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Defective glucose homeostasis during infection
Infection leads to profound alterations in whole-body metabolism, which is characterized by marked acceleration of glucose, fat and protein, and amino acid flux. One of the complications of infection, especially in the nutritionally supported setting, is hyperglycemia. The hyperglycemia is caused by...
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| Published in: | Annual review of nutrition 2005-01, Vol.25 (1), p.9-35 |
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| cites | cdi_FETCH-LOGICAL-c470t-aea7cc095e20d597e2127f27452568699e8c754b753cb7a4fce2e68e789ba0e53 |
| container_end_page | 35 |
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| container_title | Annual review of nutrition |
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| creator | McGuinness, O.P |
| description | Infection leads to profound alterations in whole-body metabolism, which is characterized by marked acceleration of glucose, fat and protein, and amino acid flux. One of the complications of infection, especially in the nutritionally supported setting, is hyperglycemia. The hyperglycemia is caused by peripheral insulin resistance and alterations in hepatic glucose metabolism. The defects in hepatic glucose metabolism include overproduction of glucose and a failure of the liver to appropriately adapt when nutritional support is administered. Investigators have suggested that multiple factors contribute to the observed defects. In this review, I focus primarily on alterations in carbohydrate metabolism, examining both the metabolic response to infection and inflammatory stress, the role of the accompanying neuroendocrine and inflammatory responses in the metabolic response, and the interaction between the endocrine response to infection and nutritional support. |
| doi_str_mv | 10.1146/annurev.nutr.24.012003.132159 |
| format | article |
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One of the complications of infection, especially in the nutritionally supported setting, is hyperglycemia. The hyperglycemia is caused by peripheral insulin resistance and alterations in hepatic glucose metabolism. The defects in hepatic glucose metabolism include overproduction of glucose and a failure of the liver to appropriately adapt when nutritional support is administered. Investigators have suggested that multiple factors contribute to the observed defects. In this review, I focus primarily on alterations in carbohydrate metabolism, examining both the metabolic response to infection and inflammatory stress, the role of the accompanying neuroendocrine and inflammatory responses in the metabolic response, and the interaction between the endocrine response to infection and nutritional support.</description><identifier>ISSN: 0199-9885</identifier><identifier>EISSN: 1545-4312</identifier><identifier>DOI: 10.1146/annurev.nutr.24.012003.132159</identifier><identifier>PMID: 16011457</identifier><identifier>CODEN: ARNTD8</identifier><language>eng</language><publisher>Palo Alto, CA: Annual Reviews</publisher><subject>Amino acids ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Biological and medical sciences ; clinical nutrition ; Emergency and intensive care: metabolism and nutrition disorders. Enteral and parenteral nutrition ; enteral feeding ; glucagon ; Gluconeogenesis ; Glucose - metabolism ; glucose tolerance ; Homeostasis ; Hormones - physiology ; Humans ; hyperglycemia ; Infection - metabolism ; inflammation ; Inflammation - metabolism ; Insulin Resistance ; Intensive care medicine ; Liver - metabolism ; Medical sciences ; neurosecretory system ; Nutritional Support ; parenteral feeding ; sepsis (infection)</subject><ispartof>Annual review of nutrition, 2005-01, Vol.25 (1), p.9-35</ispartof><rights>2006 INIST-CNRS</rights><rights>Copyright Annual Reviews, Inc. 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-aea7cc095e20d597e2127f27452568699e8c754b753cb7a4fce2e68e789ba0e53</citedby><cites>FETCH-LOGICAL-c470t-aea7cc095e20d597e2127f27452568699e8c754b753cb7a4fce2e68e789ba0e53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17052705$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16011457$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>McGuinness, O.P</creatorcontrib><title>Defective glucose homeostasis during infection</title><title>Annual review of nutrition</title><addtitle>Annu Rev Nutr</addtitle><description>Infection leads to profound alterations in whole-body metabolism, which is characterized by marked acceleration of glucose, fat and protein, and amino acid flux. One of the complications of infection, especially in the nutritionally supported setting, is hyperglycemia. The hyperglycemia is caused by peripheral insulin resistance and alterations in hepatic glucose metabolism. The defects in hepatic glucose metabolism include overproduction of glucose and a failure of the liver to appropriately adapt when nutritional support is administered. Investigators have suggested that multiple factors contribute to the observed defects. In this review, I focus primarily on alterations in carbohydrate metabolism, examining both the metabolic response to infection and inflammatory stress, the role of the accompanying neuroendocrine and inflammatory responses in the metabolic response, and the interaction between the endocrine response to infection and nutritional support.</description><subject>Amino acids</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Biological and medical sciences</subject><subject>clinical nutrition</subject><subject>Emergency and intensive care: metabolism and nutrition disorders. 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| ispartof | Annual review of nutrition, 2005-01, Vol.25 (1), p.9-35 |
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| language | eng |
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| source | Annual Reviews Sciences archive collection; SPORTDiscus with Full Text |
| subjects | Amino acids Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Biological and medical sciences clinical nutrition Emergency and intensive care: metabolism and nutrition disorders. Enteral and parenteral nutrition enteral feeding glucagon Gluconeogenesis Glucose - metabolism glucose tolerance Homeostasis Hormones - physiology Humans hyperglycemia Infection - metabolism inflammation Inflammation - metabolism Insulin Resistance Intensive care medicine Liver - metabolism Medical sciences neurosecretory system Nutritional Support parenteral feeding sepsis (infection) |
| title | Defective glucose homeostasis during infection |
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