TY - JOUR
T1 - In vivo assessment of the metabolic alterations in glucagonoma syndrome
AU - Klein, Samuel
AU - Jahoor, Farook
AU - Baba, Hidefumi
AU - Townsend, Courtney M.
AU - Shepherd, Mary
AU - Wolfe, Robert R.
N1 - Funding Information:
From the Departments of Internal Medicine. Preventive Medicine and Community Health, Surgery, and Anesthesiology, The Universiry of Texas Medical Branch and The Shriners Burns Institute. Galveston, TX. Supported by National Institutes qf Health Grant No. CA 50330, Clinical Research Grant No. RR-00073. and a grantf rom the Shriners Hospitals. Address reprint requests to Samuel Klein, MD. Division of Gastroen-ferology G-64. The University of Texas Medical Branch, Galwsrootl, TX 77550. Copyright 0 1992 by W.B. Saunders Cornpar!? 0026-0495192/4111-0005$03.00l0
PY - 1992/11
Y1 - 1992/11
N2 - Stable-isotope methodology and indirect calorimetry were used to evaluate metabolic abnormalities in a patient with glucagonoma syndrome manifested by 17% body weight loss, hypoaminoacidemia, and hyperglycemia. Energy expenditure (26 kcal/kg) was the same as that predicted by the Harris-Benedict equation. The rate of appearance (Ra) of intracellular leucine (2.70 μmol/kg/min), an index of protein breakdown, was normal, although the percentage of leucine flux oxidized (31%), an index of amino acid catabolism, was 50% greater than the normal mean value. Glucose Ra in plasma (12.9 μmol/kg/min), representing hepatic glucose production, and glycerol Ra in plasma (3.04 μmol/kg/min), a measurement of whole-body lipolysis, were 15% and 25% greater, respectively, than mean values found in normal volunteers. These results suggest that long-term alterations in energy, leucine, glucose, and lipid metabolism in patients with glucagonoma are minimal. However, small long-term metabolic alterations caused by glucagon excess, in conjunction with chronic negative energy balance, could be responsible for the weight loss, hypoaminoacidemia, and hyperglycemia observed in this patient population.
AB - Stable-isotope methodology and indirect calorimetry were used to evaluate metabolic abnormalities in a patient with glucagonoma syndrome manifested by 17% body weight loss, hypoaminoacidemia, and hyperglycemia. Energy expenditure (26 kcal/kg) was the same as that predicted by the Harris-Benedict equation. The rate of appearance (Ra) of intracellular leucine (2.70 μmol/kg/min), an index of protein breakdown, was normal, although the percentage of leucine flux oxidized (31%), an index of amino acid catabolism, was 50% greater than the normal mean value. Glucose Ra in plasma (12.9 μmol/kg/min), representing hepatic glucose production, and glycerol Ra in plasma (3.04 μmol/kg/min), a measurement of whole-body lipolysis, were 15% and 25% greater, respectively, than mean values found in normal volunteers. These results suggest that long-term alterations in energy, leucine, glucose, and lipid metabolism in patients with glucagonoma are minimal. However, small long-term metabolic alterations caused by glucagon excess, in conjunction with chronic negative energy balance, could be responsible for the weight loss, hypoaminoacidemia, and hyperglycemia observed in this patient population.
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U2 - 10.1016/0026-0495(92)90005-U
DO - 10.1016/0026-0495(92)90005-U
M3 - Article
C2 - 1435287
AN - SCOPUS:0026440005
SN - 0026-0495
VL - 41
SP - 1171
EP - 1175
JO - Metabolism
JF - Metabolism
IS - 11
ER -