Dietary soy protein isolate and isoflavones modulate hepatic thyroid hormone receptors in rats

Thyroid hormone receptors (TRs) are regulators of many genes involved in cholesterol and lipid metabolism. The purpose of this study was to examine the effect of soy protein isolate (SPI) and isoflavones on hepatic TRs in rats. In Expt. 1, Sprague-Dawley rats were fed diets containing either casein or alcohol-washed SPI with or without isoflavone supplementation (5-1250 mg/kg diet) for 70, 190, and 310 d. The offspring (F1) were fed the same diets as their parents (F0). In Expt. 2, Sprague-Dawley rats were fed diets containing casein or casein plus isoflavones (50-400 mg/kg diet) for 120 d. The mRNA and protein contents of the hepatic TRs were measured by semiquantitative RT-PCR and Western blot, respectively. TRalpha1, TRalpha2, and TRbeta2 contents were not affected by SPI. However, the content of the 52-kDa TRbeta1 protein, the major isoform present in the liver, was markedly increased by dietary SPI in both sexes of F0 and F1 compared with casein. The supplemental isoflavones had no effect on TRbeta1, whereas the high doses of isoflavones (250 and 1250 mg/kg diet) reduced the hepatic TRalpha1 protein content in F1 male rats on d 28. SPI had no effect on total T3 and T4 levels. However, higher dose of supplemental isoflavones markedly increased T4 level in female rats. Overall, this study demonstrates for the first time that SPI upregulates hepatic TRbeta1 expression, and that isoflavones reduce the hepatic TRalpha1 level in young male rats. The SPI-induced TRbeta1 may play a role in mediating the hypocholesterolemic and lipid-lowering actions of soy protein.     

Dietary soy protein isolate modifies hepatic retinoic acid receptor-beta proteins and inhibits their DNA binding activity in rats

Retinoic acid receptors (RAR) belong to the same nuclear receptor superfamily as thyroid hormone receptors (TR) that were previously shown to be modulated by dietary soy protein isolate (SPI). This study has examined the effect of dietary SPI and isoflavones (ISF) on hepatic RAR gene expression and DNA binding activity. In Expt. 1, Sprague-Dawley rats were fed diets containing 20% casein or 20% alcohol-washed SPI in the absence or presence of increasing amounts of ISF (5-1250 mg/kg diet) for 70, 190, or 310 d. In Expt. 2, weanling Sprague-Dawley rats were fed diets containing 20% casein with or without supplemental ISF (50 mg/kg diet) or increasing amounts of alcohol-washed SPI (5, 10, and 20%) for 90 d. Intake of soy proteins significantly elevated hepatic RARbeta2 protein content dose-dependently compared with a casein diet, whereas supplemental ISF had no consistent effect. Neither RARbeta protein in the other tissues measured nor the other RAR (RARalpha and RARgamma) in the liver were affected by dietary SPI, indicating a tissue and isoform-specific effect of SPI. RARbeta2 mRNA abundances were not different between dietary groups except that its expression was markedly suppressed in male rats fed SPI for 310 d. DNA binding activity of nuclear RARbeta was significantly attenuated and the isoelectric points of RARbeta2 were shifted by dietary SPI. Overall, these results show for the first time, to our knowledge, that dietary soy proteins affect hepatic RARbeta2 protein content and RARbeta DNA binding activity, which may contribute to the suppression of retinoid-induced hypertriglyceridemia by SPI as reported.     

Soy protein isolate increases hepatic thyroid hormone receptor content and inhibits its binding to target genes in rats

Our previous studies showed that intake of 20% alcohol-washed soy protein isolate (SPI) significantly increased hepatic thyroid hormone receptor (TR) beta1 protein content in rats. However, whether SPI influences the binding ability of TR to its target genes is unknown. The purpose of this study was to examine the effect of increasing amounts of dietary SPI on hepatic TRbeta1 content and the binding of TR to thyroid hormone response element (TRE) in rats. Sprague-Dawley rats (28 d old) were fed diets containing casein (20%) with or without isoflavone supplementation (50 mg/kg diet) or alcohol-washed SPI (5, 10, or 20%) for 90 d. The hepatic TRbeta1 protein content was measured by Western blot, and the binding ability of TR to DNA was examined by electrophoretic mobility shift assay. Consumption of the 20% SPI diet increased pancreatic relative weight and decreased spleen relative weight. Intake of SPI markedly elevated TRbeta1 content in both male and female rats compared with a casein-based control diet. The increase in TRbeta1 in females was much higher than that in males. Interestingly, the binding abilities of TR to DNA were significantly inhibited by increasing amounts of dietary SPI in female rats. In conclusion, this study shows for the first time that dietary SPI increases hepatic TRbeta1 protein content and inhibits the binding of TR to target genes. Modulation of hepatic TRbeta1, a key regulator of gene expression involved in lipid metabolism, by SPI may be a novel mechanism by which soy components lower blood lipid level and exert their hypocholesterolemic actions.     

A ketogenic diet increases protein phosphorylation in brain slices of rats

Ketogenic diets have been used to treat seizure disorders of children and recently it was shown to increase the drug-induced seizure threshold in rats. Protein phosphorylation is a major regulatory mechanism of signal transduction that has been implicated in modulating neuronal excitability. We investigated the basal protein phosphorylation in microslices from different brain regions (hippocampus, cerebral cortex and cerebellum) of young rats fed a ketogenic diet, and we evaluated the effect of this diet on weight development and health of these rats based on serum biochemistry. Thirty-day-old rats consumed ad libitum ketogenic (high fat) or control diets for 8 wk. Rats consuming the high fat diet had ketonemia without signs of undernutrition or illness. Microslices were incubated in media containing (32)P-phosphate, and (32)P-phosphoprotein content was analyzed by one- or two-dimensional electrophoresis followed by autoradiography. Basal protein phosphorylation was greater in brain slices from ketogenic rats. Different increments of synapsin I, GAP-43 and GFAP phosphorylation were observed in two-dimensional autoradiography. A ketogenic diet induced metabolic changes affecting the basal status of protein phosphorylation. This change could affect the mechanisms of signal transduction in neural cells involved in the increase in the seizure threshold.     

Altered expression and glucocorticoid-inducibility of hepatic CYP3A and CYP2B enzymes in male rats fed diets containing soy protein isolate.

Hepatic CYP3A and CYP2B enzymes were studied in male Sprague-Dawley rats derived from 5-7 litters fed diets in which the protein source was either casein or soy protein isolate. At age 65 d, rats were gavaged with corn oil (vehicle) or 50 mg/kg dexamethasone. Hepatic expression of CYP3A and CYP2B1 mRNA, apoprotein and associated monooxygenase activities were measured. Consumption of soy diets significantly increased monooxygenase activity toward the following: the CYP3A substrates erythromycin and ethylmorphine N-demethylase; corticosterone and testosterone 6beta-hydroxylase; and apoprotein and mRNA expression of CYP3A2 (P < 0.05). Dexamethasone significantly induced turnover of erythromycin and testosterone, expression of CYP3A apoprotein, and expression of CYP3A1 and CYP3A2 mRNA (P < 0.05). In addition, significant diet-inducer interactions were observed in the expression of CYP3A apoprotein and activities toward ethylmorphine, corticosterone and testosterone (P < 0.05). Significant diet-inducer interactions were also observed on CYP2B1-dependent pentoxyresorufin O-depentylase activity (P < 0.05). However, although dexamethasone significantly induced CYP2B1 expression at the apoprotein and mRNA level (P < 0.05), no significant diet effects were observed. These data suggest potential effects of soy consumption on the metabolism of a wide variety of CYP3A and CYP2B1 substrates, especially in situations involving coexposure to CYP inducers.     

Soy protein isolate enhances hepatic copper accumulation and cell damage in LEC rats

In a series of experiments, the effects of soy protein isolate (SPI), defatted soy (DFS) or SPI supplemented with L-methionine (SPIM) were examined in the Long-Evans rat with a cinnamon coat color (LEC rat), a model animal of Wilson's disease with a hereditary defect in the Atp7b gene resulting in defective copper metabolism and copper accumulation in hepatocytes. Milk casein in the control AIN-93G diet (20 g/100 g) was totally or 60% replaced by the soy products, SPI, DFS or SPIM (L-Met added to be equal to that in the control diet) beginning when rats were 6 wk old. Copper and iron concentrations in SPI and DFS were measured and the concentrations of these metals in the salt mix were adjusted so that test and the control diets had the same final concentrations. Food intake did not differ among groups. Rats were euthanized when they became moribund with jaundice. Survival time in the SPI diet group was shorter (14.0 +/- 0.8 wk) than in the control group (19.1 +/- 1.7 wk) (P < 0.001), and that in the DFS diet group was intermediate (16.0 +/- 1.7 wk). Survival time in the SPIM diet group did not differ from that of the SPI diet group. Copper concentrations in the livers of rats in the SPI and SPIM diet groups were approximately 80% higher than in rats fed the control diet. Liver iron concentrations did not differ among the groups. The results, including histological analyses, indicate that SPI enhances copper uptake into the liver cells and promotes liver cell damage in LEC rats. However, this did not occur in the livers of F344 rats with wild-type Atp7b. Recommendations to individuals suffering from Wilson's disease to avoid consuming soy protein may be warranted.     

Effects of iron status and soy protein on iron absorption by rats

The effects of iron nutrition and soy protein on iron absorption by rats was studied. Rats were fed semipurified diets containing either 0, 5, or 20 micrograms of added iron per gram of diet to obtain groups with different iron status. After 3 weeks the rats had mean hemoglobin concentrations of 7.0, 10.7 and 13.2 g/dl, respectively. As the rats became more anemic, percent iron absorption from casein and soy protein diets increased. The relative availability of iron from soy compared with casein-based diets was 70 to 90%. Iron status did not affect the relative iron availability among treatments. The rat trials did not indicate any significant differences between iron absorption from meals containing soy flour (SF), soy protein concentrate (SC) or soy protein isolate (SI) regardless of the iron status of the rat. These studies do not support the hypothesis that the subject's iron status will affect the relative availability of iron from foods. Recent human iron absorption studies suggest that relative iron availability from meals containing soy proteins is lower than expected based on rat studies. Furthermore, differences in iron availability between soy flour and soy isolate observed in human studies are not apparent in these rat studies.     

Pancreatic response to long-term feeding of soy protein isolate, casein or egg white in rats

Rats were fed purified diets which provided 24% protein from casein (C), soy protein isolate (SPI), or egg white (EW) for 18 mo. Groups of rats were killed at 3, 6, 12 and 18 mo; the pancreata were removed and examined histologically for occurrence of atypical nodules. The weight, protein, DNA, trypsin and chymotrypsin concentrations of the pancreas at each period were measured. Over the entire experimental period, body weight did not differ among groups. Pancreatic weight, protein and trypsin activity were highest in the EW group, followed by the SPI group, and lowest in the C group. Chymotrypsin activity was significantly higher in the EW and SPI groups than the C group. DNA content did not differ significantly among groups over the entire experimental period, although it was elevated in the SPI or EW groups compared to the C groups at some of the time periods. Only one microscopic nodule was observed in all of the animals; it was found at 3 mo in the pancreas from an animal fed EW. Overall, the results suggest that the elevation in enzyme activity and pancreatic weight associated with long-term consumption of EW and SPI did not result in development of pancreatic lesions in rats.     

Effect of dietary methionine and polychlorinated biphenyls on cholesterol metabolism in rats fed a diet containing soy protein isolate

The effects of supplementation of methionine to a 20% soy protein isolate diet on serum level of cholesterol. 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase activity, cholesterol 7 alpha-hydroxylase activity, and biliary and fecal steroids in rats with or without receiving polychlorinated biphenyls (PCB) were investigated. Supplementation of methionine and PCB did not affect the growth. Serum level of cholesterol was higher in rats fed PCB than in controls. In rats fed PCB, addition of methionine elevated serum level of cholesterol synergistically. The activity of HMG-CoA reductase was higher in rats fed the methionine-supplemented diet than in those fed the unsupplemented diet when PCB was included in the diets. Cholesterol 7 alpha-hydroxylase activity (nmol/h.100 g body weight) was higher in rats fed PCB than in controls. Biliary secretion of bile acids was higher in rats fed PCB than in controls. On the other hand, fecal excretion of bile acids decreased in PCB-treated rats, but total steroids were not affected by PCB. In rats fed PCB, the addition of methionine did not alter cholesterol 7 alpha-hydroxylase activity and biliary and fecal steroid output. The data suggest that the increase in serum level of cholesterol due to dietary addition of methionine together with PCB would be mediated through the stimulation of hepatic synthesis of cholesterol.     

Isoflavone-rich soy protein isolate attenuates bone loss in the lumbar spine of perimenopausal women

BACKGROUND: No published studies have directly examined the effect of soy protein with isoflavones on bone or bone turnover in perimenopausal women. OBJECTIVE: Our objective was to determine the effects of 24 wk of consumption of soy protein isolate with isoflavones (80.4 mg/d) in attenuating bone loss during the menopausal transition. DESIGN: Perimenopausal subjects were randomly assigned, double blind, to treatment: isoflavone-rich soy (SPI+; n = 24), isoflavone-poor soy (SPI-; n = 24), or whey (control; n = 21) protein. At baseline and posttreatment, lumbar spine bone mineral density (BMD) and bone mineral content (BMC) were measured by using dual-energy X-ray absorptiometry. At baseline, midtreatment, and posttreatment, urinary N:-telopeptides and serum bone-specific alkaline phosphatase (BAP) were measured. RESULTS: The percentage change in lumbar spine BMD and BMC, respectively, did not differ from zero in the SPI+ or SPI- groups, but loss occurred in the control group (-1.28%, P: = 0.0041; -1.73%, P: = 0.0037). By regression analysis, SPI+ treatment had a positive effect on change in BMD (5.6%; P: = 0.023) and BMC (10.1%; P: = 0.0032). Baseline BMD and BMC (P: < or = 0.0001) negatively affected the percentage change in their respective models; baseline body weight (P: = 0.0036) and bone-free lean weight (P: = 0.016) contributed positively to percentage change in BMD and BMC, respectively. Serum BAP posttreatment was negatively related to percentage change in BMD (P: = 0.0016) and BMC (P: = 0.019). Contrast coding using analyses of covariance with BMD or BMC as the outcome showed that isoflavones, not soy protein, exerted the effect. CONCLUSION: Soy isoflavones attenuated bone loss from the lumbar spine in perimenopausal women.     

Retinoic acid modulates hepatic iron homeostasis in rats by attenuating the RNA-binding activity of iron regulatory proteins

Vitamin A deficiency has been widely associated with perturbations of iron homeostasis, a consequence that can be reversed by retinoid supplementation. Despite the numerous studies that demonstrate an interaction between these 2 nutrients, the mechanistic basis for this relation has not been well characterized. Because iron regulatory proteins (IRP) have been established as central regulators of iron homeostasis, we investigated the potential role of IRP in the regulation of iron homeostasis under conditions of vitamin A deficiency and supplementation with all-trans-retinoic acid (atRA). Rats were fed a control diet or a diet deficient in either vitamin A or iron or both micronutrients. Four parallel groups of rats were supplemented with atRA daily (30 micromol/kg body weight) during the final week of this study. As expected, iron-deficient (-Fe) rats exhibited a decrease in hepatic nonheme iron levels and a subsequent increase in IRP RNA-binding activity, resulting in diminished ferritin abundance. Interestingly, atRA supplementation inhibited the increase in IRP RNA-binding activity in -Fe rats to a level that was not significantly (P = 0.139) different from control values, and it partially restored ferritin abundance. This inhibition of IRP RNA-binding activity by atRA supplementation was also associated with a 40% reduction in transferrin receptor abundance. Taken together, these results indicate that IRP represent a mechanistic link between vitamin A and the regulation of iron homeostasis, a key finding toward further understanding this important nutrient-nutrient interaction.     

Inducibility of hepatic CYP1A enzymes by 3-methylcholanthrene and isosafrole differs in male rats fed diets containing casein, soy protein isolate or whey from conception to adulthood

Hepatic cytochrome P450 (CYP)1A1 and 1A2 enzymes were studied in male Sprague-Dawley rats derived from 5-7 litters fed diets in which the protein source was casein, soy protein isolate or whey. At age 65 d, rats were gavaged with corn oil (vehicle), 40 mg/kg 3-methylcholanthrene (3-MC) or 75 mg/kg isosafrole (ISO). Hepatic expression of CYP1A1 and CYP1A2 mRNA, apoprotein and associated monooxygenase activities were measured 17 h later. No significant dietary effects were observed on basal expression of either enzyme. However, interactions between diet and the two inducers (3-MC and ISO) were observed in soy-fed rats for ethoxy- and methoxyresorufin O-dealkylase activity, CYP1A1 and CYP1A2 apoprotein and mRNA (P < 0.05). The level of induction of CYP1A1 mRNA and apoprotein was lower in rats fed soy diets than in rats fed casein diets (P < 0.05), and the level of induced CYP1A2 mRNA was lower in rats fed soy or whey (P < 0.05) after treatment with the aryl hydrocarbon (Ah) receptor-dependent inducer 3-MC. This was accompanied by a 50% reduction in constitutive levels of the Ah receptor in liver cytosol of soy-fed, relative to casein-fed rats, and a slightly smaller reduction in whey-fed rats. Expression of the Ah receptor correlated with 3-MC-inducibility of CYP1A1 mRNA in rats fed the three diets. In contrast, in rats induced with ISO, which does not bind to the Ah receptor and induces CYP1As via different mechanisms than 3-MC, ethoxyresorufin O-deethylase activity and levels of CYP1A1 apoprotein and mRNA were elevated to a greater degree in soy-fed than in casein- or whey-fed rats (P < 0.05). Moreover, after ISO treatment, induction of methoxyresorufin O-demethylase activity, CYP1A2 apoprotein and mRNA levels was observed only in rats fed soy (P < 0.05). These data suggest potential effects of dietary protein source on metabolism of a wide variety of CYP1A substrates, including environmental and dietary carcinogens, many of which induce their own metabolism.     

Myofibrillar protein synthesis following ingestion of soy protein isolate at rest and after resistance exercise in elderly men

ABSTRACT: BACKGROUND: Increased amino acid availability stimulates muscle protein synthesis, however, aged muscle appears less responsive to the anabolic effects of amino acids when compared to the young. We aimed to compare changes in myofibrillar protein synthesis (MPS) in elderly men at rest and after resistance exercise following ingestion of different doses of soy protein and compare the responses to those we previously observed with ingestion of whey protein isolate. METHODS: Thirty elderly men (age 71 +/- 5 y) completed a bout of unilateral knee-extensor resistance exercise prior to ingesting no protein (0 g), or either 20 g or 40 g of soy protein isolate (0, S20, and S40 respectively). We compared these responses to previous responses from similar aged men who had ingested 20 g and 40 g of whey protein isolate (W20 and W40). A primed constant infusion of L-[1-13C]leucine and L-[ring-13C6]phenylalanine and skeletal muscle biopsies were used to measure whole-body leucine oxidation and MPS over 4 h post-protein consumption in both exercised and non-exercised legs. RESULTS: Whole-body leucine oxidation increased with protein ingestion and was significantly greater for S20 vs. W20 (P = 0.003). Rates of MPS for S20 were less than W20 (P = 0.02) and not different from 0 g (P = 0.41) in both exercised and non-exercised leg muscles. For S40, MPS was also reduced compared with W40 under both rested and post-exercise conditions (both P < 0.005); however S40 increased MPS greater than 0 g under post-exercise conditions (P = 0.04). CONCLUSIONS: The relationship between protein intake and MPS is both dose and protein source-dependent, with isolated soy showing a reduced ability, as compared to isolated whey protein, to stimulate MPS under both rested and post-exercise conditions. These differences may relate to the lower postprandial leucinemia and greater rates of amino acid oxidation following ingestion of soy versus whey protein.     

Effect of dietary protein status on urea metabolism and hepatic arginase activity of the pig

Experiments were conducted with cross-bred pigs to determine the effect of dietary protein concentration on liver arginase activity. In Exp. 1, pigs were fed diets containing 12, 18 or 24% protein. In Exp. 2, pigs were fed diets containing 12 or 24% protein. Pigs used in Exp. 1 were slaughtered after reaching a wt of 50 kg and after reaching 30, 60 and 90 kg wt in Exp. 2. Aliquots of a 50,000 x g liver supernatant were used for determination of arginase activity as well as endogenous activation kinetics. In addition, aliquots of the supernatants were fractionated by gel chromatography to determine the molecular species of swine liver arginase. Hepatic arginase activity was similar in pigs fed diets containing either 12 or 18% protein but greater in pigs fed the 24% protein diet. The data also indicate that greater than 70% of the hypatic cytosolic manganese is associated with arginase and that arginase activation may be regulated by manganese.     

丙烯酰胺亚慢性染毒大鼠脑和脊髓线粒体某些生化指标的变化

目的 观察丙烯酰胺亚慢性染毒对大鼠脑和脊髓线粒体能量代谢的影响.方法 66只健康雄性Wistar大鼠随机分为0、2、4、6、8、10周对照组和染毒组.染毒组给予丙烯酰胺[生理氯化钠溶液(NS)]40mg/kg腹腔注射,每周3次.对照组同样方式注射NS.观察大鼠的一般情况,每周测量体质量.按设定时间点处死大鼠,留取脑和脊髓组织进行线粒体提取,检测二磷酸腺苷(ADP)和三磷酸腺苷(ATP)的比值、ATP合成酶的活力.结果 染毒组大鼠体质量增长缓慢,染毒第4周后体质量显著低于对照组(P<0.05);脊髓和脑组织线粒体的ADP和ATP比值显著高于对照组(P<0.05,P<0.01).脑和脊髓中ATP合成酶活力分别于第8周和第4周起显著低于对照组(P<0.05),且持续降低至第10周.结论 丙烯酰胺可致染毒大鼠脑和脊髓ADP/ATP比值下降,ATP合成酶活力降低.     

High dose lycopene supplementation increases hepatic cytochrome P4502E1 protein and inflammation in alcohol-fed rats

Recent in vitro evidence suggests that the antioxidant lycopene can prevent alcohol-induced oxidative stress and inflammation. However, knowledge of possible interactions in vivo between escalating doses of lycopene and chronic alcohol ingestion are lacking. In this study, we investigated potential interactions between alcohol ingestion and lycopene supplementation and their effect on hepatic lycopene concentration, cytochrome P4502E1 (CYP2E1) induction, and inflammation. Fischer 344 rats (6 groups, n = 10 per group) were fed either a liquid ethanol Lieber-DeCarli diet or a control diet (isocaloric maltodextrin substituted for ethanol) with or without lycopene supplementation at 2 doses (1.1 or 3.3 mg x kg body weight(-1) x d(-1)) for 11 wk. Plasma and hepatic concentrations of lycopene isomers were assessed by HPLC analysis. We examined expressions of hepatic CYP2E1 and tumor necrosis factor-alpha (TNFalpha) and the incidence of hepatic inflammatory foci. Both plasma and hepatic lycopene concentrations were greater in alcohol-fed rats than in control rats supplemented with identical doses of lycopene. In contrast, alcohol-fed rats had a lower percentage of lycopene cis isomers in the plasma and the liver compared with control rats fed the same dose of lycopene. Notably, lycopene supplementation at the higher dose significantly induced hepatic CYP2E1 protein, TNFalpha mRNA, and the incidence of inflammatory foci in the alcohol-fed rats but not in the control rats. These data indicate an interaction between chronic alcohol ingestion and lycopene supplementation and suggest a need for caution among individuals consuming high amounts of both alcohol and lycopene.     

Resveratrol increases cerebral glycogen synthase kinase phosphorylation as well as protein levels of drebrin and transthyretin in mice: an exploratory study

Alzheimer’s disease (AD) is characterized by intraneuronal β-amyloid plaques and hyperphosphorylated tau, leading to neuronal cell death and progressive memory losses. This exploratory work investigates if dietary resveratrol, previously shown to have broad anti-aging effects and improve AD pathology in vivo, leads to neuroprotective changes in specific protein targets in the mouse brain. Both wild-type and APP/PS1 mice, a transgenic AD mouse model, received control AIN-93G diet or AIN-93G supplemented with resveratrol. Pathology parameters and AD risk were assessed via measurements on plaque burden, levels of phosphorylated glycogen synthase kinase 3-β (GSK3-β), tau, transthyretin and drebrin. Dietary resveratrol treatment did not decrease plaque burden in APP/PS1 mice. However, resveratrol-fed mice demonstrated increases in GSK3-β phosphorylation, a 3.8-fold increase in protein levels of transthyretin, and a 2.2-fold increase in drebrin. This study broadens our understanding of specific mechanisms and targets whereby resveratrol provides neuroprotection.     

Urinary calcium and calcium balance in young women affected by high protein diet of soy protein isolate and adding sulfur-containing amino acids and/or potassium

The effects of sulfur-containing amino acids (SAA) and potassium (K) on urinary excretion and retention of calcium (Ca) of 27 young Japanese women were studied. A basal diet low in protein level (50 g per day) was fortified by meat or soy protein isolate (SPI) to a protein level of 100 g per day, and effects of addition of apple to these high protein diets, and addition of SAA and/or potassium (K) to the high SPI diet, especially on urinary Ca excretion, were studied. The addition of meat which increased protein intake to 100 g caused the increase in apparent absorption and urinary excretion of Ca with increased excretion of urinary sulfur (S), phosphate, ammonia, and titratable acids (TA), whereas addition of SPI did not. The addition of apple to high meat diet decreased absorption and urinary excretion of Ca. Urinary Ca, S, K, ammonia, and TA excretion increased by the addition of SAA to high SPI diet in a manner similar to the meat diet. Consequently, SAA-supplemented diet had a significantly negative effect on Ca retention. In SPI+SAA,K diet period, urinary K excretion markedly increased, and increments in urinary Ca, ammonia, and TA excretion were reversed. These changes observed in SPI+SAA, K diet period were similar to those by adding apple to meat diet without any effect on Ca absorption. The results suggest that the hypercalciuria induced by high meat diet is mainly caused by high content of SAA and may be reversed by the ingestion of K-rich foodstuffs, and soy protein does not induce hypercalciuria because of it contains less SAA than animal protein.