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Insulin plays a critical role in amino acid‐induced heat accumulation during anesthesia
Author(s) -
Yamaoka Ippei,
Doi Masako,
Kawano Yuichi,
Nakayama Mitsuo,
Watanabe Yosuke,
Ohba Kanae,
Sugahara Kunio,
Yoshizawa Fumiaki
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a161-c
Subject(s) - somatostatin , medicine , endocrinology , insulin , chemistry , saline , phosphorylation , stimulation , biochemistry
We aimed to assess the contribution of insulin, which was markedly elevated following infusion of an amino acid (AA) mixture during anesthesia, to heat storage and stimulation in muscle protein synthesis. We administered an AA mixture or saline (Sal) intravenously for 3 h to propofol‐anesthetized rats with or without somatostatin treatment in a primed‐constant manner. Combined infusion of AA with somatostatin maintained plasma insulin concentrations at the same levels seen in both Sal groups. AA administration attenuated the decrease in intraperitoneal temperature, while this thermogenic response was entirely blocked by somatostatin treatment. AA administration raised the plasma levels of most AAs, and somatostatin treatment further augmented this elevation. Somatostatin treatment abolished the stimulatory effects of AA on muscle protein synthesis. Somatostatin treatment with AA attenuated the phosphorylation of PKB to a comparable degree as in the Sal group; however, AA‐induced phosphorylation of mTOR, 4E‐BP1 and S6K1 were partially, but not completely blocked. Collectively, our findings strongly suggest that insulin is markedly elevated by AA administration during anesthesia and facilitates thermal accumulation in the body. The AA‐induced rise in muscle protein synthesis and up‐regulation of translation initiation factors probably play important in the mechanism.