In vivo assessment of the metabolic alterations in glucagonoma syndrome.
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 mumol/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 mumol/kg/min), representing hepatic glucose production, and glycerol Ra in plasma (3.04 mumol/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.
Klein
S
S
Department of Internal Medicine, University of Texas Medical Branch, Galveston 77550.
Jahoor
F
F
Baba
H
H
Townsend
C M
CM
Shepherd
M
M
Wolfe
R R
RR
D000328:Adult; D000596:Amino Acids / Q000097:blood; D001786:Blood Glucose / Q000032:analysis; D004734:Energy Metabolism; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005934:Glucagon / Q000097:blood; D005935:Glucagonoma / Q000378:metabolism*; D006801:Humans; D006885:Hydroxybutyrates / Q000097:blood; D008297:Male; D008875:Middle Aged; D010101:Oxygen Consumption; D010190:Pancreatic Neoplasms / Q000378:metabolism*; D012016:Reference Values; D013577:Syndrome
D000596:Amino Acids; D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D006885:Hydroxybutyrates; D005934:Glucagon