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Results for “PALMITIC ACID”

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PubMed1976

Chain elongation and desaturation of palmitic acid in liver microsomes of rats subjected to hyperbaric exposure.

The enzyme activities associated with chain elongation and desaturation of fatty acid in hepatic microsomes from rats held at 1 ATA of air, 1 ATA of He-O2, and 20 ATA of He-O2 were studied. It was found that both the microsomal chain elongation and desaturation of fatty acids were depressed in rats held at 1 ATA of He-O2 as compared to animals held at 1 ATA of air. When animals were exposed to an environment of 20 ATA of He-O2, the chain elongation of fatty acid was about the same as for rats held at 1 ATA of air and was two times greater than for the rats held at 1 ATA of He-O2. The desaturase activity was depressed as compared to the two groups of control animals held at 1 ATA of air and 1 ATA of He-O2.

Air Pressure↗
PubMed1983

Stimulation of gluconeogenesis by palmitic acid in rat hepatocytes: evidence that this effect can be dissociated from the provision of reducing equivalents.

When hepatocytes isolated from fasted rats were incubated in medium containing 5 mmol/L pyruvate, addition of albumin-bound palmitate (0.5 mmol/L) increased fatty acid oxidation and the conversion of pyruvate to glucose. Similar stimulation of gluconeogenesis occurred when palmitate was added to hepatocytes in medium containing 5 mmol/L alanine. Addition of 0.5 mmol/L (+)-octanoylcarnitine, an inhibitor of fatty acid oxidation, prevented the increment in beta-oxidation, but not the increase in glucose formation from pyruvate or alanine, induced by palmitate. These studies and other data to be considered subsequently indicate that palmitate can stimulate hepatic gluconeogenesis from three-carbon precursors under conditions that preclude an increase in the formation of reducing equivalents by beta-oxidation.

Animals↗
PubMed1996

Dithionite-supported hydroxylation of palmitic acid by cytochrome P450BM-3.

The ability of dithionite, an inexpensive reducing agent routinely used to produce the ferrous-carbonyl form of P450, to support P450BM-3-catalyzed hydroxylation of palmitate was studied. The hydroxylation products in the presence of dithionite were 15, 14, and 13-hydroxyhexadecanoate, with relative distributions similar to those observed with NADPH. The hydroxylation reaction was carried out in two separate steps, anaerobic reduction and subsequent oxidation of P450BM-3 by oxygen bubbling. The reduction step was much slower than the oxidation step, thus limiting the overall rate of hydroxylation. Upon addition of dithionite, the reductase domain of P450BM-3 seemed to be reduced before significant reduction of the heme domain occurred. The discovery of new reducing agents for P450-catalyzed reaction raises the possibility of replacing NADPH in specialty chemical hydroxylation catalyzed by P450s, especially catalytically self-sufficient P450s, such as P450BM-3 or recombinant fusion proteins of P450 covalently linked to a reductase.

Bacterial Proteins↗
PubMed1991

Effect of palmitic acid and fatty acid binding protein on ventricular fibrillation threshold in the perfused rat heart.

The effects of increased free fatty acid (FFA) levels on ventricular arrhythmias remain controversial. Using ventricular fibrillation threshold (VFT), we examined the relationship between FFA levels and ventricular arrhythmias. Isolated rat hearts were perfused with palmitate bound to either albumin or fatty acid binding protein (FABP) by Langendorf's method. The VFT was determined by electrical stimulation. Perfusion with 0.12 mM albumin alone, 0.12 mM palmitate bound to 0.12 mM albumin, and 0.36 mM palmitate bound to 0.12 mM albumin did not lower the VFT significantly. However, 0.60 mM palmitate bound to 0.12 mM albumin lowered VFT from 2.19 +/- 0.20 mA to 1.56 +/- 0.13 mA. The perfusion of 0.36 mM palmitate bound to 0.12 mM FABP lowered the VFT from 2.05 +/- to 0.19 mA to 1.47 +/- 0.23 mA, but 0.12 mM FABP alone did not affect the VFT. Perfusion with 0.36 mM palmitate bound to 0.12 mM FABP caused the VFT to fall more than perfusion with 0.36 mM palmitate bound to 0.12 mM albumin. Then the effects of verapamil perfusion or a low concentration of perfusate Ca2+ on VFT were examined. VFT was determined by electrical stimulation. Palmitate (0.6 mM) bound to 0.12 mM albumin lowered VFT. Verapamil 10(-7) M perfusion and a low concentration of Ca2+ (Ca2+ 1.67 mM) suppressed the FFA-induced fall of VFT. These results suggested that the arrhythmogenic action of FFA was related to Ca2+ overload in myocardial cells.

Albumins↗