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Polyenoic acids, administration

Indeed, these polyenoic acids are metabolized rapidly, linoleic, linolenic, and the isomers as well. The low value in one of the linoleic acid experiments must be related to a delayed resorption 74% of the activity was still present in the intestine at the end of the experiment. Only after 5 hours following administration of the substance did the expired CO2 become radioactive, whereas in all other experiments this occurred after 1 hour. It is remarkable that animals on a normal diet oxidize these substances at a faster rate than those on a fat-free diet, supplemented with the corresponding inactive acid over a period of 3-4 weeks. [Pg.14]

Numerous studies have dealt with the epithelium of the small intestine. Entry of fat from the bowel lumen into the mucosal cells appears to proceed as evidenced by the extreme degree of fat accumulation in these cells. Steatorrhea may result when the maximal absorptive capacity of these cells is exceeded. There is no evidence of selective absorption of certain fats, as could be shown by analysis of mucosal lipids and feces. In particular, the lowering of plasma linoleic acid concentration in a-jff-lipoproteinemia and other forms of malabsorption does not appear to be due to impairment of absorption of, essential fatty acids. After administration of diets rich in polyenoic acids Ways and Parmentier (1963) found more linoleic acid in mucosal phospholipids and triglycerides than was found with the normal diet. There was a simultaneous increase in the proportion of linoleate in plasma cholesterol esters. Linoleic acid, given for a period of three years, was absorbed to about 97 per cent (Frezal et al. 1966). Its administration resulted in a significant increase of the proportion of linoleic acid in the plasma lipid fatty acids. Normal values were reached in the triglyceride and phospholipid fractions (see table 6). [Pg.395]

In addition to other systemic manifestations, essential fatty acid deficiency in rats has been known to be accompanied by a relative increase in eicosatrienoic and palmitoleic acid and a relative decrease in tetraenoic acid in the heart (Rieckehoff et al., 1949 Mead, 1957). Holman and Peifer (1960) showed that the administration of dietary cholesterol to rats already deficient in essential fatty acids promoted the accumulation of polyenoic acids in the heart with an even higher proportion of trienoic acid and a lower proportion of tetraenoic acid, which they interpreted as an intensification of the essential fatty acid deficiency. It would be of great interest to know whether essential fatty acid deficiency and/or cholesterol feeding causes a change in fatty acid synthetic rate by isolated heart mitochondria or microsomes. Either of these organelles could readily modify the heart s lipids by pathways of elongation and desaturation. [Pg.153]

To examine the fetal accumulation of polyenoates we have used guinea-pigs at about 25-30 days pregnant. They were dosed orally with 25-50 yCi of labelled a-linolenic acid. The animals were killed at time intervals up to 96 hours after administration. [Pg.140]


See other pages where Polyenoic acids, administration is mentioned: [Pg.10]    [Pg.11]   
See also in sourсe #XX -- [ Pg.395 ]




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