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Post-oral fat-induced satiation is mediated by endogenous CCK and GLP-1 in a fat self-administration mouse model

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Vana, V, Lærke, MK, Kleberg, K, Mroz, PA, Lindberg, BL, Ekberg, JH, Rehfeld, JF, Schwartz, TW & Hansen, HS 2021, 'Post-oral fat-induced satiation is mediated by endogenous CCK and GLP-1 in a fat self-administration mouse model', Physiology & Behavior, bind 234, 113315, s. 113315. https://doi.org/10.1016/j.physbeh.2021.113315

APA

Vana, V., Lærke, M. K., Kleberg, K., Mroz, P. A., Lindberg, B. L., Ekberg, J. H., Rehfeld, J. F., Schwartz, T. W., & Hansen, H. S. (2021). Post-oral fat-induced satiation is mediated by endogenous CCK and GLP-1 in a fat self-administration mouse model. Physiology & Behavior, 234, 113315. [113315]. https://doi.org/10.1016/j.physbeh.2021.113315

CBE

MLA

Vancouver

Author

Vana, Vasiliki ; Lærke, Michelle K ; Kleberg, Karen ; Mroz, Piotr A ; Lindberg, Birgit L ; Ekberg, Jeppe H ; Rehfeld, Jens F ; Schwartz, Thue W ; Hansen, Harald S. / Post-oral fat-induced satiation is mediated by endogenous CCK and GLP-1 in a fat self-administration mouse model. I: Physiology & Behavior. 2021 ; Bind 234. s. 113315.

Bibtex

@article{13a6d77362554d7c8310ec0a0f16f6e4,
title = "Post-oral fat-induced satiation is mediated by endogenous CCK and GLP-1 in a fat self-administration mouse model",
abstract = "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.",
keywords = "CCK1 receptor, Fat, GLP-1 receptor, Jant4-C16, Satiation, Y receptor",
author = "Vasiliki Vana and L{\ae}rke, {Michelle K} and Karen Kleberg and Mroz, {Piotr A} and Lindberg, {Birgit L} and Ekberg, {Jeppe H} and Rehfeld, {Jens F} and Schwartz, {Thue W} and Hansen, {Harald S}",
note = "Copyright {\textcopyright} 2021. Published by Elsevier Inc.",
year = "2021",
month = may,
day = "15",
doi = "10.1016/j.physbeh.2021.113315",
language = "English",
volume = "234",
pages = "113315",
journal = "Physiology and Behavior",
issn = "0031-9384",
publisher = "Elsevier Inc",

}

RIS

TY - JOUR

T1 - Post-oral fat-induced satiation is mediated by endogenous CCK and GLP-1 in a fat self-administration mouse model

AU - Vana, Vasiliki

AU - Lærke, Michelle K

AU - Kleberg, Karen

AU - Mroz, Piotr A

AU - Lindberg, Birgit L

AU - Ekberg, Jeppe H

AU - Rehfeld, Jens F

AU - Schwartz, Thue W

AU - Hansen, Harald S

N1 - Copyright © 2021. Published by Elsevier Inc.

PY - 2021/5/15

Y1 - 2021/5/15

N2 - 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.

AB - 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.

KW - CCK1 receptor

KW - Fat

KW - GLP-1 receptor

KW - Jant4-C16

KW - Satiation

KW - Y receptor

UR - http://www.scopus.com/inward/record.url?scp=85102039085&partnerID=8YFLogxK

U2 - 10.1016/j.physbeh.2021.113315

DO - 10.1016/j.physbeh.2021.113315

M3 - Journal article

C2 - 33460676

VL - 234

SP - 113315

JO - Physiology and Behavior

JF - Physiology and Behavior

SN - 0031-9384

M1 - 113315

ER -

ID: 65558075