1988 Fiscal Year Final Research Report Summary
Hormone insensitivity of critically ill patients - in relation to hepatic energy metabolism
| Project/Area Number |
61570643
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Digestive surgery
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| Research Institution | YAMANASHI Medical College |
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Principal Investigator |
SUGAHARA Katsuhiko Yamanashi Medical College, 外科学講座第1, 教授 (90009944)
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| Co-Investigator(Kenkyū-buntansha) |
FUJII Hideki Yamanashi Medical College, 外科学講座第1, 助手 (30181316)
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| Project Period (FY) |
1986 – 1988
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| Keywords | obstructive jaundice / arterial ketone body ratio / 動脈血中ケトン体比 / アラニン / hormone insensitivity |
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| Research Abstract |
In the postoperative course follwing major surgery such as massive liver resection or radical operation for bile duct cancer or pancreatic cancer accompanying severe obstructive jaundice, intractable glucose intolerance sometimes appears and it is not controlled by an insulin infusion. The present research project was to analyze this pathological status from the aspect of the hepatic energy metabolism experimentally after summarizing this clinical entity. Main reasons of postoperative jaundice withe no mechanical obstruction were circulatroty disturbance of the liver and persistent infection. This jaundice is an ominous sign of the multiple organ failure. The hepatic energy status of these patients, demonstrated as the arterial ketone body ratio remained in a lower critical state, below 0.4, had organ failures more than 3 and sometimes exhibited non ketonic hyperglycemia by a glucose infusion and hypoglycemia by no glucose infusion. In this lower hepatic energy status, interrelationship of the substrate-supply and -utilization between the liver and peripheral organs were disturbed, and no more mitochondrial function to produce ATP was reversible. On the other hand, in obstructive-jaundiced rabbits and 70% hepatectomized rabbits, when the energy status of the liver, demonstrated as the energy charge, decreased in accordance with a decrease in the oxidative phosphorylative activity of the liver mitochondria. In the lower status under that about 70% of operated rabbits died, glucose tolerance was severely depressed. Cyctic AMP response after glucagon infusion was also depressed. Gluconeogenesis occurring after glucagon infusion was also depressed. Gluconeogenesis occurring after glucagon infusion needs energy consumption. In a lower energy status of the liver, energy consuming suquences such as gluconeogenesis was also inhibited.
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