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 M.
AU - Klein, S.
N1 - Funding Information:
From the Department of Internal Medicine, Washington University School of Medicine, St Louis, MO; Children’s Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston; and the Department of Surgery, The University of Texas Medical Branch, Galveston, TX. Submitted August 28, 2000; accepted December 8, 2000. Supported by the National Institutes of Health Grants No. DK 37948, RR-00036 (General Clinical Research Center), RR-00954 (Mass Spectrometry Resource), AG 13629 (Claude Pepper Older American Independence Center), and DK 56341 (Clinical Nutrition Research Unit). Address reprint requests to Samuel Klein, MD, Washington University School of Medicine, 660 S. Euclid Ave, Box 8031, St Louis, MO 63110. Copyright © 2001 by W.B. Saunders Company 0026-0495/01/5006-0015$35.00/0 doi:10.1053/meta.2001.23306
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.
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U2 - 10.1053/meta.2001.23306
DO - 10.1053/meta.2001.23306
M3 - Article
C2 - 11398151
AN - SCOPUS:0034966519
SN - 0026-0495
VL - 50
SP - 720
EP - 722
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
IS - 6
ER -