., Choi, S. J., Taylor, G. M., Heath, M. M., Lambert, P. D., et al. (1996) · Nature · doi:10.1038/379069a0 · Cited by 1,950
Elliott, R. M., Morgan, L. M., Tredger, J. A., Deacon, S., Wright, J., & Marks, V. (1993) · Journal of Endocrinology · doi:10.1677/joe.0.1380159 · Cited by 695
Larsen, P. J., Tang-Christensen, M., Holst, J. J., & Ørskov, C. (1997) · Neuroscience · doi:10.1016/s0306-4522(96)00434-4 · Cited by 663
Cited by
Glucagon-like peptide 1 (GLP-1)
Müller, T. D., Finan, B., Bloom, S. R., D'Alessio, D., Drucker, D. J., Flatt, P. R., Fritsche, A., Gribble, F., Grill, H. J., Habener, J. F., et al. (2019) · Molecular Metabolism · doi:10.1016/j.molmet.2019.09.010 · Cited by 1,868
The arcuate nucleus mediates GLP-1 receptor agonist liraglutide-dependent weight loss
Secher, A., Jelsing, J., Baquero, A. F., Hecksher-Sørensen, J., Cowley, M. A., Dalbøge, L. S., Hansen, G., Grove, K. L., Pyke, C., Raun, K., et al. (2014) · Journal of Clinical Investigation · doi:10.1172/jci75276 · Cited by 961
Alhadeff, A. L., Rupprecht, L. E., & Hayes, M. R. (2012) · Endocrinology · doi:10.1210/en.2011-1443 · Cited by 515
Central Control of Body Weight and Appetite
Woods, S. C., & D'Alessio, D. A. (2008) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2008-1630 · Cited by 458
Gastrointestinal hormones and food intake
Strader, A. D., & Woods, S. C. (2005) · Gastroenterology · doi:10.1053/j.gastro.2004.10.043 · Cited by 447
Metadata
- Authors
- McMahon, L. R., & Wellman, P. J.
- Venue
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
- Publisher
- American Physiological Society
- Published
- 1998-01-01
- Volume
- 274
- Issue
- 1
- Pages
- R23-R29
- ISSN
- 0363-6119 (ISSN-L)
- 1522-1490
- OpenAlex
- W2114699589
- Cited by
- 199
- References
- 3
- FWCI
- 2.48
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: PVN infusion of GLP-1-(7—36) amide suppresses feeding but does not induce aversion or alter locomotion in rats. https://app.cochat.ai/papers/10.1152/ajpregu.1998.274.1.r23
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- McMahon, L. R., & Wellman, P. J. (1998). PVN infusion of GLP-1-(7—36) amide suppresses feeding but does not induce aversion or alter locomotion in rats. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. https://doi.org/10.1152/ajpregu.1998.274.1.r23
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
