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K Moukabary

Publications and source records attributed to K Moukabary.

3 recordsLinked to original sources

Effects of eicosapentaenoic and gamma-linolenic acids (dietary lipids) on pulmonary surfactant composition and function during porcine endotoxemia.

STUDY OBJECTIVES: To investigate whether a diet enriched with fish and borage oils, with their high polyunsaturated fatty acid (PUFA) content, alters surfactant composition and function during endotoxemia. DESIGN: Prospective, randomized, blinded, controlled animal study. SETTING: Research laboratory at a medical center. PARTICIPANTS: Thirty-six 15- to 25-kg, disease-free, castrated male pigs. DIETS AND MEASUREMENTS: Three groups of pigs (n = 12 per group) were fed for 8 days diets containing either omega-6 fatty acids (FAs) (corn oil; diet A), or omega-3 FAs (fish oil; diet B), or a combination of omega-6 and omega-3 FAs (borage and fish oils; diet C). Eight of 12 pigs in each group received a 0.1-mg/kg bolus of Escherichia coli endotoxin followed by a continuous infusion (0. 075 mg/kg/h). One lung was subsequently isolated ex vivo, and pressure-volume curves were measured. The contralateral lung was lavaged, and surfactant was analyzed for total and individual phospholipids and FA composition. Minimum and maximum surface tension was measured by bubble surfactometry. RESULTS: Pigs fed either diet B or C had increased oleic acid (C(18:1) omega-9), eicosapentaenoic acid (EPA; C(20:5) omega-3), docosahexaenoic acid (C(22:6) omega-3), and total omega-3 and monounsaturated FAs in their surfactant PUFA pools. The relative percentage of linoleic acid (C(18:2) omega-6) and total omega-6 FAs were significantly lower from pigs fed diets B and C compared with diet A. Palmitic acid (C(16:0)) concentrations, the primary FA in surfactant, had a tendency to be lower in pigs fed diets B and C. There were no demonstrable effects on surfactant function or pulmonary compliance. CONCLUSIONS: Diets containing EPA or EPA and gamma-linolenic acid altered the PUFA composition of pulmonary surfactant, but without demonstrable effects on surfactant function during porcine endotoxemia.

Animals↗

Hepatocellular 22Na+ uptake: effect of oleate.

Whether cellular oleate uptake is Na+ coupled remains controversial. Our present studies document that hepatocellular [3H]oleate uptake is unaltered by isomotic substitution of Na+ with K+, Li+, or sucrose in Hanks' HEPES buffer. In parallel studies 22Na+ uptake was significantly (P less than 0.02) increased by concentrations of alanine that yielded [3H]-alanine uptakes greater than 24% of basal 22Na+ uptake when both were expressed as nanomoles per minute per 10(6) hepatocytes. Although [3H]glutamine uptake exceeded this threshold, maximal specific [3H]taurocholate uptake did not. Consistent with the observations with alanine, addition of glutamine, but not taurocholate, to the incubations resulted in a significant increase in 22Na+ uptake. The ionophore monensin increased uptake of 22Na+ under all conditions. Both in the absence and in the presence of HCO3- (4 and 25 mM), specific [3H]oleate uptake was sufficient to elicit a readily detectable effect on 22Na+ uptake, if Na+ and oleate were cotransported. However, addition of 1 mM oleate did not affect 22Na+ uptake in the absence of HCO3- (5.4 +/- 0.6 vs. control 5.4 +/- 0.4 nmol.min-1.10(6) cells-1) as well as in the presence of 4mM HCO3- (10.4 +/- 1.8 vs. control 9.9 +/- 1.1) and 25 mM HCO3- (10 +/- 1.3 vs. control 10.8 +/- 0.5). These data indicate that the predominant component of hepatocellular oleate uptake is not directly associated with Na+ influx. They do not exclude, however, a more complex or indirect link.

Alanine↗