Brewer's yeast was grown on a defined medium containing tracer 51Cr with or without added chromium. The two batches of yeast contained 10 μg/g (high-Cr) or 80 ng/g (low-Cr). Extracts were prepared and fractionated. A third batch of yeast (third batch) was grown with added Cr, and fractionated. Rats were reared on either rat cubes (normal diet) or on a low-Cr diet (low-Cr), or on rat cubes with added cholestyramine (cholestyramine diet). Preparations of rat liver, both cell-free and intact hepatocytes, incorporated acetate-carbon into fatty acids and cholesterol. These processes were inhibited by a yeast fraction containing small, neutral, water-soluble compounds. The degree of inhibition was the same whether the liver came from normal rats or rats fed on the low-Cr diet. Similarly the inhibitory effect was found with identical amounts of extracts from low- or high-Cr yeasts. Therefore, Cr compounds do not appear to account for the inhibitory effects of brewer's yeast. Use of other substrates indicated that the site of inhibition of sterol synthesis was apparently between acetyl-CoA and mevalonate. One inhibitory substance was isolated from yeast and was found to be nicotinamide riboside. This may have been produced from NAD(P) during the preparation of yeast extracts, and it may be produced from dietary yeast supplements during digestion in vivo. Nicotinamide riboside may be partly responsible for the reported effects of yeast supplements on plasma lipids in humans.
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