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Stress.

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General Adaptation Syndrome↗
PubMed1981

Formalin stress reaction of germfree and conventional mice treated with Bordetella pertussis vaccine.

Germfree and conventional mice responded similarly to pertussis vaccine treatment. In both groups, lymphocytosis and splenomegaly developed in a similar proportion. The formalin stress reaction of germfree and conventional mice with hypertrophic lymphoid organs induced by pertussis vaccine differed from that of untreated mice: the treated germfree and conventional mice showed a acute increase of lymphocytosis without an significant change in splenomegaly.

Animals↗
PubMed1993

Regulation of protein metabolism during stress.

Stress induces a hypermetabolic state of increased urinary nitrogen loss and increased metabolic rate. The principal reason for such a response is the mobilization of amino acids and the production of glucose to provide energy for the cells involved in the host immune response and wound repair. The endocrine hormones, eg, cortisol, the catecholamines, and glucagon, are largely responsible for these effects. Insulin and growth hormone administration can produce anabolic effects to block the loss of body protein. Administration of specific amino acids, such as glutamine, also appears to be beneficial. However, the hypermetabolic state goes beyond derangement of endocrine hormone levels. Although the cytokines are also important mediators, it is not clear how these mediators, in concert with hormonal changes, produce all of the manifestations of the hypermetabolic state seen in stress.

Amino Acids↗
PubMed1993

Lipid fuel metabolism in health and disease.

Rates of adipose tissue lipolysis are increased in critically ill patients, thus increasing the systemic supply of free fatty acids. This increase in the availability of free fatty acids is probably mediated by various factors including increases in counterregulatory hormones and tumor necrosis factor alpha. The cytokines tumor necrosis factor and interleukin-1 also promote de novo lipogenesis in the liver and may be responsible for impaired triglyceride removal in peripheral tissues; these effects together contribute to the hypertriglyceridemia often seen in septic states. This hypertriglyceridemia may have a teleologic basis, because triglyceride-rich lipoproteins have been shown to bind and inactivate endotoxin. When present in excess, free fatty acids may be responsible for tissue injury in the cold-stored liver allograft, in ischemic-reperfusion cardiac injury, and in ischemic brain injury. Hypoketonemia commonly occurs in septic states and may be due to the combination of a defect in hepatic ketogenesis and accelerated ketone body uptake by peripheral tissues. Both tumor necrosis factor and interleukin-1 have a hypoketonemic effect in animals. Whether ketone bodies have significant protein-sparing properties remains controversial.

Adipose Tissue↗