This study suggests that a significant subclinical Mg deficit, not detected by serum Mg, was present in many of these healthy elderly subjects. Mg supplementation improved Mg status and renal function.
Two groups of rats were fed diets containing 20% by weight of either partially hydrogenated marine oil supplemented with sunflower seed oil (PHMO) or palm oil (PO) for 8 wk. Using a liver perfusion system, the effect of dietary long chain monoenoic fatty acids on the uptake and metabolism of [14-14C]erucic acid was studied. The perfusion times were 15 and 60 min, respectively. The two groups showed equal ability for erucic acid uptake in the liver but differed in the channeling of the fatty acids into various metabolic pathways. A higher metabolic turnover of 22:1 in the PHMO livers relative to the PO livers was demonstrated by an increased recovery of total [14C]labeling in the triglyceride (TG) and phospholipid (PL) fractions, already evident after 15 min of perfusion. The chain-shortening capacity was highest in the PHMO group, reflected by a higher [14C]18:1 incorporation in both TG and PL, and increasing from 15 to 60 min of perfusion. The amount of [14C]18:1 found in PL and TG after 60 min of perfusion of livers from rats fed PO corresponded to that shown for the PHMO group after 15 min. The PL demonstrated a discrimination against 22:1 compared to TG, and, when available, 18:1 was highly preferred for PL-synthesis. The total fatty acid distribution in the TG, as determined by gas liquid chromatography (GLC), reflected the composition of the dietary fats. In the total liver PL, 22:1 and 20:1 were present in negligible amounts, although the PHMO diet contained 12-13% of both 22:1 and 20:1. In the free fatty acid fraction (FFA), the major part of the radioactivity (approximately 80%) was [14-14C]erucic acid, and only small amounts of [14C]18:1 (less than 2%) were present, even after 60 min of perfusion. The shortened-chain 18:1 was readily removed from the FFA pool and preferentially used for lipid esterification.
Forty men with mild to moderate hypertension were given one of two dietary supplements for 6 weeks: 20 capsules of fish oil (MaxEPA) or placebo (olive and corn oil). The MaxEPA supplement provided about 7 g omega-3-fatty acids pr day, whereas the placebo contained about 7 g omega-6-fatty acids and only 0.2 g omega-3-fatty acids. A clinical insignificant reduction in blood pressure was noted in both groups. In the fish oil group, the serum triglyceride levels fell by 30%. A decrease in the ratio total cholesterol/high density lipoprotein (HDL-) cholesterol was noted in both groups, most pronounced in the placebo group. No significant effect on total serum cholesterol level was observed during this study.
The liver metabolism of erucic acid, 22:1 n-9, was studied in rat livers perfused with 14–14C-labelled erucic acid for 15 and 60 min, determining the distribution of radioactivity in the perfusate and in the lipids of the liver cell organelles. The rats were adapted to a high-fat diet containing either partially hydrogenated marine oil (PHMO) or palm oil (PO), both adjusted to a 10% content of linoleic acid. The results showed an efficient uptake and metabolism of erucic acid with the secretion to the perfusate medium of labelled free fatty acids other than erucic acid, labelled phospholipids as well as water soluble oxidation products. Only minor amounts of secreted labelled triglycerides were found within 60 min of perfusion. In the liver, labelled lipids accumulated in the endoplasmic reticulum, after 15 min mainly as free fatty acids, after 60 min as triglycerides. The esterification pathway, including the erucic acid given as well as chain-shortened fatty acids, seemed to be preferred under the experimental conditions and with adequate linoleic acid in the diet. A chain shortening of erucic acid probably took place in both peroxisomes and mitochondria shown by the presence of labelled 18:1 and 20:1 in the organelle-bound phospholipids. A chain shortening was found in both dietary groups, and is assumed to be an affect of the adaptation to a high-fat diet rather than an effect of dietary very long chain monoenoic fatty acids. Somewhat higher levels were found in the PHMO group, but the difference in the dietary fat was not a major factor in the liver lipid adaptation.
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