linoleic-acid and Bacterial-Infections

Increased mortality from sepsis is associated with high levels of thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (PGF1 alpha). Linoleic acid, an n-6 essential fatty acid, is the usual precursor of TXB2 and PGF1 alpha, while fish oil is rich in n-3 essential fatty acid, the precursor of less active moieties. Rats were fed chow, an essential fatty acid-deficient diet, or an essential fatty acid-deficient diet supplemented with linoleic acid or fish oil for 2 weeks. The animals then underwent a sham operation or cecal ligation and puncture to induce sepsis. Six hours later, blood was obtained for analysis. The chow and linoleic acid diets produced significant (twofold to fivefold) increases in levels of both TXB2 and PGF1 alpha after sepsis. The essential fatty acid-deficient diet and fish oil diet protected against increases in levels of TXB2 or PGF1 alpha during sepsis. Dietary restriction of linoleic acid or fish oil supplementation may play an important role in altering the inflammatory mediator response to sepsis.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Bacterial Infections; Cecum; Dietary Fats; Epoprostenol; Fatty Acids, Essential; Fatty Acids, Unsaturated; Fish Oils; Linoleic Acid; Linoleic Acids; Male; Rats; Rats, Inbred Strains; Thromboxane A2; Thromboxane B2

The effects of exogenous insulin on oxidation of glucose and fatty acid were investigated in septic (n = 20) and control rats (n = 20). Sepsis was induced by ligation and puncture of the caecum. The rats received intravenous nutrition with glucose as a non-protein calorie for 27 hours. Ten rats in each group received insulin intravenously at a rate of 0.64U/kg/hr during the last 6 hours of the intravenous nutrition, U-14C-glucose or 1-14C-linoleic acid at a dose of 1.563 microCi each was injected as a bolus at the 21st hour of the intravenous nutrition. Cumulative 14CO2 production was measured for 6 hours after the injection of the radioactive substrates. 14CO2 production from both glucose and linoleic acid was inhibited by the sepsis. 14CO2 production from glucose was accelerated by exogenous insulin in the control rats, while it was not accelerated in the septic rats. Exogenous insulin did not affect 14CO2 production from linoleic acid in both the control and the septic rats. These results indicate that, under the condition of sepsis, lowering blood sugar level with exogenous insulin does not refLect an increase in oxidation of glucose.

Topics: Animals; Bacterial Infections; Glucose; Insulin; Linoleic Acid; Linoleic Acids; Oxidation-Reduction; Rats; Rats, Inbred Strains