Energy substrate metabolism during stress
Sugimoto, H.
Nihon Geka Gakkai Zasshi 97(9): 726-732
1996
ISSN/ISBN: 0301-4894 PMID: 8940683 Document Number: 458312
Energy substrate metabolism during stress is characterized by increased REE (resting energy expenditure), hyperglycemia, hyperlactatemia and protein catabolism. This stress-induced hypermetabolic responses are closely related to increased secretion of neurohormonal and cytokine mediators. The insulin resistance hyperglycemia has been called "stress diabetes" or "surgical diabetes". Glucose disposal has been thought to be impaired in this condition. However, glucose uptake in most tissue is non-insulin mediated. Recent studies showed glucose uptake elevated in sepsis or TNF infusion. Insulin-regulatable glucose transporter (GLUT4) is present only in muscle, heart and adipose tissues. It was demonstrated that insulin binding to membrane receptors in these tissues was intact. This hyperglycemia in stress diabetes results from a postreceptor mechanism. Stress hyperlactatemia is thought to be caused by decreased pyruvate dehydrogenase activity rather than tissue hypoperfusion. Hyperlactatemia may promote gluconeogenesis. Glucose is a essential energy substrate in some tissues such as brain, erythrocyte and leukocyte. Hyperglycemia may be viewed as a beneficial response during stress.