Post-oral fat-induced satiation is mediated by endogenous CCK and GLP-1 in a fat self-administration mouse model
Copyright © 2021. Published by Elsevier Inc..
Triacylglycerol is the most abundant dietary lipid, and a strong stimulator of satiation. Absorption of triacylglycerol in the small intestine occurs in the form of free fatty acids and 2-monoacylglycerol, a process known to trigger not only the release of cholecystokinin (CCK) but also glucagon-like peptide 1 (GLP-1) and peptide YY (PYY). It remains controversial, however, whether endogenously released GLP-1 and PYY are required for fat-induced satiation. Using a self-administration model where mice are trained to self-administer Intralipid 30% intragastrically, we show that blocking the CCK1 receptors with intraperitoneal devazepide diminishes the post-oral satiation effect of ingested fat. Similarly, s.c. administration of a GLP-1 receptor antagonist with a prolonged half-life (Jant4-C16) also reduced the post-oral satiation effect of ingested fat. Importantly, coadministration of the GLP-1 antagonist together with devazepide increased fat self-infusions to a level equal to the combined blockade of each individual peptide action alone, indicating an additive effect of endogenous CCK and GLP-1 in fat satiation signaling. Blocking the PYY Y2 receptor did not further enhance the fat intake in devazepide-treated mice. Consistent with the above, we show that voluntary post-oral ingestion of fat increases CCK and GLP-1 plasma levels and is correlated positively with CCK and GLP-1 plasma concentrations. Taken together, our results support the role of endogenous GLP-1 in the regulation of fat intake and suggest that both CCK and GLP-1 are required for the fat satiation signaling.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2021 |
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| Erschienen: |
2021 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:234 |
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| Enthalten in: |
Physiology & behavior - 234(2021) vom: 15. Mai, Seite 113315 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Vana, Vasiliki [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 25.06.2021 Date Revised 25.06.2021 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1016/j.physbeh.2021.113315 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM320232492 |
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| 245 | 1 | 0 | |a Post-oral fat-induced satiation is mediated by endogenous CCK and GLP-1 in a fat self-administration mouse model |
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| 520 | |a Copyright © 2021. Published by Elsevier Inc. | ||
| 520 | |a Triacylglycerol is the most abundant dietary lipid, and a strong stimulator of satiation. Absorption of triacylglycerol in the small intestine occurs in the form of free fatty acids and 2-monoacylglycerol, a process known to trigger not only the release of cholecystokinin (CCK) but also glucagon-like peptide 1 (GLP-1) and peptide YY (PYY). It remains controversial, however, whether endogenously released GLP-1 and PYY are required for fat-induced satiation. Using a self-administration model where mice are trained to self-administer Intralipid 30% intragastrically, we show that blocking the CCK1 receptors with intraperitoneal devazepide diminishes the post-oral satiation effect of ingested fat. Similarly, s.c. administration of a GLP-1 receptor antagonist with a prolonged half-life (Jant4-C16) also reduced the post-oral satiation effect of ingested fat. Importantly, coadministration of the GLP-1 antagonist together with devazepide increased fat self-infusions to a level equal to the combined blockade of each individual peptide action alone, indicating an additive effect of endogenous CCK and GLP-1 in fat satiation signaling. Blocking the PYY Y2 receptor did not further enhance the fat intake in devazepide-treated mice. Consistent with the above, we show that voluntary post-oral ingestion of fat increases CCK and GLP-1 plasma levels and is correlated positively with CCK and GLP-1 plasma concentrations. Taken together, our results support the role of endogenous GLP-1 in the regulation of fat intake and suggest that both CCK and GLP-1 are required for the fat satiation signaling | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a CCK1 receptor | |
| 650 | 4 | |a Fat | |
| 650 | 4 | |a GLP-1 receptor | |
| 650 | 4 | |a Jant4-C16 | |
| 650 | 4 | |a Satiation | |
| 650 | 4 | |a Y(2) receptor | |
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| 650 | 7 | |a Cholecystokinin |2 NLM | |
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| 700 | 1 | |a Lærke, Michelle K |e verfasserin |4 aut | |
| 700 | 1 | |a Kleberg, Karen |e verfasserin |4 aut | |
| 700 | 1 | |a Mroz, Piotr A |e verfasserin |4 aut | |
| 700 | 1 | |a Lindberg, Birgit L |e verfasserin |4 aut | |
| 700 | 1 | |a Ekberg, Jeppe H |e verfasserin |4 aut | |
| 700 | 1 | |a Rehfeld, Jens F |e verfasserin |4 aut | |
| 700 | 1 | |a Schwartz, Thue W |e verfasserin |4 aut | |
| 700 | 1 | |a Hansen, Harald S |e verfasserin |4 aut | |
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