Journal
ANNUAL REVIEW OF NUTRITION
Volume 25, Issue -, Pages 9-35Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev.nutr.24.012003.132159
Keywords
glucagon; insulin resistance; sepsis; nutritional support; enteral nutrition; parenteral nutrition; hyperglycemia; gluconeogenesis; lactate
Categories
Funding
- NIDDK NIH HHS [DK-20593, DK-43748, P30-DK-26657] Funding Source: Medline
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK026657, R01DK043748, P60DK020593, R56DK043748, R29DK043748] Funding Source: NIH RePORTER
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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.
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