Effect of Dietary Linolenate on the Pathogenesis of Fever
The effects of a reduction in the level of arachidonic acid 20:4(ω6) by increases in linoleic acid 18:2(ω6) and/or linolenic acid 18:3(ω3) in a febrile condition, induced by gram- negative bacterial pyrogens, are unknown. Yet it is recognized that endotoxin fever in humans and rabbits is arachidonate dependent (Spawinski et al., 1978). It is also recognized that increasing amounts of linolenate, 18:3(ω3), reduce the metabolites of linoleic acid, 18:2(ω6) (Machlin, 1962; Mohrhauer and Holman, 1963; Rahm and Holman, 1964; Anding and Hwang, 1986) by acting as a competitor for the same cyclo-oxygenase (Pace-Asciak and Wolfe, 1968), thereby not only influencing the formation of arachidonic acid but suppressing its metabolites as well. The metabolites of arachidonic acid have been implicated in the biochemical sequences leading to fever induced by bacterial endotoxin (Feldberg and Saxena, 1975; Milton, 1976; Skarnes et al., 1981). Therefore, deficiency in arachidonic acid diminishes the fever response (Kenedi et al., 1984), which, in the course of constant stimulation by endotoxin, leads to tolerance of the fever (Atkins, 1960; Kanoh et al, 1977). The physiological consequences of tolerance in the body, induced by increased intake in linolenate, together with chronic induction of fever, have not been associated with a diseased condition, as the biochemical mechanism leading to tolerance had been unknown until the present study. According to Bernheim et al. (1979), a “true” fever is a disorder of thermoregulation in which the body actively seeks to raise its temperature by increasing heat production (Bernheim et al., 1979). Heat is the result of oxidative catabolism in the body, and there is a relationship between the amount of O2 absorbed and the amount of CO2 eliminated (Benedict, 1907; Fritz, 1961).
KeywordsArachidonic Acid Fever Response Dietary Linolenate Clean Test Tube Increase Heat Production
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