In vivo assessment of the metabolic alterations in glucagonoma syndrome

Samuel Klein, Farook Jahoor, Hidefumi Baba, Courtney Townsend, Mary Shepherd, Robert R. Wolfe

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1171-1175
Number of pages5
JournalMetabolism
Volume41
Issue number11
DOIs
StatePublished - 1992

Fingerprint

Glucagonoma
Leucine
Glucose
Hyperglycemia
Weight Loss
Indirect Calorimetry
Lipolysis
Glucagon
Lipid Metabolism
Isotopes
Glycerol
Energy Metabolism
Healthy Volunteers
Reference Values
Body Weight
Amino Acids
Liver
Population
Proteins

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Klein, S., Jahoor, F., Baba, H., Townsend, C., Shepherd, M., & Wolfe, R. R. (1992). In vivo assessment of the metabolic alterations in glucagonoma syndrome. Metabolism, 41(11), 1171-1175. https://doi.org/10.1016/0026-0495(92)90005-U

In vivo assessment of the metabolic alterations in glucagonoma syndrome. / Klein, Samuel; Jahoor, Farook; Baba, Hidefumi; Townsend, Courtney; Shepherd, Mary; Wolfe, Robert R.

In: Metabolism, Vol. 41, No. 11, 1992, p. 1171-1175.

Research output: Contribution to journalArticle

Klein, S, Jahoor, F, Baba, H, Townsend, C, Shepherd, M & Wolfe, RR 1992, 'In vivo assessment of the metabolic alterations in glucagonoma syndrome', Metabolism, vol. 41, no. 11, pp. 1171-1175. https://doi.org/10.1016/0026-0495(92)90005-U
Klein, Samuel ; Jahoor, Farook ; Baba, Hidefumi ; Townsend, Courtney ; Shepherd, Mary ; Wolfe, Robert R. / In vivo assessment of the metabolic alterations in glucagonoma syndrome. In: Metabolism. 1992 ; Vol. 41, No. 11. pp. 1171-1175.
@article{5f3e9e3d827d4bccaa151ff7198a3b26,
title = "In vivo assessment of the metabolic alterations in glucagonoma syndrome",
abstract = "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.",
author = "Samuel Klein and Farook Jahoor and Hidefumi Baba and Courtney Townsend and Mary Shepherd and Wolfe, {Robert R.}",
year = "1992",
doi = "10.1016/0026-0495(92)90005-U",
language = "English (US)",
volume = "41",
pages = "1171--1175",
journal = "Metabolism: Clinical and Experimental",
issn = "0026-0495",
publisher = "W.B. Saunders Ltd",
number = "11",

}

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

AU - Shepherd, Mary

AU - Wolfe, Robert R.

PY - 1992

Y1 - 1992

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.

UR - http://www.scopus.com/inward/record.url?scp=0026440005&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026440005&partnerID=8YFLogxK

U2 - 10.1016/0026-0495(92)90005-U

DO - 10.1016/0026-0495(92)90005-U

M3 - Article

VL - 41

SP - 1171

EP - 1175

JO - Metabolism: Clinical and Experimental

JF - Metabolism: Clinical and Experimental

SN - 0026-0495

IS - 11

ER -