Glucagon Clearance Is Decreased in Chronic Kidney Disease but Preserved in Liver Cirrhosis
It is not completely clear which organs are responsible for glucagon elimination in humans, and disturbances in the elimination of glucagon could contribute to the hyperglucagonemia observed in chronic liver disease and chronic kidney disease (CKD). Here, we evaluated kinetics and metabolic effects...
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| Published in | Diabetes (New York, N.Y.) Vol. 73; no. 10; pp. 1641 - 1647 |
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| Main Authors | , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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United States
American Diabetes Association
01.10.2024
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| Abstract | It is not completely clear which organs are responsible for glucagon elimination in humans, and disturbances in the elimination of glucagon could contribute to the hyperglucagonemia observed in chronic liver disease and chronic kidney disease (CKD). Here, we evaluated kinetics and metabolic effects of exogenous glucagon in individuals with stage 4 CKD (n = 16), individuals with Child-Pugh A-C cirrhosis (n = 16), and matched control individuals (n = 16), before, during, and after a 60-min glucagon infusion (4 ng/kg/min). Individuals with CKD exhibited a significantly lower mean metabolic clearance rate of glucagon (14.0 [95% CI 12.2;15.7] mL/kg/min) compared with both individuals with cirrhosis (19.7 [18.1;21.3] mL/kg/min, P < 0.001) and control individuals (20.4 [18.1;22.7] mL/kg/min, P < 0.001). Glucagon half-life was significantly prolonged in the CKD group (7.5 [6.9;8.2] min) compared with individuals with cirrhosis (5.7 [5.2;6.3] min, P = 0.002) and control individuals (5.7 [5.2;6.3] min, P < 0.001). No difference in the effects of exogenous glucagon on plasma glucose, amino acids, or triglycerides was observed between groups. In conclusion, CKD, but not liver cirrhosis, leads to a significant reduction in glucagon clearance, supporting the kidneys as a primary site for human glucagon elimination. |
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| AbstractList | It is not completely clear which organs are responsible for glucagon elimination in humans, and disturbances in the elimination of glucagon could contribute to the hyperglucagonemia observed in chronic liver disease and chronic kidney disease (CKD). Here, we evaluated kinetics and metabolic effects of exogenous glucagon in individuals with stage 4 CKD (n = 16), individuals with Child-Pugh A-C cirrhosis (n = 16), and matched control individuals (n = 16), before, during, and after a 60-min glucagon infusion (4 ng/kg/min). Individuals with CKD exhibited a significantly lower mean metabolic clearance rate of glucagon (14.0 [95% CI 12.2;15.7] mL/kg/min) compared with both individuals with cirrhosis (19.7 [18.1;21.3] mL/kg/min, P < 0.001) and control individuals (20.4 [18.1;22.7] mL/kg/min, P < 0.001). Glucagon half-life was significantly prolonged in the CKD group (7.5 [6.9;8.2] min) compared with individuals with cirrhosis (5.7 [5.2;6.3] min, P = 0.002) and control individuals (5.7 [5.2;6.3] min, P < 0.001). No difference in the effects of exogenous glucagon on plasma glucose, amino acids, or triglycerides was observed between groups. In conclusion, CKD, but not liver cirrhosis, leads to a significant reduction in glucagon clearance, supporting the kidneys as a primary site for human glucagon elimination. It is not completely clear which organs are responsible for glucagon elimination in humans, and disturbances in the elimination of glucagon could contribute to the hyperglucagonemia observed in chronic liver disease and chronic kidney disease (CKD). Here, we evaluated kinetics and metabolic effects of exogenous glucagon in individuals with stage 4 CKD (n = 16), individuals with Child-Pugh A-C cirrhosis (n = 16), and matched control individuals (n = 16), before, during, and after a 60-min glucagon infusion (4 ng/kg/min). Individuals with CKD exhibited a significantly lower mean metabolic clearance rate of glucagon (14.0 [95% CI 12.2;15.7] mL/kg/min) compared with both individuals with cirrhosis (19.7 [18.1;21.3] mL/kg/min, P < 0.001) and control individuals (20.4 [18.1;22.7] mL/kg/min, P < 0.001). Glucagon half-life was significantly prolonged in the CKD group (7.5 [6.9;8.2] min) compared with individuals with cirrhosis (5.7 [5.2;6.3] min, P = 0.002) and control individuals (5.7 [5.2;6.3] min, P < 0.001). No difference in the effects of exogenous glucagon on plasma glucose, amino acids, or triglycerides was observed between groups. In conclusion, CKD, but not liver cirrhosis, leads to a significant reduction in glucagon clearance, supporting the kidneys as a primary site for human glucagon elimination.It is not completely clear which organs are responsible for glucagon elimination in humans, and disturbances in the elimination of glucagon could contribute to the hyperglucagonemia observed in chronic liver disease and chronic kidney disease (CKD). Here, we evaluated kinetics and metabolic effects of exogenous glucagon in individuals with stage 4 CKD (n = 16), individuals with Child-Pugh A-C cirrhosis (n = 16), and matched control individuals (n = 16), before, during, and after a 60-min glucagon infusion (4 ng/kg/min). Individuals with CKD exhibited a significantly lower mean metabolic clearance rate of glucagon (14.0 [95% CI 12.2;15.7] mL/kg/min) compared with both individuals with cirrhosis (19.7 [18.1;21.3] mL/kg/min, P < 0.001) and control individuals (20.4 [18.1;22.7] mL/kg/min, P < 0.001). Glucagon half-life was significantly prolonged in the CKD group (7.5 [6.9;8.2] min) compared with individuals with cirrhosis (5.7 [5.2;6.3] min, P = 0.002) and control individuals (5.7 [5.2;6.3] min, P < 0.001). No difference in the effects of exogenous glucagon on plasma glucose, amino acids, or triglycerides was observed between groups. In conclusion, CKD, but not liver cirrhosis, leads to a significant reduction in glucagon clearance, supporting the kidneys as a primary site for human glucagon elimination. It is not completely clear which organs are responsible for glucagon elimination in humans, and disturbances in the elimination of glucagon could contribute to the hyperglucagonemia observed in chronic liver disease and chronic kidney disease (CKD). Here, we evaluated kinetics and metabolic effects of exogenous glucagon in individuals with stage 4 CKD (n = 16), individuals with Child-Pugh A–C cirrhosis (n = 16), and matched control individuals (n = 16), before, during, and after a 60-min glucagon infusion (4 ng/kg/min). Individuals with CKD exhibited a significantly lower mean metabolic clearance rate of glucagon (14.0 [95% CI 12.2;15.7] mL/kg/min) compared with both individuals with cirrhosis (19.7 [18.1;21.3] mL/kg/min, P < 0.001) and control individuals (20.4 [18.1;22.7] mL/kg/min, P < 0.001). Glucagon half-life was significantly prolonged in the CKD group (7.5 [6.9;8.2] min) compared with individuals with cirrhosis (5.7 [5.2;6.3] min, P = 0.002) and control individuals (5.7 [5.2;6.3] min, P < 0.001). No difference in the effects of exogenous glucagon on plasma glucose, amino acids, or triglycerides was observed between groups. In conclusion, CKD, but not liver cirrhosis, leads to a significant reduction in glucagon clearance, supporting the kidneys as a primary site for human glucagon elimination. Article Highlights It is not completely clear which organs are responsible for glucagon elimination in humans, and disturbances in the elimination of glucagon could contribute to the hyperglucagonemia observed in chronic liver disease and chronic kidney disease (CKD). Here, we evaluated kinetics and metabolic effects of exogenous glucagon in individuals with stage 4 CKD ( n = 16), individuals with Child-Pugh A–C cirrhosis ( n = 16), and matched control individuals ( n = 16), before, during, and after a 60-min glucagon infusion (4 ng/kg/min). Individuals with CKD exhibited a significantly lower mean metabolic clearance rate of glucagon (14.0 [95% CI 12.2;15.7] mL/kg/min) compared with both individuals with cirrhosis (19.7 [18.1;21.3] mL/kg/min, P < 0.001) and control individuals (20.4 [18.1;22.7] mL/kg/min, P < 0.001). Glucagon half-life was significantly prolonged in the CKD group (7.5 [6.9;8.2] min) compared with individuals with cirrhosis (5.7 [5.2;6.3] min, P = 0.002) and control individuals (5.7 [5.2;6.3] min, P < 0.001). No difference in the effects of exogenous glucagon on plasma glucose, amino acids, or triglycerides was observed between groups. In conclusion, CKD, but not liver cirrhosis, leads to a significant reduction in glucagon clearance, supporting the kidneys as a primary site for human glucagon elimination. |
| Author | Hartmann, Bolette Holst, Jens J Lange, Andreas H Kofod, Dea H Gluud, Lise L Lund, Asger B Knop, Filip K Trammell, Samuel A J Christensen, Mikkel B Grøndahl, Magnus F G Grevengoed, Trisha J Vilsbøll, Tina Suppli, Malte P Hornum, Mads Bagger, Jonatan I van Hall, Gerrit Thing, Mira |
| AuthorAffiliation | 5 Department of Nephrology, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark 10 Copenhagen Center for Translational Research, Copenhagen University Hospital - Bispebjerg and Frederiksberg, Copenhagen, Denmark 2 Clinical Research, Steno Diabetes Center Copenhagen, Herlev, Denmark 3 Gastro Unit, Medical Unit, Copenhagen University Hospital Hvidovre, Hvidovre, Denmark 9 Department of Clinical Pharmacology, Copenhagen University Hospital - Bispebjerg and Frederiksberg, Copenhagen, Denmark 4 Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark 11 Novo Nordisk A/S, Bagsværd, Denmark 6 Clinical Metabolomics Core Facility, Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark 7 Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark 8 Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Heal |
| AuthorAffiliation_xml | – name: 1 Center for Clinical Metabolic Research, Copenhagen University Hospital - Herlev and Gentofte, Hellerup, Denmark – name: 9 Department of Clinical Pharmacology, Copenhagen University Hospital - Bispebjerg and Frederiksberg, Copenhagen, Denmark – name: 6 Clinical Metabolomics Core Facility, Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark – name: 7 Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – name: 10 Copenhagen Center for Translational Research, Copenhagen University Hospital - Bispebjerg and Frederiksberg, Copenhagen, Denmark – name: 2 Clinical Research, Steno Diabetes Center Copenhagen, Herlev, Denmark – name: 11 Novo Nordisk A/S, Bagsværd, Denmark – name: 3 Gastro Unit, Medical Unit, Copenhagen University Hospital Hvidovre, Hvidovre, Denmark – name: 4 Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – name: 8 Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – name: 5 Department of Nephrology, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark |
| Author_xml | – sequence: 1 givenname: Magnus F G surname: Grøndahl fullname: Grøndahl, Magnus F G organization: Center for Clinical Metabolic Research, Copenhagen University Hospital - Herlev and Gentofte, Hellerup, Denmark – sequence: 2 givenname: Andreas H surname: Lange fullname: Lange, Andreas H organization: Center for Clinical Metabolic Research, Copenhagen University Hospital - Herlev and Gentofte, Hellerup, Denmark – sequence: 3 givenname: Malte P surname: Suppli fullname: Suppli, Malte P organization: Center for Clinical Metabolic Research, Copenhagen University Hospital - Herlev and Gentofte, Hellerup, Denmark – sequence: 4 givenname: Jonatan I surname: Bagger fullname: Bagger, Jonatan I organization: Clinical Research, Steno Diabetes Center Copenhagen, Herlev, Denmark – sequence: 5 givenname: Mira surname: Thing fullname: Thing, Mira organization: Gastro Unit, Medical Unit, Copenhagen University Hospital Hvidovre, Hvidovre, Denmark – sequence: 6 givenname: Lise L surname: Gluud fullname: Gluud, Lise L organization: Gastro Unit, Medical Unit, Copenhagen University Hospital Hvidovre, Hvidovre, Denmark – sequence: 7 givenname: Dea H surname: Kofod fullname: Kofod, Dea H organization: Department of Nephrology, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark – sequence: 8 givenname: Mads surname: Hornum fullname: Hornum, Mads organization: Department of Nephrology, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark – sequence: 9 givenname: Gerrit surname: van Hall fullname: van Hall, Gerrit organization: Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 10 givenname: Samuel A J surname: Trammell fullname: Trammell, Samuel A J organization: Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 11 givenname: Trisha J surname: Grevengoed fullname: Grevengoed, Trisha J organization: Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 12 givenname: Bolette orcidid: 0000-0001-8509-2036 surname: Hartmann fullname: Hartmann, Bolette organization: Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 13 givenname: Jens J orcidid: 0000-0001-6853-3805 surname: Holst fullname: Holst, Jens J organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 14 givenname: Tina surname: Vilsbøll fullname: Vilsbøll, Tina organization: Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 15 givenname: Mikkel B surname: Christensen fullname: Christensen, Mikkel B organization: Copenhagen Center for Translational Research, Copenhagen University Hospital - Bispebjerg and Frederiksberg, Copenhagen, Denmark – sequence: 16 givenname: Asger B surname: Lund fullname: Lund, Asger B organization: Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 17 givenname: Filip K orcidid: 0000-0002-2495-5034 surname: Knop fullname: Knop, Filip K organization: Novo Nordisk A/S, Bagsværd, Denmark |
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| Cites_doi | 10.1056/NEJM197401312900502 10.1210/js.2018-00321 10.2337/db21-0024 10.1016/0026-0495(95)90051-9 10.2337/diab.23.3.199 10.1007/s11892-014-0555-4 10.1007/s00125-014-3283-z 10.1016/0016-5085(78)90696-0 10.1016/0026-0495(94)90161-9 10.1172/JCI108330 10.1152/ajpendo.00488.2020 10.1152/ajpgi.00216.2017 10.1007/s00125-006-0566-z 10.1007/BF00315314 10.1210/jcem-58-2-287 10.2337/db16-0994 10.1016/j.celrep.2017.10.034 10.1152/ajpendo.00125.2003 10.1111/jgh.12981 10.1038/ki.2012.460 10.2337/db09-1414 10.1111/j.1365-2265.1979.tb03093.x |
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| References_xml | – volume: 290 start-page: 239 year: 1974 ident: 2024092018510373100_B12 article-title: Hyperglucagonemia in Laennec’s cirrhosis. 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| Snippet | It is not completely clear which organs are responsible for glucagon elimination in humans, and disturbances in the elimination of glucagon could contribute to... |
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| SubjectTerms | Adult Aged Case-Control Studies Female Glucagon - blood Glucagon - metabolism Humans Liver Cirrhosis - metabolism Male Metabolic Clearance Rate Metabolism Middle Aged Renal Insufficiency, Chronic - metabolism |
| Title | Glucagon Clearance Is Decreased in Chronic Kidney Disease but Preserved in Liver Cirrhosis |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/39052774 https://www.proquest.com/docview/3084772713/abstract/ https://pubmed.ncbi.nlm.nih.gov/PMC11417434 |
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