Cholesterol propionate

Ammonium sulfate triolein, oleic acid, androsten-3,17-dione, xanthanonic acid, cholesterol-propionate, N-methy Ipheny lalanine, D-glucose fluorescence after heating to 150 — 180 °C, exposure to tert-butyl hypochlorite [203]... 

Propionate is not a quantitatively significant gluconeogenic precursor in humans, but it is a major source of glucose in ruminants. It is derived from the catabolism of isolecucine, valine, methionine, and threonine from jd-oxidation of odd-chain fatty acids and from the degradation of the side chain of cholesterol. Propionate enters gluconeogenesis via the TCA cycle after conversion to succinyl-CoA (Chapter 18). 

Methylmalonyl CoA mutase, leucine aminomutase, and methionine synthase (Figure 45-14) are vitamin Bj2-dependent enzymes. Methylmalonyl CoA is formed as an intermediate in the catabolism of valine and by the carboxylation of propionyl CoA arising in the catabolism of isoleucine, cholesterol, and, rarely, fatty acids with an odd number of carbon atoms—or directly from propionate, a major product of microbial fer-... 

A metabolic product of fiber fermentation, propionate may mediate some of the hypocholesterolemic effects of certain soluble plant fibers. In cholesterol-fed rats, propionate decreases serum cholesterol and liver triglyceride level where no changes in hepatic histology in response to propionate intake have been detected (Wang and Ng, 1999). 

Differences in incorporation of radioactivity from the C-1 and C-2 carbons of propionate into cholesterol and bile acids by biliary fistula rats have been demonstrated. It appears that incorporation of propionate via HCO3" is not the major pathway. Feeding experiments with sodium [ C]bicarbonate produced no labelled cholesterol or bile acids. 

Fig. 11.6.1. HPLC separation of cholesterol and cholesteryl ester standards. Chromatographic conditions column, Supelcosil LC-18 (250x4.6 mm I.D.) mobile phase, acetonitrile-methanol-chloroform (1 1 1, v/v/v) flow rate, 1.0 ml/min temperature, ambient detection, differential refractometer. Peaks 1, cholesterol, 2, acetate 3, propionate 4, butyrate 5, nonanoate 6, decanoate 7, arachidonate 8, laurate 9, linoleate 10, oleate 11, elaidate 12, palmitate 13, stearate. The average mass of lipid chromatographed was 20-40 ng. Reproduced from Perkins et al. (1981), with...

Sathali et al. formulated a topical gel containing clobetasol propionate niosomes to prolong the duration of action and prevent side effects. The clobetasol propionate niosomes were prepared by altering the ratio of various non-ionic surfectants (Span 40,60, and 80) to cholesterol by the thin film hydration method. The in vivo results showed that the niosomal gel had a sustained as well as a prolonged action. 

With respect to the oxidation of the side chain in chenodeoxycholic acid formation, it may be inferred from the early studies with mitochondrial preparations that it involves an co-oxidation followed by a / -oxidation (cf. Section IIB). More direct evidence has been presented by Dean and White-house (87,91), who showed that mitochondrial preparations from rat liver catalyze the oxidation of 5-cholestene-3/ ,26-diol into 3/ -hydroxy-5-choles-tenoic acid and the formation of propionic acid from 3/5-hydroxy-5-choles-tenoic acid. Mitropoulos and Myant (97) have shown that mitochondrial preparations from rat liver catalyze the conversion of cholesterol into 5-cholestene-3/ ,26-diol, 3/ -hydroxy-5-cholestenoic acid, 3/5-hydroxy-5-chole-noic acid, lithocholic acid, and chenodeoxycholic acid (Fig. 5). Additional evidence for a pathway to chenodeoxycholic acid involving the successive, intermediary formation of above-mentioned compounds is provided by the finding that 3/ -hydroxy-5-cholenoic acid is converted into lithocholic acid and chenodeoxycholic acid by mitochondrial preparations (98). 

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