Unique effects of infectious or inflammatory stress on fat metabolism in rats.
Infectious or inflammatory stress in the rat causes very typical functional and metabolic alterations. Among the most typical are elevation in body temperature, insulin, and glucagon and depression in the concentrations of plasma ketones and free fatty acids. These changes occur only with infectious or inflammatory stress and not with noninflammatory stresses such as femoral fracture, screen restraint, or exercise. It appears that the depression in plasma ketone bodies during infection or inflammation is closely related to the rise in plasma insulin. During infection imposed on experimentally induced diabetes, inhibition of plasma ketones is not apparent. In a similar fashion, infection in hypophysectomized rats causes no elevation in plasma insulin and no depression in plasma ketones. Discussion concerning the implications of these observations in the rat and primate is included.
D000818:Animals; D004685:Encephalomyelitis, Venezuelan Equine / Q000378:metabolism; D005264:Femoral Fractures / Q000378:metabolism; D005934:Glucagon / Q000097:blood; D007016:Hypophysectomy; D007239:Infections / Q000378:metabolism*; D007249:Inflammation / Q000378:metabolism*; D007328:Insulin / Q000097:blood; D050356:Lipid Metabolism; D005082:Physical Exertion; D011018:Pneumonia, Pneumococcal / Q000378:metabolism; D051381:Rats; D012149:Restraint, Physical; D013312:Stress, Physiological / Q000378:metabolism*; D013965:Thyroidectomy; D014406:Tularemia / Q000378:metabolism
D007328:Insulin; D005934:Glucagon