Defective glucose homeostasis during infection

• Published in: Annual review of nutrition 2005-01, Vol.25 (1), p.9-35
• Main Author: McGuinness, O.P
• Format: Article
• Language: English
• 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)
• ISSN: 0199-9885; 1545-4312
• DOI: 10.1146/annurev.nutr.24.012003.132159

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.