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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:dateCreated |
1989-10-12
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| pubmed:abstractText |
The metabolic response to injury may be presumed to be adaptive, at least in terms of days to weeks. In the wild state where these patterns developed, the wounded organism has poor access to food and must live off its own stores of nutrients, mainly fat, and tissue proteins, mainly from muscle. In fasting, without injury, the organism conserves protein. In this condition there are reductions in blood glucose and insulin levels and increases in glucagon and fatty acid levels. Insulin-dependent tissues stop using glucose; the liver converts fatty acids to ketone bodies, which increase about 100-fold in the fasting human; and the brain substitutes ketone bodies for more than one half of what would otherwise be an obligatory consumption of 100 to 150 g glucose per day in humans. This substitution spares the amount of muscle protein required for gluconeogenesis in liver and kidney, and net N losses can be reduced to less than 6 g per day. Energy expenditure decreases up to 30%. The fasted, injured subject has additional nutritional requirements. Regeneration of the wound and rapidly proliferating white and red blood cells require a source of amino acids and other nutrients. Synthesis of acute-phase proteins required for host defense also needs amino acids. In addition, the wound, regenerating tissue, and white blood cells require large amounts of glucose for glycolysis. That the wound is poorly vascularized may be the major reason for hyperglycemia, which provides a glucose gradient between plasma and tissue high enough for extraction of sufficient glucose. The wound does not increase net consumption of glucose; rather, lactate returns to the liver to be converted again to glucose. Hyperglycemia due to the wound increases the requirements for gluconeogenesis from muscle protein, however. The high concentrations of counterregulatory hormones, cortisol, epinephrine, and glucagon will minimize glucose utilization by insulin-sensitive tissues, despite high concentrations of both glucose and insulin, but these hormones are not able to prevent suppression of ketone body synthesis in the liver. As a result, the brain continues to derive almost all its energy from oxidation of glucose. Synthesis of this glucose in liver is the biggest consumer of amino acids made available by net degradation of muscle protein. The metabolic response to injury, initiated by afferent nerve impulses and cytokines and mediated by increases in counterregulatory hormones and sympathetic activity, is a well-coordinated, well-regulated process controlled largely by the hypothalamus. Increased consumption of nutrients occurs simultaneously with but is not caused by increase in production.(ABSTRACT TRUNCATED AT 400 WORDS)
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:status |
MEDLINE
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| pubmed:issn |
0199-9885
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
9
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
445-73
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| pubmed:dateRevised |
2004-11-17
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| pubmed:meshHeading | |
| pubmed:year |
1989
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| pubmed:articleTitle |
The effects of injury and sepsis on fuel utilization.
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| pubmed:affiliation |
Department of Orthopedic Surgery, Columbia University, New York, NY 10032.
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| pubmed:publicationType |
Journal Article,
Review
|