The DOI matches its Crossref record; 67 of the 67 references it cites were found in a registry or an index.
Peripheral Exendin-4 and Peptide YY3–36 Synergistically Reduce Food Intake through Different Mechanisms in Mice
Abstract
Glucagon-like peptide-17–36NH2 (GLP-1) and peptide YY3–36NH2 (PYY3–36NH2) are cosecreted from the intestine in response to nutrient ingestion. Peripheral administration of GLP-1 or PYY3–36NH2 decreases food intake (FI) in rodents and humans; however, the exact mechanisms by which these peptides regulate FI remain unclear. Male C57BL/6 mice were injected (ip) with exendin-41–39 (Ex4, a GLP-1 receptor agonist) and/or PYY3–36NH2 (0.03–3 μg), and FI was determined for up to 24 h. Ex4 and PYY3–36NH2 alone decreased FI by up to 83 and 26%, respectively (P < 0.05–0.001), whereas a combination of the two peptides (0.06 μg Ex4 plus 3 μg PYY3–36NH2) further reduced FI for up to 8 h in a synergistic manner (P < 0.05–0.001). Ex4 and/or PYY3–36NH2 delayed gastric emptying by a maximum of 19% (P < 0.01–0.001); however, there was no significant effect on locomotor activity nor was there induction of taste aversion. Capsaicin pretreatment prevented the inhibitory effect of Ex4 on FI (P < 0.05), but had no effect on the anorexigenic actions of PYY3–36NH2. Similarly, exendin-49–39 (a GLP-1 receptor antagonist) partially abolished Ex4-induced anorexia (P < 0.05), but did not affect the satiation produced by PYY3–36NH2. Conversely, BIIE0246 (a Y2 receptor antagonist) completely blocked the anorexigenic effects of PYY3–36NH2 (P < 0.001), but had no effect on Ex4-induced satiety. Thus, Ex4 and PYY3–36NH2 suppress FI via independent mechanisms involving a GLP-1 receptor-dependent, sensory afferent pathway (Ex4) and a Y2-receptor mediated pathway (PYY3–36NH2). These findings suggest that administration of low doses of Ex4 together with PYY3–36NH2 may increase the suppression of FI without inducing significant side effects.
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Cites
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Glucagon-like peptide-1 7–36: a physiological incretin in man
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Cited by
Biology of Incretins: GLP-1 and GIP
Baggio, L. L., & Drucker, D. J. (2007) · Gastroenterology · doi:10.1053/j.gastro.2007.03.054 · Cited by 3,639
Self-citationGastrointestinal regulation of food intake
Cummings, D. E., & Overduin, J. (2007) · Journal of Clinical Investigation · doi:10.1172/jci30227 · Cited by 1,216
The role of incretins in glucose homeostasis and diabetes treatment
Kim, W., & Egan, J. M. (2008) · Pharmacological Reviews · doi:10.1124/pr.108.000604 · Cited by 824
Gut hormones and the regulation of energy homeostasis
Murphy, K. G., & Bloom, S. R. (2006) · Nature · doi:10.1038/nature05484 · Cited by 778
Unimolecular Dual Incretins Maximize Metabolic Benefits in Rodents, Monkeys, and Humans
Finan, B., Ma, T., Ottaway, N., Müller, T. D., Habegger, K. M., Heppner, K. M., Kirchner, H., Holland, J., Hembree, J., Raver, C., et al. (2013) · Science Translational Medicine · doi:10.1126/scitranslmed.3007218 · Cited by 696
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Metadata
- Authors
- Talsania, T., Anini, Y., Siu, S., Drucker, D. J., & Brubaker, P. L.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2005-09-01
- Volume
- 146
- Issue
- 9
- Pages
- 3748-3756
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W1983901940
- Cited by
- 306
- References
- 67
- FWCI
- 8.02
- Type
- journal article
- Language
- en
- Open access
- closed
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