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Oleic acid induction

Fig. 4 A, B. Time profiles of A cell dry weight and PHA concentration B PHA content (wt %) and 3HV fraction in PHA (mol%) during the fed-batch culture of XLl-Blue(pJC4) with oleic acid supplementation after acetic acid induction. The feeding solution was added to increase the concentrations of glucose and propionic acid to 20 g/1 and to 5 mmol/1, respectively, after each feeding (reproduced from [62] with permission)... [Pg.191]

The fact that PR3 could utilize triolein to produce DOD indicated the possibility that lipase induction could release free fatty acids from triolein before it was used as substrate for DOD production. When Chang and colleagues monitored the time-dependent activity of extracellular lipase, they reported that triolein, not oleic acid, induced lipase activity. The induction of lipase activity was observed 12h after substrate addition, and DOD production... [Pg.561]

Nucleation from the melt has been studied for palm oil, composed of triglycerides of palmitic and oleic acids, and exhibiting at least three polymorphs (van Putte and Bakker 1987). Nucleation curves (induction time x vs temperature T) of palm oil and palm stearin show discontinuities at 297 and 306 °C respectively, indicating the onset of nucleation, and the demarcation of the occurrence of the polymorphs, as confirmed by isothermal Differential Scanning Calorimetry (DSC) studies (Ng I990a,b). [Pg.72]

The endothelial dysfunction during the postprandial phase after a meal rich in oxidized fat is almost certainly due to the cellular response to oxidized fat originating from this repeatedly heated fat. As in so many cases, the precise identity of this factor is not known. It is often assumed that it is a reactive molecule, derived from quantitatively the most important unsaturated fatty acid (linoleic acid) in the diet. Thus 9-, 11-, and 13-hydroperoxy-linoleic acids are possibilities, as are 8,9- or 11,12-epoxy-linoleic acids. However, the relative amount of epoxy fatty acids in the diet is much less than that of hydroperoxy fats. Photooxidation products of oleic acid cannot be excluded either, and it is worth pointing out that this unsaturated fatty acid is quantitatively the most important fatty acid in Western and Mediterranean diets. What is also not clear is whether endothelial dysfunction during postprandial lipemia requires the induction of enzymes. [Pg.209]

A6-Desaturase Gene Expression. In liver, A6D gene expression (Fig. 4) increased, irrespective of the source of lipids. Oleic acid provided in the diet as the only source of lipids yielded the highest induction of A6D gene expression. LA had a greater effect than ALA on this gene. However, in brain (Fig. 5) and kidney (Fig. 6), A6-desaturase expression did not change, irrespective of the fatty acid provided. [Pg.271]

The induction of formation of endoplasmic reticulum membranes by phenobarbital leads to a considerable change in Upid composition of the membranes. The molar ratio of cholesterol/total phospholipid in the membranes of the endoplasmic reticulum faUs to 73 % of the control and the proportion of Unoleic acid in phosphatidylchoUne and phosphati-dylethanolamine rises to 120-125% of the control, whereas the proportion of oleic acid, arachidonic acid docosahexaenoic acid decreases (Davison and Wills 1976). The capacity of reducing added hydroperoxides is increased in isolated microsomal fi actions from phenobarbital-pretreated rats as compared to controls (Sies and Summer 1975). [Pg.637]

The effect of hormones on the A6 desaturation of linoleic, a-linolenic and oleic acids was shown as early as 1966 (Mercuri et al, 1966, 1967). It was found that alloxan diabetes depressed the A 6 desaturase activity of rat liver microsomes and insulin injection corrected the defect in less than 38 h. The simultaneous injection of actinomycin D or Puromycin that abolished protein synthesis imparted the reparative effect of insulin and suggested that insulin effect might involve A6 desaturase induction. However... [Pg.92]

Shake flask cultures (2(X) ml) of C. cloacae parent w ere grown on sucrose overnight then induced with oleic acid. Samples were taken at several timepoints for enzyme assays. Results are shown in Fig. 1. A comparison of induction in parent and mutant strains showed that alcohol oxidase w as induced to levels... [Pg.268]

The role of dietary fat in predisposing thrombosis has been given impetus by Hornstra. He demonstrated the induction of arterial thrombosis in rats and the use of the filtragometer technique for evaluating the tendency to venous thrombosis in man. In rat studies (6,7) where arterial thrombosis was evaluated by an arterial loop technique, it was found that the primary thrombogenic components of the diet were myristic, palmitic, and stearic acids, but that linoleic acid had an anti-thrombotic effect and oleic acid a neutral effect. Fig. 3 shows the effect of sunflower-seed oil, an oil rich in polyunsaturated fatty acids, on the thrombotic ob-... [Pg.194]

Figure 3. Effect of oleic acid (10%) on the allo-purinol (0.75 gs/kg) induction of XDH in chick liver. Chicks were fed Startena (18% protein) for three weeks before materials were added to this diet. Controls ( ), allopurinol (O), oleic acid (A ), and allopurinol plus oleic acid ( ). The allopurinol was removed prior to measuring XDH activities (6). Figure 3. Effect of oleic acid (10%) on the allo-purinol (0.75 gs/kg) induction of XDH in chick liver. Chicks were fed Startena (18% protein) for three weeks before materials were added to this diet. Controls ( ), allopurinol (O), oleic acid (A ), and allopurinol plus oleic acid ( ). The allopurinol was removed prior to measuring XDH activities (6).

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See also in sourсe #XX -- [ Pg.192 ]




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