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Tumor necrosis factor alpha stimulates gluconeogenesis from alanine in vivo
Author(s) -
Blumberg David,
Hochwald Steven,
Burt Michael,
Donner David,
Brennan Murray F.
Publication year - 1995
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.2930590404
Subject(s) - in vivo , medicine , gluconeogenesis , tumor necrosis factor alpha , alpha (finance) , alanine , cancer research , necrosis , endocrinology , biochemistry , biology , amino acid , surgery , metabolism , genetics , construct validity , patient satisfaction
An increase in gluconeogenesis contributes to the cachexia seen in severe injury, sepsis, and malignancy by converting amino acids from skeletal muscle to glucose. Since tumor necrosis factor α (TNFα) may mediate this cachexia, we examined the effect of this cytokine on gluconeogenesis. Twenty‐eight male Fischer rats were injected intraperitoneally with TNFα (250 μg/kg) or saline, and after 4 hours, isolated hepatocytes were obtained by in situ collagenase liver perfusion. Hepatocytes were incubated with alanine (10 mM), and rates of gluconeogenesis were determined. Plasma lactate, glucose, insulin, glucagon, cortisol, and amino acids were measured. TNFα administration resulted in a 50% increase in gluconeogenesis from alanine ( P <0.05) and a three‐fold increase in plasma glucagon ( P = 0.01). Total and glucogenic plasma amino acids decreased with TNFα injection ( P < 0.05). In vivo TNFα causes an increase in hepatic gluconeogenesis associated with increased plasma glucagon.