Gerard A. Walsh

The effects of dietary supplementation with Yucca schidigera extract or fractions thereof on nitrogen metabolism and gastrointestinal fermentation processes in the rat

Yucca schidigera was fractionated with butan-1-ol, yielding a butanol-extractable (BE) fraction, containing all the in vitro antimicrobial activity, and the aqueous, non-butanol-extractable (NBE) fraction. Four groups of five female rats (12 weeks old) were allowed ad libitum access to diets supplemented with water (control) or 200 mg kg -1 total Y. schidigera (TOT) or its fraction equivalent of NBE or BE for 64 days. The effects of the fractions and their interactions in the TOT treatment were analysed according to the factorial experimental structure by two-way ANOVA. NBE reduced serum urea (-50%, P = 0.019) and ammonia (-46%, P = 0.037) concentrations, serum/urine concentration quotients of urea (-79%, P = 0.009) and ammonia (-57%, P = 0.002). NBE also reduced hindgut acetate/propionate (-12%, P = 0.007) but increased faecal ammonia concentration (+87%, P = 0.039). BE reduced hindgut indoles (-25%, P = 0.023) and interacted synergystically with NBE in the TOT treatment to further reduce hindgut acetate/propionate by 6% (P = 0.006). NBE increased (+27%, P = 0.002) and BE decreased (-57%, P = 0.005) hindgut urease activity levels, resulting in essentially no change (+4%) in the TOT treatment. The in vitro antimicrobial activity of Y. schidigera is an unlikely explanation for most of its effects in vivo because these are caused by NBE and in vitro antimicrobial activity is exclusive to BE. Sarsasapogenin and smilagenin were also exclusive (>98%) to BE and cannot account for the effects of Y. schidigera on N metabolism.

CORRELATION OF RAT HEPATIC PHENYLALANINE HYDROXYLASE, WITH TETRAHYDROBIOPTERIN AND GTP CONCENTRATIONS

Hepatic phenylalanine hydroxylase is reported to be more abundant in experimentally-diabetic rats; whereas livers of animals fed a high protein diet, where gluconeogenesis also prevails, have normal amounts of this enzyme. In this study, in addition to seeking an explanation for this effect of experimental diabetes, we also examined the effects of providing alternative dietary gluconeogenic substrates. In rats fed a diet composed of 40% (w/w) glycerol, the specific activities of hepatic phenylalanine hydroxylase are decreased to about 60% of control values. There is no effect on the apparent state of phosphorylation of the enzyme. However, studies on the incorporation of radiolabelled leucine into liver phenylalanine hydroxylase suggested that there was a decreased rate of synthesis. Similarly, animals fed a diet containing 85% (w/w) fructose also have diminished phenylalanine hydroxylase activities. Under all of the above circumstances and also in streptozotocin-induced diabetic animals, alterations in the concentrations of the hydroxylase cofactor, tetrahydrobiopterin and of GTP closely correlate with the effects on the enzyme activities. They are elevated in livers of diabetic animals and significantly diminished in livers of rats fed diets rich in glycerol or fructose. These observations suggest that in adult rat both liver tetrahydrobiopterin concentrations and the expression of hepatic phenylalanine hydroxylase are regulated by GTP [210].