Liraglutide changes postprandial responses of gut hormones involved in the regulation of gallbladder motility
Aim Liraglutide treatment is associated with gallbladder‐related disorders and has been shown to delay postprandial gallbladder refilling. The gut hormones cholecystokinin (CCK), fibroblast growth factor 19 (FGF19) and glucagon‐like peptide 2 (GLP‐2), are known to regulate gallbladder motility and m...
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| Veröffentlicht in: | Diabetes, obesity & metabolism obesity & metabolism, 2023-06, Vol.25 (6), p.1632-1637 |
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| creator | Nerild, Henriette H. Brønden, Andreas Gether, Ida M. Hellmann, Pernille H. Baekdal, Mille Gillum, Matthew P. Svenningsen, Jens S. Hartmann, Bolette Rathor, Naveen Kudiyanur Muniraju, Hanna Angelene Rehfeld, Jens F. Holst, Jens J. Vilsbøll, Tina Sonne, David P. Knop, Filip K. |
| description | Aim
Liraglutide treatment is associated with gallbladder‐related disorders and has been shown to delay postprandial gallbladder refilling. The gut hormones cholecystokinin (CCK), fibroblast growth factor 19 (FGF19) and glucagon‐like peptide 2 (GLP‐2), are known to regulate gallbladder motility and may be implicated in gallbladder‐related disorders associated with liraglutide treatment.
Materials and Methods
In a double‐blind, 12‐week trial, 52 participants [50% male, age 47.6 ± 10.0 years, body mass index 32.6 ± 3.4 kg/m2 (mean ± standard deviation)] with obesity were randomized 1:1 to once‐daily subcutaneous liraglutide (escalated from 0.6 mg to 3.0 mg once‐daily) or placebo. During liquid meal tests performed at baseline, after the first dose and following 12 weeks of treatment, we evaluated postprandial gallbladder dynamics and plasma responses of CCK, FGF19 and GLP‐2.
Results
Liraglutide reduced postprandial FGF19 after the first dose [area under the curve (AUC)0‐240 min 24.8 vs. 48.0 min × ng/ml, treatment ratio (TR) (95% confidence interval) 0.52 (0.39; 0.69)] and following 12 weeks of treatment [AUC0‐240 min 33.7 vs. 48.5 ng/ml × min, TR 0.69 (0.52; 0.93)]. Liraglutide also reduced postprandial GLP‐2 responses (AUC0‐240 min 3650 vs. 4894 min × pmol/L, TR 0.75 (0.62; 0.90)] following the first dose as well as after 12 weeks [AUC0‐240 min 3760 vs. 4882 min × pmol/L, TR 0.77 (0.60; 0.99)]. Liraglutide increased postprandial responses of CCK after the first dose [AUC0‐240 min 762 vs. 670 min × pmol/L; TR 1.14 (0.97; 1.33)] and following 12 weeks of treatment [AUC0‐240 min 873 vs. 628 min × pmol/L; TR 1.39 (1.12; 1.73)].
Conclusion
Compared with placebo, treatment with liraglutide decreased postprandial FGF19 and GLP‐2 concentrations and increased postprandial CCK concentrations, which may explain the delayed postprandial gallbladder refilling observed in individuals with obesity treated with liraglutide. |
| doi_str_mv | 10.1111/dom.15017 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2776515628</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2776515628</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3887-8238730c29387d03862660f05dc21e12e4dfc2528b91a19520ff0daafca5bc973</originalsourceid><addsrcrecordid>eNp10c9PwyAUB3BiNG5OD_4DpokXPXQDuhZ6NPNnMrOLngkF2rHQUqGd2X8vrtODiVzeg3zyzQsPgEsEpyicmbT1FKUQkSMwRvMsiVGCs-N9j2OaQzwCZ95vIITzhJJTMEoyQhHFcAzqpXa8Mn2npYrEmjeV8lFrfdc63kjNTeSUb23jw7Mto6rvorV1tW3CXTdba7ZKhibq1irIqje807bZU25MYbiUykW17bTR3e4cnJTceHVxqBPw_vjwtniOl6unl8XdMhYJpSSmOIyZQIHzUCVMaIazDJYwlQIjhbCay1LgFNMiRxzlKYZlCSXnpeBpIXKSTMDNkNs6-9Er37Fae6GM4Y2yvWeYkCxFaYZpoNd_6Mb2rgnTMUwhTSEhCAV1OyjhrPdOlax1uuZuxxBk3ztgYQdsv4Ngrw6JfVEr-St_Pj2A2QA-tVG7_5PY_ep1iPwCY-GRLg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2808507711</pqid></control><display><type>article</type><title>Liraglutide changes postprandial responses of gut hormones involved in the regulation of gallbladder motility</title><source>MEDLINE</source><source>Wiley Journals</source><creator>Nerild, Henriette H. ; Brønden, Andreas ; Gether, Ida M. ; Hellmann, Pernille H. ; Baekdal, Mille ; Gillum, Matthew P. ; Svenningsen, Jens S. ; Hartmann, Bolette ; Rathor, Naveen ; Kudiyanur Muniraju, Hanna Angelene ; Rehfeld, Jens F. ; Holst, Jens J. ; Vilsbøll, Tina ; Sonne, David P. ; Knop, Filip K.</creator><creatorcontrib>Nerild, Henriette H. ; Brønden, Andreas ; Gether, Ida M. ; Hellmann, Pernille H. ; Baekdal, Mille ; Gillum, Matthew P. ; Svenningsen, Jens S. ; Hartmann, Bolette ; Rathor, Naveen ; Kudiyanur Muniraju, Hanna Angelene ; Rehfeld, Jens F. ; Holst, Jens J. ; Vilsbøll, Tina ; Sonne, David P. ; Knop, Filip K.</creatorcontrib><description>Aim
Liraglutide treatment is associated with gallbladder‐related disorders and has been shown to delay postprandial gallbladder refilling. The gut hormones cholecystokinin (CCK), fibroblast growth factor 19 (FGF19) and glucagon‐like peptide 2 (GLP‐2), are known to regulate gallbladder motility and may be implicated in gallbladder‐related disorders associated with liraglutide treatment.
Materials and Methods
In a double‐blind, 12‐week trial, 52 participants [50% male, age 47.6 ± 10.0 years, body mass index 32.6 ± 3.4 kg/m2 (mean ± standard deviation)] with obesity were randomized 1:1 to once‐daily subcutaneous liraglutide (escalated from 0.6 mg to 3.0 mg once‐daily) or placebo. During liquid meal tests performed at baseline, after the first dose and following 12 weeks of treatment, we evaluated postprandial gallbladder dynamics and plasma responses of CCK, FGF19 and GLP‐2.
Results
Liraglutide reduced postprandial FGF19 after the first dose [area under the curve (AUC)0‐240 min 24.8 vs. 48.0 min × ng/ml, treatment ratio (TR) (95% confidence interval) 0.52 (0.39; 0.69)] and following 12 weeks of treatment [AUC0‐240 min 33.7 vs. 48.5 ng/ml × min, TR 0.69 (0.52; 0.93)]. Liraglutide also reduced postprandial GLP‐2 responses (AUC0‐240 min 3650 vs. 4894 min × pmol/L, TR 0.75 (0.62; 0.90)] following the first dose as well as after 12 weeks [AUC0‐240 min 3760 vs. 4882 min × pmol/L, TR 0.77 (0.60; 0.99)]. Liraglutide increased postprandial responses of CCK after the first dose [AUC0‐240 min 762 vs. 670 min × pmol/L; TR 1.14 (0.97; 1.33)] and following 12 weeks of treatment [AUC0‐240 min 873 vs. 628 min × pmol/L; TR 1.39 (1.12; 1.73)].
Conclusion
Compared with placebo, treatment with liraglutide decreased postprandial FGF19 and GLP‐2 concentrations and increased postprandial CCK concentrations, which may explain the delayed postprandial gallbladder refilling observed in individuals with obesity treated with liraglutide.</description><identifier>ISSN: 1462-8902</identifier><identifier>EISSN: 1463-1326</identifier><identifier>DOI: 10.1111/dom.15017</identifier><identifier>PMID: 36781820</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adult ; Antidiabetics ; Blood Glucose - metabolism ; Body Mass Index ; Cholecystokinin ; clinical trial ; Diabetes Mellitus, Type 2 - complications ; Double-Blind Method ; Female ; Fibroblast growth factors ; Gallbladder ; Gallbladder - metabolism ; Gastric motility ; GLP1 ; GLP‐1 analogue ; Glucagon ; Humans ; incretin physiology ; incretin therapy ; liraglutide ; Liraglutide - pharmacology ; Liraglutide - therapeutic use ; Male ; Middle Aged ; Motility ; Obesity ; Obesity - complications ; Placebos ; Postprandial Period</subject><ispartof>Diabetes, obesity & metabolism, 2023-06, Vol.25 (6), p.1632-1637</ispartof><rights>2023 The Authors. published by John Wiley & Sons Ltd.</rights><rights>2023 The Authors. Diabetes, Obesity and Metabolism published by John Wiley & Sons Ltd.</rights><rights>2023. This article is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3887-8238730c29387d03862660f05dc21e12e4dfc2528b91a19520ff0daafca5bc973</citedby><cites>FETCH-LOGICAL-c3887-8238730c29387d03862660f05dc21e12e4dfc2528b91a19520ff0daafca5bc973</cites><orcidid>0000-0002-4898-2256 ; 0000-0002-0456-6787 ; 0000-0002-3529-8228 ; 0000-0002-2495-5034 ; 0000-0003-1262-3769</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fdom.15017$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fdom.15017$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36781820$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nerild, Henriette H.</creatorcontrib><creatorcontrib>Brønden, Andreas</creatorcontrib><creatorcontrib>Gether, Ida M.</creatorcontrib><creatorcontrib>Hellmann, Pernille H.</creatorcontrib><creatorcontrib>Baekdal, Mille</creatorcontrib><creatorcontrib>Gillum, Matthew P.</creatorcontrib><creatorcontrib>Svenningsen, Jens S.</creatorcontrib><creatorcontrib>Hartmann, Bolette</creatorcontrib><creatorcontrib>Rathor, Naveen</creatorcontrib><creatorcontrib>Kudiyanur Muniraju, Hanna Angelene</creatorcontrib><creatorcontrib>Rehfeld, Jens F.</creatorcontrib><creatorcontrib>Holst, Jens J.</creatorcontrib><creatorcontrib>Vilsbøll, Tina</creatorcontrib><creatorcontrib>Sonne, David P.</creatorcontrib><creatorcontrib>Knop, Filip K.</creatorcontrib><title>Liraglutide changes postprandial responses of gut hormones involved in the regulation of gallbladder motility</title><title>Diabetes, obesity & metabolism</title><addtitle>Diabetes Obes Metab</addtitle><description>Aim
Liraglutide treatment is associated with gallbladder‐related disorders and has been shown to delay postprandial gallbladder refilling. The gut hormones cholecystokinin (CCK), fibroblast growth factor 19 (FGF19) and glucagon‐like peptide 2 (GLP‐2), are known to regulate gallbladder motility and may be implicated in gallbladder‐related disorders associated with liraglutide treatment.
Materials and Methods
In a double‐blind, 12‐week trial, 52 participants [50% male, age 47.6 ± 10.0 years, body mass index 32.6 ± 3.4 kg/m2 (mean ± standard deviation)] with obesity were randomized 1:1 to once‐daily subcutaneous liraglutide (escalated from 0.6 mg to 3.0 mg once‐daily) or placebo. During liquid meal tests performed at baseline, after the first dose and following 12 weeks of treatment, we evaluated postprandial gallbladder dynamics and plasma responses of CCK, FGF19 and GLP‐2.
Results
Liraglutide reduced postprandial FGF19 after the first dose [area under the curve (AUC)0‐240 min 24.8 vs. 48.0 min × ng/ml, treatment ratio (TR) (95% confidence interval) 0.52 (0.39; 0.69)] and following 12 weeks of treatment [AUC0‐240 min 33.7 vs. 48.5 ng/ml × min, TR 0.69 (0.52; 0.93)]. Liraglutide also reduced postprandial GLP‐2 responses (AUC0‐240 min 3650 vs. 4894 min × pmol/L, TR 0.75 (0.62; 0.90)] following the first dose as well as after 12 weeks [AUC0‐240 min 3760 vs. 4882 min × pmol/L, TR 0.77 (0.60; 0.99)]. Liraglutide increased postprandial responses of CCK after the first dose [AUC0‐240 min 762 vs. 670 min × pmol/L; TR 1.14 (0.97; 1.33)] and following 12 weeks of treatment [AUC0‐240 min 873 vs. 628 min × pmol/L; TR 1.39 (1.12; 1.73)].
Conclusion
Compared with placebo, treatment with liraglutide decreased postprandial FGF19 and GLP‐2 concentrations and increased postprandial CCK concentrations, which may explain the delayed postprandial gallbladder refilling observed in individuals with obesity treated with liraglutide.</description><subject>Adult</subject><subject>Antidiabetics</subject><subject>Blood Glucose - metabolism</subject><subject>Body Mass Index</subject><subject>Cholecystokinin</subject><subject>clinical trial</subject><subject>Diabetes Mellitus, Type 2 - complications</subject><subject>Double-Blind Method</subject><subject>Female</subject><subject>Fibroblast growth factors</subject><subject>Gallbladder</subject><subject>Gallbladder - metabolism</subject><subject>Gastric motility</subject><subject>GLP1</subject><subject>GLP‐1 analogue</subject><subject>Glucagon</subject><subject>Humans</subject><subject>incretin physiology</subject><subject>incretin therapy</subject><subject>liraglutide</subject><subject>Liraglutide - pharmacology</subject><subject>Liraglutide - therapeutic use</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Motility</subject><subject>Obesity</subject><subject>Obesity - complications</subject><subject>Placebos</subject><subject>Postprandial Period</subject><issn>1462-8902</issn><issn>1463-1326</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><recordid>eNp10c9PwyAUB3BiNG5OD_4DpokXPXQDuhZ6NPNnMrOLngkF2rHQUqGd2X8vrtODiVzeg3zyzQsPgEsEpyicmbT1FKUQkSMwRvMsiVGCs-N9j2OaQzwCZ95vIITzhJJTMEoyQhHFcAzqpXa8Mn2npYrEmjeV8lFrfdc63kjNTeSUb23jw7Mto6rvorV1tW3CXTdba7ZKhibq1irIqje807bZU25MYbiUykW17bTR3e4cnJTceHVxqBPw_vjwtniOl6unl8XdMhYJpSSmOIyZQIHzUCVMaIazDJYwlQIjhbCay1LgFNMiRxzlKYZlCSXnpeBpIXKSTMDNkNs6-9Er37Fae6GM4Y2yvWeYkCxFaYZpoNd_6Mb2rgnTMUwhTSEhCAV1OyjhrPdOlax1uuZuxxBk3ztgYQdsv4Ngrw6JfVEr-St_Pj2A2QA-tVG7_5PY_ep1iPwCY-GRLg</recordid><startdate>202306</startdate><enddate>202306</enddate><creator>Nerild, Henriette H.</creator><creator>Brønden, Andreas</creator><creator>Gether, Ida M.</creator><creator>Hellmann, Pernille H.</creator><creator>Baekdal, Mille</creator><creator>Gillum, Matthew P.</creator><creator>Svenningsen, Jens S.</creator><creator>Hartmann, Bolette</creator><creator>Rathor, Naveen</creator><creator>Kudiyanur Muniraju, Hanna Angelene</creator><creator>Rehfeld, Jens F.</creator><creator>Holst, Jens J.</creator><creator>Vilsbøll, Tina</creator><creator>Sonne, David P.</creator><creator>Knop, Filip K.</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>24P</scope><scope>WIN</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4898-2256</orcidid><orcidid>https://orcid.org/0000-0002-0456-6787</orcidid><orcidid>https://orcid.org/0000-0002-3529-8228</orcidid><orcidid>https://orcid.org/0000-0002-2495-5034</orcidid><orcidid>https://orcid.org/0000-0003-1262-3769</orcidid></search><sort><creationdate>202306</creationdate><title>Liraglutide changes postprandial responses of gut hormones involved in the regulation of gallbladder motility</title><author>Nerild, Henriette H. ; Brønden, Andreas ; Gether, Ida M. ; Hellmann, Pernille H. ; Baekdal, Mille ; Gillum, Matthew P. ; Svenningsen, Jens S. ; Hartmann, Bolette ; Rathor, Naveen ; Kudiyanur Muniraju, Hanna Angelene ; Rehfeld, Jens F. ; Holst, Jens J. ; Vilsbøll, Tina ; Sonne, David P. ; Knop, Filip K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3887-8238730c29387d03862660f05dc21e12e4dfc2528b91a19520ff0daafca5bc973</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Adult</topic><topic>Antidiabetics</topic><topic>Blood Glucose - metabolism</topic><topic>Body Mass Index</topic><topic>Cholecystokinin</topic><topic>clinical trial</topic><topic>Diabetes Mellitus, Type 2 - complications</topic><topic>Double-Blind Method</topic><topic>Female</topic><topic>Fibroblast growth factors</topic><topic>Gallbladder</topic><topic>Gallbladder - metabolism</topic><topic>Gastric motility</topic><topic>GLP1</topic><topic>GLP‐1 analogue</topic><topic>Glucagon</topic><topic>Humans</topic><topic>incretin physiology</topic><topic>incretin therapy</topic><topic>liraglutide</topic><topic>Liraglutide - pharmacology</topic><topic>Liraglutide - therapeutic use</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Motility</topic><topic>Obesity</topic><topic>Obesity - complications</topic><topic>Placebos</topic><topic>Postprandial Period</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nerild, Henriette H.</creatorcontrib><creatorcontrib>Brønden, Andreas</creatorcontrib><creatorcontrib>Gether, Ida M.</creatorcontrib><creatorcontrib>Hellmann, Pernille H.</creatorcontrib><creatorcontrib>Baekdal, Mille</creatorcontrib><creatorcontrib>Gillum, Matthew P.</creatorcontrib><creatorcontrib>Svenningsen, Jens S.</creatorcontrib><creatorcontrib>Hartmann, Bolette</creatorcontrib><creatorcontrib>Rathor, Naveen</creatorcontrib><creatorcontrib>Kudiyanur Muniraju, Hanna Angelene</creatorcontrib><creatorcontrib>Rehfeld, Jens F.</creatorcontrib><creatorcontrib>Holst, Jens J.</creatorcontrib><creatorcontrib>Vilsbøll, Tina</creatorcontrib><creatorcontrib>Sonne, David P.</creatorcontrib><creatorcontrib>Knop, Filip K.</creatorcontrib><collection>Wiley-Blackwell Open Access Titles</collection><collection>Wiley Free Content</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetes, obesity & metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nerild, Henriette H.</au><au>Brønden, Andreas</au><au>Gether, Ida M.</au><au>Hellmann, Pernille H.</au><au>Baekdal, Mille</au><au>Gillum, Matthew P.</au><au>Svenningsen, Jens S.</au><au>Hartmann, Bolette</au><au>Rathor, Naveen</au><au>Kudiyanur Muniraju, Hanna Angelene</au><au>Rehfeld, Jens F.</au><au>Holst, Jens J.</au><au>Vilsbøll, Tina</au><au>Sonne, David P.</au><au>Knop, Filip K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Liraglutide changes postprandial responses of gut hormones involved in the regulation of gallbladder motility</atitle><jtitle>Diabetes, obesity & metabolism</jtitle><addtitle>Diabetes Obes Metab</addtitle><date>2023-06</date><risdate>2023</risdate><volume>25</volume><issue>6</issue><spage>1632</spage><epage>1637</epage><pages>1632-1637</pages><issn>1462-8902</issn><eissn>1463-1326</eissn><abstract>Aim
Liraglutide treatment is associated with gallbladder‐related disorders and has been shown to delay postprandial gallbladder refilling. The gut hormones cholecystokinin (CCK), fibroblast growth factor 19 (FGF19) and glucagon‐like peptide 2 (GLP‐2), are known to regulate gallbladder motility and may be implicated in gallbladder‐related disorders associated with liraglutide treatment.
Materials and Methods
In a double‐blind, 12‐week trial, 52 participants [50% male, age 47.6 ± 10.0 years, body mass index 32.6 ± 3.4 kg/m2 (mean ± standard deviation)] with obesity were randomized 1:1 to once‐daily subcutaneous liraglutide (escalated from 0.6 mg to 3.0 mg once‐daily) or placebo. During liquid meal tests performed at baseline, after the first dose and following 12 weeks of treatment, we evaluated postprandial gallbladder dynamics and plasma responses of CCK, FGF19 and GLP‐2.
Results
Liraglutide reduced postprandial FGF19 after the first dose [area under the curve (AUC)0‐240 min 24.8 vs. 48.0 min × ng/ml, treatment ratio (TR) (95% confidence interval) 0.52 (0.39; 0.69)] and following 12 weeks of treatment [AUC0‐240 min 33.7 vs. 48.5 ng/ml × min, TR 0.69 (0.52; 0.93)]. Liraglutide also reduced postprandial GLP‐2 responses (AUC0‐240 min 3650 vs. 4894 min × pmol/L, TR 0.75 (0.62; 0.90)] following the first dose as well as after 12 weeks [AUC0‐240 min 3760 vs. 4882 min × pmol/L, TR 0.77 (0.60; 0.99)]. Liraglutide increased postprandial responses of CCK after the first dose [AUC0‐240 min 762 vs. 670 min × pmol/L; TR 1.14 (0.97; 1.33)] and following 12 weeks of treatment [AUC0‐240 min 873 vs. 628 min × pmol/L; TR 1.39 (1.12; 1.73)].
Conclusion
Compared with placebo, treatment with liraglutide decreased postprandial FGF19 and GLP‐2 concentrations and increased postprandial CCK concentrations, which may explain the delayed postprandial gallbladder refilling observed in individuals with obesity treated with liraglutide.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>36781820</pmid><doi>10.1111/dom.15017</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0002-4898-2256</orcidid><orcidid>https://orcid.org/0000-0002-0456-6787</orcidid><orcidid>https://orcid.org/0000-0002-3529-8228</orcidid><orcidid>https://orcid.org/0000-0002-2495-5034</orcidid><orcidid>https://orcid.org/0000-0003-1262-3769</orcidid><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1462-8902 |
| ispartof | Diabetes, obesity & metabolism, 2023-06, Vol.25 (6), p.1632-1637 |
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| subjects | Adult Antidiabetics Blood Glucose - metabolism Body Mass Index Cholecystokinin clinical trial Diabetes Mellitus, Type 2 - complications Double-Blind Method Female Fibroblast growth factors Gallbladder Gallbladder - metabolism Gastric motility GLP1 GLP‐1 analogue Glucagon Humans incretin physiology incretin therapy liraglutide Liraglutide - pharmacology Liraglutide - therapeutic use Male Middle Aged Motility Obesity Obesity - complications Placebos Postprandial Period |
| title | Liraglutide changes postprandial responses of gut hormones involved in the regulation of gallbladder motility |
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