Abundance of dimethylamine in seafoods: possible implications in the incidence of human cancer

Levels of secondary and primary amines in various squids and other seafoods were determined by the newly developed dabsylation-HPLC method. Ammonia and dimethylamine were found in all of the seafoods analyzed, and some of them also contained methylamine, isobutylamine, ethylamine, and/or diethylamine. Extremely high levels of dimethylamine and methylamine were detected in all squids analyzed and in certain other seafoods. Very high activity of trimethylamine oxidase was observed in fresh squid tissue. Pyrolysis of sarcosine HCl and trimethylamine HCl yielded high levels of dimethylamine and methylamine. Various cooking conditions (extracting, frying, and broiling) had profound effects on amine content. Broiling was found to elevate the amine contents in most seafoods.     

A method of studying metabolic variation between individual tumors: A preliminary report

Levels of secondary and primary amines in various squids and other seafoods were determined by the newly developed dabsylation‐HPLC method. Ammonia and dimethylamine were found in all of the seafoods analyzed, and some of them also contained methylamine, isobutylamine, ethylamine, and/or diethylamine. Extremely high levels of dimethylamine and methylamine were detected in all squids analyzed and in certain other seafoods. Very high activity of trimethylamine oxidase was observed in fresh squid tissue. Pyrolysis of sarcosine HCl and trimethylamine HCl yielded high levels of dimethylamine and methylamine. Various cooking conditions (extracting, frying, and broiling) had profound effects on amine content. Broiling was found to elevate the amine contents in most seafoods. (Nutr Cancer 6,148–159, 1984)     

Conversion of dietary choline to trimethylamine and dimethylamine in rats: dose-response relationship

Trimethylamine (TMA) and dimethylamine (DMA) are normal components of human urine and are precursors of dimethylnitrosamine, a potent carcinogen. In part, DMA and TMA are products of the metabolism of dietary choline by intestinal bacteria. Most TMA formed in the intestinal tract is later oxidized and excreted as trimethylamine oxide (TMAO). Humans treated with large doses of choline smell "fishy" (the odor of TMA). Humans ingest choline as part of foods, and yet rarely smell fishy, suggesting that TMA formation must depend upon the dose of choline ingested. We found that, in adult rats, at low doses of choline (1.5 mmol/kg body wt) only 9 mumol choline (6% of the dose) reached the part of the intestine which is colonized by bacteria (the cecum and colon). After administration of 15 mmol choline/kg body wt, 237 mumol (16% of the dose) reached the cecum and colon. At both doses, 64-65% of the administered choline was absorbed from the intestine by 3 h after the dose. We found that orally administered choline slightly increased TMA and TMAO excretion at doses of choline smaller than 7 mmol/kg body wt, but that there was a disproportionately large increase in TMA excretion per 24 h when larger doses were administered (from 11 mumol TMA and 100 mumol TMAO per kg body wt in controls to 226 mumol TMA and 3617 mumol TMAO per kg body wt in rats treated with 15 mmol choline/kg body wt).(ABSTRACT TRUNCATED AT 250 WORDS)     

A study of the effects of dietary gum arabic in the rat

Gum arabic (GA) is a water-soluble polysaccharide (molecular weight approximately 850 000) containing rhamnose, arabinose, glucuronic acid and galactose. The metabolism of GA has been studied in the rat. Adult male Wistar rats were given GA incorporated into either an Oxoid breeders (OB) diet or an elemental (Elem) diet. Intestinal contents were examined for precipitable GA using acidified ethanol. GA was found from stomach to small intestine but not in the caecum, colon or rectum. Caecal excision and restoration of intestinal continuity resulted in GA recovery from stomach to rectum. Excreted methane, hydrogen and volatile fatty acids (VFA) were measured as indicators of bacterial activity in the caecum and colon. Methane excretion increased on the OB + GA diet and H2 concentrations remained unaltered. The Elem diet abolished gas production. When the animals were given the Elem + GA diet, H2 and methane were only produced after 28 d. Faecal VFA increased with increasing GA intake, acetate concentration increased and butyrate concentration decreased with increasing GA dosage. Significant decreases in concentrations of VFA were found from caecum to left colon and from left colon to faeces. It can be concluded that GA degradation occurs in the caecum and is associated with increased methane excretion, increased VFA concentrations and changes in the proportions of various VFA in the faeces.     

Phosphorus-induced nephrocalcinosis and kidney function in female rats

The question was addressed whether dietary phosphorus-induced nephrocalcinosis in rats is associated with impaired kidney function. Weanling female rats were fed purified diets containing either 0.4 or 0.6% (wt/wt) phosphorus for 28 d. The diet containing 0.6% phosphorus produced marked kidney calcification, as determined both by chemical analysis of kidney calcium and histological examination in kidney sections. Histological examination did not show calcification in stomach, lung, heart or thoracic aorta, which are predisposition sites of metastatic calcification in secondary renal hyperparathyroidism. In rats fed the 0.6% phosphorus diet, phosphorus retention and urinary excretion were greater compared with rats fed the 0.4% phosphorus diet. The following indicators of kidney function were examined: water intake, urinary volume, urine and plasma osmolality, urine and plasma creatinine, urine and plasma urea, urea and creatinine clearance and urinary albumin excretion. Of these indicators, only urinary albumin excretion was significantly increased in rats fed the nephrocalcinogenic diet. In a further experiment, the increase of urinary albumin was reproduced. After pooling the results of the two experiments, in individual rats fed the 0.6% phosphorus diet, the concentration of kidney calcium was found to be positively related with kidney weight expressed relative to body weight (r = 0.82, n = 22) and with albumin excretion in urine (r = 0.79, n = 28). The increased weight of calcinotic kidneys was mainly due to both calcium deposition and tubular hyperplasia. It is concluded that dietary phosphorus-induced nephrocalcinosis is associated with impaired kidney function in rats.     

Effects of two fermentable carbohydrates (inulin and resistant starch) and their combination on calcium and magnesium balance in rats

Resistant starch and inulin are complex carbohydrates that are fermented by the microflora and known to increase colonic absorption of minerals in animals. The fermentation of these substrates in the large bowel to short-chain fatty acids is the main reason for this increase in mineral absorption. The purpose of the present study was to examine the potential synergistic effect of a combination of these two fermentable carbohydrates. For this purpose, thirty-two adult male Wistar rats weighing 200 g were used in the present study. The rats were distributed into four groups, and fed for 21 d a fibre-free basal purified diet or diet containing 100 g inulin, or 150 g resistant starch (raw potato starch)/kg diet or a blend of 50 g inulin and 75 g resistant starch/kg diet. After an adaptation period of 14 d, the rats were then transferred to metabolic cages and dietary intake, faeces and urine were monitored for 5 d. The animals were then anaesthetized and caecal Ca and Mg absorption were measured. Finally, the rats were killed and blood, caecum and tissues were sampled. Ca and Mg levels were assessed in diets, faeces, urine, caecum and plasma by atomic absorption spectrometry. Our results confirmed that inulin and resistant starch ingestion led to considerable caecal fermentation in the three experimental groups compared with the control group diet. Moreover, both carbohydrates significantly increased the intestinal absorption and balance of Ca and Mg, without altering the plasma level of these two minerals. Interestingly, the combination of the studied carbohydrates increased significantly the caecal soluble Ca and Mg concentrations, the apparent intestinal absorption and balance of Ca, and non-significantly the plasma Mg level. In conclusion, a combination of different carbohydrates showed synergistic effects on intestinal Ca absorption and balance in rats. Further studies with other types of carbohydrate combinations should be carried out to extend these findings.     

Comparative effects of choline chloride and phosphatidylcholine on plasma and liver lipid levels in rats fed a choline-deficient high cholesterol diet

The effects of dietary choline chloride and phosphatidylcholine (PC) on plasma and liver lipid levels were investigated with rats fed a choline-deficient high cholesterol diet. The plasma cholesterol level significantly increased as the dietary level of choline chloride was increased. The addition of PC to the choline-free diet also resulted in an increase in the plasma cholesterol level, but the magnitude of the increase was significantly lower than that by choline chloride. There was no difference, on the other hand, in the effect of choline chloride and PC on the plasma triglyceride level. The contents of cholesterol and triglyceride in the liver markedly decreased in rats fed a diet containing PC at a high level. The fecal excretion of neutral sterol significantly increased by the addition of PC at a high level, but not at a low level. The results indicate that the plasma cholesterol level, but not triglyceride, is differentially influenced by dietary choline chloride and PC, and that PC has both hyper- and antihypercholesterolemic effects when compared with a choline-free diet and a diet supplemented with choline chloride, respectively.     

Effects of prenatal ethanol exposure on postnatal renal function and structure in the rat

Effects of prenatal ethanol exposure on postnatal renal function and structure in the rat. Renal function and morphology were studied in 90-day-old offspring of ethanol-fed (E) rats and were compared to pair-fed control (C) animals. Compared to C rats, E rats were smaller at birth, had higher fractional sodium excretion (p less than 0.01) and lower fractional potassium excretion (p less than 0.01). In E rats, sodium (Na) restriction resulted in a significant increase in urine flow and Na wastage, whereas C rats remained in Na balance. E rats developed hyperkalemia, when potassium (K) intake was increased from 2.8 to 14 mEq/day. Baseline creatinine clearance, urine and blood osmolalities and pH, plasma electrolytes and aldosterone concentrations were similar in both groups. There was no significant difference in wet or dry kidney weight, renal water content, or renal tissue concentrations of Na or K between the two groups. No difference was found in gross morphology or light microscopic appearances of the kidneys between E and C rats. Thus rats exposed to ethanol during fetal life have a defect in urine concentration and Na conservation when fed a low Na diet and a defect in K excretion when given a K load without evidence of any gross or light microscopic renal structural abnormalities at 90 days of age.     

Biotin studies in pigs. 5. The post-ileal absorption of biotin

Six pigs were given a biotin-deficient diet (10 micrograms biotin/kg) for 14 weeks. The pigs were given the same diet for a further 42 d with one of three biotin treatments: no supplement, 400 micrograms biotin/d given orally, 400 micrograms biotin/d infused into the caecum. The concentrations of biotin in the liver, kidney and heart, at the conclusion of 42 d were greater in the pigs given the oral biotin supplement than in the unsupplemented pigs. The values for the pigs given the caecal infusion of biotin were intermediate. The excretion of biotin in faeces was increased from 35 to 101 micrograms/d by the caecal biotin infusion, and the urinary excretion was increased from 35 to 83 micrograms/d. The oral dose of biotin increased urinary biotin excretion from 35 to 345 micrograms/d, but there was no change in faecal biotin excretion. Two pigs were fitted with ileal cannulas and catheters in the vena cava. The pigs were given a dose of [14C] biotin either into the caecum, when the ileum was occluded by a bladder catheter, or orally. [14C] biotin was measured in the urine and plasma and showed that post-ileal biotin absorption was 8% as efficient as the absorption of biotin after oral dosing.     

Evidence that polyunsaturated lecithin induces a reduction in plasma cholesterol level and favorable changes in lipoprotein composition in hypercholesterolemic rats

For 30 d adult rats were fed a hypercholesterolemic (H) diet (25% saturated fat, 1% cholesterol and 0.5% cholic acid) containing different amounts of saponins (1% or 0.2%) and/or purified polyunsaturated lecithin (2.5% or 0.7%). Lecithin induced a striking reduction in the plasma levels of very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL) and low density lipoprotein (LDL) cholesterol as well as an increase in the level of high density lipoprotein (HDL) cholesterol. Saponins had only a very slight effect in lowering the level of VLDL cholesterol. Apoprotein A-I was unexpectedly present in VLDL, IDL and LDL after feeding rats the H diet and disappeared only after lecithin feeding. The activity of plasma lecithin-cholesterol acyltransferase was higher when the two lecithin diets were fed than when the other diets were fed. Fecal excretion of neutral sterols was unmodified by the various diets whereas acid steroid excretion increased after lecithin feeding. Saponins, when added with lecithin to the diet, reduced the beneficial effect of lecithin. The results indicate that polyunsaturated lecithin induced a reduction in plasma cholesterol, possibly through an increased formation of HDL particles.     

Consumption of fructooligosaccharides and nitrogen excretion in cats

In a cross-over study with adult cats the effect on nitrogen (N) excretion of a diet supplemented with fructooligosaccharides (FOS) was compared with a diet supplemented with an equal amount of fructose and glucose. FOS raised N excretion with faeces by 26% (P < 0.05) and non-significantly lowered N excretion with urine by 5%. Thus, there was a shift in N excretion from urine to faeces. The amount of faecal dry matter was significantly higher (by 23.3%) when FOS was consumed.     

Effects of dietary fibre and tannins from apple pulp on the composition of faeces in rats.

The present study was undertaken to explore the effect of apple pulp on weight and composition of faeces. This material is rich in dietary fibre (DF; 620 g dry matter/kg) and contains appreciable amounts of polyphenols. Recent reports indicate that both condensed tannins (CT) and soluble polyphenols form cross-links with protein and inhibit digestive enzymes, affecting the protein digestibility, and may produce a stimulation of endogenous nitrogen excretion. Two groups of male Wistar rats were fed on either a control diet free of DF or a diet containing 100 g apple pulp DF/kg during 7 d after a 4 d adaptation period. Body-weight and food intake were monitored daily and faeces and urine were collected once daily. DF, water content and polyphenolic compounds were measured in faeces, and N content in both faeces and urine. Faecal weight increased in the fibre group by 280 and 240% when compared with wet and dry faecal weights of animals fed on the fibre-free diet. Soluble dietary fibre (SDF) excreted in faeces was 10.9% of the SDF ingested, which suggested a low resistance to fermentation of this fraction. Of the insoluble DF, 43% of the ingested fibre was fermented. Polyphenols were degraded in the intestinal tract. Of the ingested CT, 68.6% was recovered in faeces, while the soluble polyphenols were extensively degraded (85.7% of that ingested). On the other hand, a higher faecal N excretion was observed for the fibre-fed group, suggesting a decrease in the digestibility of the dietary protein and lower apparent digestibility of the dietary protein and lower apparent digestibility and N balance indices.     

Effects of sulphate- and bicarbonate-rich mineral waters on net and fractional intestinal absorption and urinary excretion of magnesium in rats

Summary. Magnesium (Mg) intake is below the recommended daily allowances in many developed countries. Mg-rich mineral waters can provide significant amounts of energy-free Mg and thus help to meet Mg requirements. We assessed the effects of different Mg-rich mineral waters on overall intestinal Mg absorption and urinary Mg excretion in 40 rats split into four groups: one received distilled water, another a solution of MgCl₂ and the others two different mineral waters, sulphated water (Hépar) and carbonated water (Badoit) mixed with the diet and as drinking water, for four weeks. The rats were given 3 mg of ²⁶Mg orally and 0.5 mg of ²⁵Mg intravenously. They were placed in metabolic cages, and diet consumption, and faeces and urine excretion were monitored during the last four days of the experiment. The rats were then sacrificed and blood was sampled. Mg levels in the diet, faeces, urine and biological samples were measured by atomic absorption spectrometry. Mg stable isotope measurements were performed by ICP/MS. Mg-rich mineral waters significantly increased net intestinal absorption of Mg by more than 30%, but the proportions of both apparent and true intestinal absorption of Mg were similar in all four groups. Thus, net and fractional retention of Mg were similar in the three Mg-supplemented groups. In conclusion, both types of Mg-rich mineral waters studied similarly increased both absorption and urinary excretion of Mg with no positive effect on the overall retention of Mg, probably because the Mg status of the rats was already satisfactory.Ca Calcium - Mg Magnesium     

Increase of urinary ketone body excretion in selenium-deficient rats is a ketone-specific change.

The effects of selenium (Se) deficiency on urinary ketone body excretion in starved rats were examined. Rats were fed a basal diet which was Se-deficient (Se content: 0.011 micrograms/g) or a Se-adequate diet (the basal diet supplemented with 0.1 micrograms Se/g as sodium selenite). On the 11th and 22nd week of the feeding period, Se-deficient status in rats fed the basal diet was verified by the observation that the Se content and glutathione peroxidase activity in their plasma, erythrocytes, and livers were markedly lowered. On the 4th, 6th, 11th, 15th, and 22nd week, the rats were starved for 48 h and the urinary excretion of ketone bodies (acetoacetate (AcAc) and 3-hydroxybutyrate (3-OHBA)), urea, and creatinine were examined. The urinary excretion of AcAc and 3-OHBA during the second 24 h of the 48-h starvation period were markedly higher in the Se-deficient rats than in the Se-adequate rats for all weeks examined, while the urine volume and the excretion of urea and creatinine were similar in the Se-deficient and Se-adequate rats, irrespective of the feeding period and the number of hours of starvation. On the 22nd week, the plasma ketone body levels were also determined and significantly higher plasma 3-OHBA levels were observed in the Se-deficient rats than in the Se-adequate rats 72 h after starvation began. These results indicate that Se deficiency causes an increase of urinary ketone body excretion in starved rats and that the increase is ketone-specific with no changes in major urinary profiles.     

The effect of a single oral dose of ethyl linoleate on urinary prostaglandin E2 excretion in essential fatty acid-deficient rats

The effects of a single oral dose of ethyl linoleate on urinary prostaglandin E2 (PGE2) excretion and urine output were investigated in essential fatty acid (EFA)-deficient rats. Weanling male rats were fed a fat-free diet. After 13 wk of feeding, eight rats received an oral dose of 400 mg of ethyl oleate. Seven days later the same eight rats received 400 mg of ethyl linoleate. The oleate dosage served as control. Another seven EFA-deficient rats received an oral dose of 100 mg of ethyl linoleate. The 24-h urine collections from each animal were analyzed for PGE2 by radioimmunoassay. Within 24 h the oleate dose resulted in a 1.3-fold increase in urinary PGE2 excretion. The 400-mg dose of ethyl linoleate induced a 2- to 3-fold increase in urinary PGE2 excretion during 7 d. The 100-mg dose of ethyl linoleate resulted in a 1.3- to 1.5-fold increase for 2 d. Neither the ethyl oleate dose nor the low dose of ethyl linoleate had any effect on urine output, whereas the high dose of ethyl linoleate induced a slow increase during the following 6 d. The present results show that a single dose of 400 mg of ethyl linoleate increased urinary PGE2 excretion and urine output in EFA-deficient rats. However, these two parameters do not seem to be correlated. The amount of urinary PGE2 excreted in excess of baseline urinary PGE2 excretion accounted on a molar basis for less than 1 ppm of the administered dose of ethyl linoleate.     

Effect of potassium salts in rats adapted to an acidogenic high-sulfur amino acid diet

Low-grade metabolic acidosis, consecutive to excessive catabolism of sulfur amino acids and a high dietary Na:K ratio, is a common feature of Western food habits. This metabolic alteration may exert various adverse physiological effects, especially on bone, muscle and kidneys. To assess the actual effects of various K salts, a model of the Westernised diet has been developed in rats: slight protein excess (20 % casein); cations provided as non-alkalinising salts; high Na:K ratio. This diet resulted in acidic urine (pH 5.5) together with a high rate of divalent cation excretion in urine, especially Mg. Compared with controls, K supplementation as KCl accentuated Ca excretion, whereas potassium bicarbonate or malate reduced Mg and Ca excretion and alkalinised urine pH (up to 8). In parallel, citraturia was strongly increased, together with 2-ketoglutarate excretion, by potassium bicarbonate or malate in the diet. Basal sulfate excretion, in the range of 1 mmol/d, was slightly enhanced in rats fed the potassium malate diet. The present model of low-grade metabolic acidosis indicates that potassium malate may be as effective as KHCO3 to counteract urine acidification, to limit divalent cation excretion and to ensure high citrate concentration in urine.     

Urinary felinine excretion in intact male cats is increased by dietary cystine

Felinine is a branched-chain sulfur amino acid present in the urine of certain Felidae, including domestic cats. The objective of the present study was to determine if additional cystine and/or dietary N would increase felinine and N-acetylfelinine excretion by intact male cats fed a low-protein(LP) diet. Feeding five adult intact male cats an LP diet (18.8% of metabolisable energy (ME) as protein) v. a high-protein diet (38.6% of ME as protein) resulted in a trend (P=0.08) for decreased urinary felinine and no change in N-acetylfelinine excretion. In a 23 d study, when the LP diet was supplemented with L-cystine at 9.3 g/kg DM, urinary felinine:creatinine ratio showed a linear two-fold (121 %) increase (P<0.01) from 0.24 (SEM 0.05) to 0.53 (SEM 0.13) after 10 d. Subsequent feeding of the LP diet resulted in a decrease in felinine excretion to base levels. Plasma gamma-glutamyl felinylglycine concentrations were consistent with the excretion of felinine. Supplementation of the LP diet with L-cystine (9.3 g/kg DM),dispensable amino acids and arginine to a second group (n 5) also resulted in a significant (P<0.01) but smaller (+72 %) increase in the daily felinine:creatinine ratio (0.25 (SEM 0.04) to 0.43 (SEM 0.05)). The degree of felinine N-acetylation within groups was unaffected by dietary addition and withdrawal of amino acids. The results indicate that felinine synthesis is regulated by cystine availability, and that arginine may be physiologically important in decreasing felinine biosynthesis in intact male cats.     

THE UTILIZATION OF THE METHYL GROUP OF METHIONINE IN THE BIOLOGICAL SYNTHESIS OF CHOLINE AND CREATINE

The transfer of methyl groups from methionine to choline and creatine has been demonstrated by the isolation of deuteriocholine and deuteriocreatine from the tissues, and of deutriocreatinine from the urine, or rats fed methionine containg a deuteriomethyl group. It was found from the deuterium ocntents of the isolated compounds that at the end of a given experimental period, each of the isolated compounds had derived approximately the same percentage of methyl groups from the deuteriomethionine of the diet. All the deuterium in the isolated choline was shown to be in the methyl grops. The concentraion of deuterium in the methyl gorups of the choline and creatine from the tissues as well as of the urinary creatinine rose to 85 per cent of that of the deuterio-methionine fed over a period of 14 weeks, strongly indicating that there was no other precursor of methyl groups in the diet employed.
The transfer of methyl groups from choline to creatime has been demonstrated by the isolation of deuteriocreatime from the tissues and of deuteriocreattnine from the urine of rats maintained on a diet containing deuteriocholine and homocystine.
Thus direct proof has been afforded to substantiate the hypothesis previously presentd that methionine may be a precursor of choline in so far as the methyl groups are concerned. The significance of these findings with regard to the prevention of fatty infiltraton of the liver and to the prevention of hemorrhagic kidneys resulting from a choline-deficient diet has been pointed out. The data support the hypothesis that the body is incapable of generationg methyl groups for certain methlations and that methyl groups must be supplied in the diet in a biologically labile from such as occurs in methionine and choline.     

Differences in uricogenic effects of dietary purine bases, nucleosides and nucleotides in rats

The uricogenic effects of dietary free purines (adenine, guanine, hypoxanthine and xanthine), their nucleosides (adenosine, monophosphate, guanosine monophosphate and inosine monophosphate) were studied in rats. Casein-based diets (20% protein) supplemented with 30 mmol/kg diet of each of the free purine base, nucleoside or nucleotide were fed to male Sprague-Dawley rats (100 +/- 5 g) for 14 d. Addition of adenine resulted in less weight gain than in controls, greater kidney weight, greater urine volume and higher levels of blood urea nitrogen, serum uric acid, creatinine and allantoin but lower urinary levels of allantoin, uric acid and creatinine. The adenine diet also caused nephropathy characterized by nephromegaly and deposition of crystals. A microscopic examination of the kidneys revealed deposition of crystals mainly in the lumen of convoluted tubules of the cortex. Feeding of diets containing other purine bases, nucleosides and nucleotides had no adverse effects on kidney weight or structure, urine volume, serum uric acid or creatinine. Urinary allantoin excretion, however, was greater in rats fed hypoxanthine, xanthine, nucleoside and nucleotide diets than in control rats. Adenine produced adverse effects only when fed in the free form and not when fed as the nucleoside or nucleotide, suggesting a metabolic significance for free adenine in predicting hyperuricemic effects of foods.     

Calculogenic potential of galactose and fructose in relation to urinary excretion of lithogenic substances in vitamin B6 deficient and control rats.

Calculogenic potential of refined sugars galactose and fructose was examined in vitamin B6 deficient and control rats in terms of their capacity to increase urinary excretion of lithogens.

Male albino rats were fed vitamin B6 deficient diet with 51.7% sucrose+ starch or galactose or fructose as the source of carbohydrate. Pair-fed controls were maintained for all the groups for a period of four weeks. Twenty-four hour urine samples obtained at weekly intervals were analyzed for creatinine, calcium, oxalate, phosphate and uric acid. Microscopic urinalysis was performed at the end of the study.

Urinary calcium excretion increased with respect to baseline in all groups except vitamin B6 control group. On day 28, galactose and fructose-fed rats demonstrated significant hypercalciuria as compared to the sucrose + starch fed group. Vitamin B6 deficient rats (irrespective of the sugar fed) excreted significantly greater urinary calcium compared to pair-fed controls. Oxalate excretion was significantly increased in rats fed galactose compared to those fed fructose or sucrose + starch. Vitamin B6 deficiency further increased oxalate excretion by 1.5, 1.9 and 1.7 fold in sucrose + starch, fructose or galactose fed animals, respectively. Urinary uric acid excretion was enhanced only in fructose-fed rats. There was no change in urinary excretion of creatinine and phosphate in different experimental and control groups. Increased urinary saturation with lithogens caused pronounced crystalluria in all the vitamin B6 deficient groups as well as galactose control group.

The results suggest galactose ingestion is associated with a greater propensity to form calcium oxalate kidney stones than fructose. Calculogenic potential of galactose and fructose is further enhanced in vitamin B6 deficiency.