Amino acid, glucose, and lipid kinetics after palliative resection in a patient with glucagonoma syndrome

M. Bernstein, F. Jahoor, Courtney Townsend, S. Klein

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Glucagon excess causes catabolic changes, including enhanced glucose production, lipolysis, and amino acid oxidation. In this study, we evaluate the metabolic effects of debulking surgery on a patient with glucagon-producing tumor. Stable isotope tracer methods were used to measure glucose, glycerol, and α-ketoisocaproic acid (αKICA) rates of appearance (Ra) into plasma. Measurements were obtained 25 days after surgery in the basal state and during hormonal suppression of glucagon production by infusing somatostatin with insulin replacement. Basal plasma glucagon concentration (14,100 pg/mL) remained high after debulking surgery. Somatostatin infusion decreased plasma glucagon concentration to 6,735 pg/mL and basal substrate kinetics (α-KICA Ra from 1.97 to 1.48 μmol/kg/min; glucose Ra from 16.89 to 11.56 μmol/kg/min; and glycerol Ra from 3.33 to 2.74 μmol/kg/min). We conclude that debulking surgery fails to adequately suppress glucagon production and the alterations in substrate metabolism associated with excess glucagon. In these patients, somatostatin therapy can be an effective method to suppress secretion of glucagon and help attenuate its catabolic effects.

Original languageEnglish (US)
Pages (from-to)720-722
Number of pages3
JournalMetabolism: Clinical and Experimental
Volume50
Issue number6
DOIs
StatePublished - 2001

Fingerprint

Glucagonoma
Glucagon
Lipids
Amino Acids
Glucose
Somatostatin
Glycerol
Acids
Lipolysis
Ambulatory Surgical Procedures
Isotopes
Insulin

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Amino acid, glucose, and lipid kinetics after palliative resection in a patient with glucagonoma syndrome. / Bernstein, M.; Jahoor, F.; Townsend, Courtney; Klein, S.

In: Metabolism: Clinical and Experimental, Vol. 50, No. 6, 2001, p. 720-722.

Research output: Contribution to journalArticle

@article{f5ea63633bd746c3a3dc6847400501fb,
title = "Amino acid, glucose, and lipid kinetics after palliative resection in a patient with glucagonoma syndrome",
abstract = "Glucagon excess causes catabolic changes, including enhanced glucose production, lipolysis, and amino acid oxidation. In this study, we evaluate the metabolic effects of debulking surgery on a patient with glucagon-producing tumor. Stable isotope tracer methods were used to measure glucose, glycerol, and α-ketoisocaproic acid (αKICA) rates of appearance (Ra) into plasma. Measurements were obtained 25 days after surgery in the basal state and during hormonal suppression of glucagon production by infusing somatostatin with insulin replacement. Basal plasma glucagon concentration (14,100 pg/mL) remained high after debulking surgery. Somatostatin infusion decreased plasma glucagon concentration to 6,735 pg/mL and basal substrate kinetics (α-KICA Ra from 1.97 to 1.48 μmol/kg/min; glucose Ra from 16.89 to 11.56 μmol/kg/min; and glycerol Ra from 3.33 to 2.74 μmol/kg/min). We conclude that debulking surgery fails to adequately suppress glucagon production and the alterations in substrate metabolism associated with excess glucagon. In these patients, somatostatin therapy can be an effective method to suppress secretion of glucagon and help attenuate its catabolic effects.",
author = "M. Bernstein and F. Jahoor and Courtney Townsend and S. Klein",
year = "2001",
doi = "10.1053/meta.2001.23306",
language = "English (US)",
volume = "50",
pages = "720--722",
journal = "Metabolism: Clinical and Experimental",
issn = "0026-0495",
publisher = "W.B. Saunders Ltd",
number = "6",

}

TY - JOUR

T1 - Amino acid, glucose, and lipid kinetics after palliative resection in a patient with glucagonoma syndrome

AU - Bernstein, M.

AU - Jahoor, F.

AU - Townsend, Courtney

AU - Klein, S.

PY - 2001

Y1 - 2001

N2 - Glucagon excess causes catabolic changes, including enhanced glucose production, lipolysis, and amino acid oxidation. In this study, we evaluate the metabolic effects of debulking surgery on a patient with glucagon-producing tumor. Stable isotope tracer methods were used to measure glucose, glycerol, and α-ketoisocaproic acid (αKICA) rates of appearance (Ra) into plasma. Measurements were obtained 25 days after surgery in the basal state and during hormonal suppression of glucagon production by infusing somatostatin with insulin replacement. Basal plasma glucagon concentration (14,100 pg/mL) remained high after debulking surgery. Somatostatin infusion decreased plasma glucagon concentration to 6,735 pg/mL and basal substrate kinetics (α-KICA Ra from 1.97 to 1.48 μmol/kg/min; glucose Ra from 16.89 to 11.56 μmol/kg/min; and glycerol Ra from 3.33 to 2.74 μmol/kg/min). We conclude that debulking surgery fails to adequately suppress glucagon production and the alterations in substrate metabolism associated with excess glucagon. In these patients, somatostatin therapy can be an effective method to suppress secretion of glucagon and help attenuate its catabolic effects.

AB - Glucagon excess causes catabolic changes, including enhanced glucose production, lipolysis, and amino acid oxidation. In this study, we evaluate the metabolic effects of debulking surgery on a patient with glucagon-producing tumor. Stable isotope tracer methods were used to measure glucose, glycerol, and α-ketoisocaproic acid (αKICA) rates of appearance (Ra) into plasma. Measurements were obtained 25 days after surgery in the basal state and during hormonal suppression of glucagon production by infusing somatostatin with insulin replacement. Basal plasma glucagon concentration (14,100 pg/mL) remained high after debulking surgery. Somatostatin infusion decreased plasma glucagon concentration to 6,735 pg/mL and basal substrate kinetics (α-KICA Ra from 1.97 to 1.48 μmol/kg/min; glucose Ra from 16.89 to 11.56 μmol/kg/min; and glycerol Ra from 3.33 to 2.74 μmol/kg/min). We conclude that debulking surgery fails to adequately suppress glucagon production and the alterations in substrate metabolism associated with excess glucagon. In these patients, somatostatin therapy can be an effective method to suppress secretion of glucagon and help attenuate its catabolic effects.

UR - http://www.scopus.com/inward/record.url?scp=0034966519&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034966519&partnerID=8YFLogxK

U2 - 10.1053/meta.2001.23306

DO - 10.1053/meta.2001.23306

M3 - Article

C2 - 11398151

AN - SCOPUS:0034966519

VL - 50

SP - 720

EP - 722

JO - Metabolism: Clinical and Experimental

JF - Metabolism: Clinical and Experimental

SN - 0026-0495

IS - 6

ER -