The Pathways of Oxalate Biosynthesis

Richardson, K.E.; Farinelli, Michael P.

doi:10.1007/978-1-4684-8977-4_137

Cited by 4 publications

(1 citation statement)

References 16 publications

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“…when low levels of xylulokinase are assumed for humans, predicted by the kinetic computer model (39). The major metabolic precursors of oxalate, glycolate, and glyoxalate are known to have several metabolic precursors besides xylitol and several metabolic fates besides oxalate (see reviews 7,76,126). It has been suggested that the conversion of xylitol to oxalate is regulated primarily at the level of glyoxalate or glycolate metabolism (7,15).…”

Section: Dillsmentioning

confidence: 99%

Sugar Alcohols as Bulk Sweeteners

Dills¹

1989

Annu. Rev. Nutr.

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The polyols are a family of bulk sweeteners, some of which are currently used in the United States and in other nations. The use of these compounds is likely to increase in the future. The greatest advantage of polyols as sweeteners is their reduced cariogenicity compared with sucrose, fructose, or glucose. This reduced cariogenicity has been observed with all of the polyols considered in this review. Furthermore, evidence suggests that one of these polyols, xylitol, may have cariostatic properties. More research is needed to clarify the mechanism of this cariostatic effect. Evidence suggests that moderate usage of the polyols in human diets over long periods is not likely to produce many toxic effects. This conclusion is supported by the facts that (a) both sorbitol and mannitol have been used as sweeteners for some time without apparent side effects, and (b) extensive long-term studies with dietary xylitol in Europe have not yielded any reports of toxicity. At this point there is no reason to believe that the disaccharide polyols differ significantly in a qualitative sense from sorbitol or mannitol with regard to their effects in humans. There are some research needs with regard to the inclusion of the polyol sweeteners in human diets: 1. All of the polyols can cause osmotic diarrhea in humans if higher levels are consumed. This fact is noted in the labelling of products containing mannitol and sorbitol in the United States (see "Current Regulatory Status"). If the disaccharide polyols are to be used as bulk sweeteners, further studies of the dose levels that can cause diarrhea may be needed. 2. The polyols, like other slowly absorbed carbohydrates, enhance the absorption of certain minerals, particularly divalent cations. More comparative and mechanistic studies of this effect are needed. 3. All of the polyols, lactose, and other slowly absorbed carbohydrates appear to cause adrenal medullary hyperplasia at high doses in laboratory rats. Evidence suggests that these lesions are linked in some way to the lactose or polyol-induced changes in calcium homeostasis. Despite long-term use of lactose, sorbitol, and mannitol in human diets, similar lesions in humans have not been reported and some investigators have concluded that the lesion in rats has no relevance to humans. Nevertheless further studies are needed to elucidate the mechanisms of the dietary lactose and polyol-induced adrenal hyperplasias in rats to ascertain definitively if they also operate in other species.(ABSTRACT TRUNCATED AT 400 WORDS)

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Section: Dillsmentioning

confidence: 99%

Sugar Alcohols as Bulk Sweeteners

Dills¹

1989

Annu. Rev. Nutr.

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Primary Hyperoxaluria

Watts¹,

Mansell²

1988

Oxalate Metabolism in Relation to Urinary Stone

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Extrarenal clearance of oxalate increases with progression of renal failure in the rat.

Costello

Smith²,

Stolarski³

et al. 1992

Journal of the American Society of Nephrology

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Oxalic acid is an end product of metabolism, and no significant degradation of oxalate occurs in mammals. The sole route of oxalate excretion is believed to be via the kidney. The extrarenal clearance of oxalate in control rats (N = 16) and in 5/6 nephrectomized rats (N = 25) with renal insufficiency was investigated. [14C]oxalic acid, approximately 2 microCi/day, was infused sc by a mini osmotic pump over 4 days. Excretion of 14C was measured in urine, in feces, and in expired CO2. The 14C content of kidney, heart, liver, muscle and bone was also determined at the time the animals were killed. Plasma oxalate was determined by an enzymatic method and by an isotopic dilution procedure. Creatinine clearance in the controls was 1.82 +/- 0.1 mL/min (mean +/- SE) compared with 0.31 +/- 0.04 mL/min (P < 0.0005) in the nephrectomized rats. Plasma oxalate was 5.6 +/- 0.6 mumol/L in controls and 27.0 +/- 3.9 (mean +/- SE; N = 24) in nephrectomized animals (P < 0.0005). The total 14C recovered in urine, feces, and CO2 combined was similar in both groups. The 14C excreted in the feces over the 4-day period was 27.8 +/- 1.5% (of the 14C recovered) in rats with renal failure and 6.5 +/- 0.5% in controls (P < 0.0005). Percent fecal 14C excretion in nephrectomized rats was inversely correlated with creatinine clearance (r = 0.80; P < 0.0001) and directly correlated with plasma oxalate (r = 0.66; P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

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The Pathways of Oxalate Biosynthesis

Cited by 4 publications

References 16 publications

Sugar Alcohols as Bulk Sweeteners

Sugar Alcohols as Bulk Sweeteners

Primary Hyperoxaluria

Extrarenal clearance of oxalate increases with progression of renal failure in the rat.

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