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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. 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