The effect of boron supplementation on its urinary excretion and selected cardiovascular risk factors in healthy male subjects

Boron (B) is an essential trace element for plants and its interrelationship with mineral and bone metabolism and endocrine function in humans has been proposed. Relatively little is known about the occurrence of B in the food chain and hence a biomarker which reflects its intake is required. Two studies were carried out to quantify the urinary B concentration of subjects consuming their habitual diet and the effect of supplementation. In addition, the effect of supplementation on plasma lipoprotein cholesterol concentrations and susceptibility to oxidation and plasma steroid hormones were determined. Boron excretion, obtained on two different occasions from 18 healthy male subjects, was found to be in the range 0.35–3.53 mg/day, with no significant difference between the two occasions. Supplementation with 10 mg B/d for 4 wk resulted in 84% of the supplemented dose being recovered in the urine. Plasma estradiol concentrations increased significantly as a result of supplementation (51.9±21.4 to 73.9±22.2 pmol/L;p<0.004) and there was a trend for plasma testosterone levels to be increased. However, there was no difference in plasma lipids or the oxidizability of low-density lipoprotein Our studies suggest that the absorption efficiency of B is very high and estimation of the urinary B concentration may provide a useful reflection of B intake. In addition, the elevation of endogenous estrogen as a result of supplementation suggests a protective role for B in atherosclerosis.     

Determining human dietary requirements for boron

A dietary requirement is defined as the lowest continuing intake of a nutrient that for a specified indicator of adequacy, will maintain a defined level of nutriture in an individual. An essential dietary component is one that the body cannot synthesize in sufficient quantities to maintain health. Recommended dietary allowances (RDAs) are based on estimates of the dietary requirements, and are designed to prevent deficiency diseases and promote health through an adequate diet. In 1996, the Food and Nutrition Board (FNB) began a revision process of the RDAs using as criteria specific indicators of adequacy and functional end points for reducing the risk of chronic disease. Boron (B) is a dietary component, and evidence from animal studies indicates that it is a dietary essential; it cannot be synthesized in tissues, and organisms exposed to very low levels of B show developmental defects. In humans, there is evidence of homeostatic regulation of B and an interrelationship with bone metabolism. To understand better the relationship between dietary B and B homeostasis, we measured the dietary B intake and urinary B losses in seven male participants of a controlled metabolic study of Zn homeostasis. Average dietary B intake for the repeated menu days, days 1, 2, and 3, was 4.56, 1.87, and 4.75 mg/d, respectively. Urinary B excretion during the 42-d collection period averaged 3.20 ± 0.41 mg/d. When dietary B was low, urinary B loss (2.92 mg/d) was significantly lower than when B intake was higher (3.15 and 3.54 mg/d). Our study showed that urinary B excretion changes rapidly with changes in B intake, indicating that the kidney is the site of homeostatic regulation. To enable establishment of a dietary requirement for B in the future, further research of homeostatic regulation and functional markers of B metabolism need to be performed, followed by epidemiological studies to identify health conditions associated with inadequate dietary B.     

Effects of allopurinol on beer-induced increases in plasma concentrations and urinary excretion of purine bases (uric acid, hypoxanthine, and xanthine).

To determine the effects of allopurinol on beer-induced increases in plasma and urinary excretion of purine bases (hypoxanthine, xanthine, and uric acid), we performed three experiments on five healthy study participants. In the first experiment (combination study), the participants ingested beer (10 ml/kg body weight) eleven hours after taking allopurinol (300 mg). In the second experiment (beer-only study), the same participants ingested beer (10 ml/kg body weight) alone, while in the third experiment (allopurinol-only study), they took allopurinol (300 mg) alone. There was a two-week interval between each of the studies. Beer-induced increases in plasma concentration and urinary excretion of hypoxanthine in the combination study were markedly higher than those in the beer-only study. On the other hand, the sum of increases in plasma concentrations of purine bases in the beer-only study was greater than in the combination study, whereas the increase in plasma uridine concentration in the combination study did not differ from the beer-only study. In addition, allopurinol administration inhibited the beer-induced increase in plasma concentration of uric acid. These results suggest that abrupt adenine nucleotide degradation may increase plasma concentration and urinary excretion of hypoxanthine under conditions of low xanthine dehydrogenase activity, which is mostly ascribable to allopurinol. Further, the difference in the sum of increases in plasma concentrations of purine bases between the combination study and beer-only study was largely ascribable to a greater increase in urinary excretion of hypoxanthine in the combination study. In addition, allopurinol intake seems to be effective in controlling the rapid increase in plasma uric acid caused by ingestion of alcoholic beverages.     

Urinary metabolites of flavonoids and hydroxycinnamic acids in humans after application of a crude extract from Equisetum arvense.

Flavonoids and hydroxycinnamic acids are polyphenolic compounds present in our daily diet in form of tea and vegetables as well as in herbal remedies used in phytomedicine. A wide range of in-vitro activities, in particular their antioxidant properties, have been studied intensively. However, in-vivo-data on absorption, bioavailability and metabolism after oral intake are scarce and contradictory. In order to examine the metabolism and renal excretion of these compounds a standardized extract from horsetail (Equisetum arvense) was administered to 11 volunteers following a flavonoid-free diet for 8 d. 24 h urine samples were collected and analyzed by HPLC-DAD. The putative quercetin metabolites, 3,4-dihydroxyphenylacetic acid or 3,4-dihydroxytoluene could not be detected in urine in any sample. The endogenous amount of homovanillic acid, generally regarded as one of the main quercetin metabolites, was 4 +/- 1 mg/d and did not increase significantly. However, hippuric acid, the glycine conjugate of benzoic acid, increased twofold after drug intake. Thus, the degradation to benzoic acid derivatives rather than phenylacetic acid derivatives seems to be a predominant route of metabolism. The results of this pilot study give rise to additional, substantial pharmacokinetic investigations in humans.     

Elimination of oxalate by fat sand rats (Psammomys obesus): wild and laboratory-bred animals compared

Wild fat sand rats (Psammomys obesus) can feed exclusively on plants containing much oxalate, but little calcium; oxalate intake may exceed 300 mg/d, while calcium intake is approximately 30 mg/day. By contrast, for generations, laboratory bred P. obesus have been fed a low-oxalate (<100 mg/day), high-calcium (approximately 150 mg/day) rodent chow. We compared oxalate intake and excretion between wild and laboratory-bred animals, both fed the natural high-oxalate diet, to determine whether these different dietary histories are reflected in the animal's ability to eliminate dietary oxalate. Since both wild and laboratory-bred P. obesus harbor intestinal oxalate-degrading bacteria, we predicted that their oxalate intake and excretion would be similar. Indeed, we found no significant differences in oxalate intake or excretion between the groups fed either saltbush or alfalfa (p>0.05). However, due to the differences in dietary calcium intake between the two diets, in both groups only part (23-25%) of the ingested oxalate was excreted when the animals were fed the oxalate-rich saltbush, yet most (87-90%) was excreted when feeding on calcium-rich alfalfa. Thus, even after generations of feeding on a commercial low-oxalate diet, fat sand rats maintain intestinal oxalate-degrading bacteria that appear to increase in number and activity when presented with their natural diet.     

Chronic activation of plasma renin is log-linearly related to dietary sodium and eliminates natriuresis in response to a pulse change in total body sodium

Responses to acute sodium loading depend on the load and on the level of chronic sodium intake. To test the hypothesis that an acute step increase in total body sodium (TBS) elicits a natriuretic response, which is dependent on the chronic level of TBS, we measured the effects of a bolus of NaCl during different low-sodium diets spanning a 25-fold change in sodium intake on elements of the renin-angiotensin-aldosterone system (RAAS) and on natriuresis. To custom-made, low-sodium chow (0.003%), NaCl was added to provide four levels of intake, 0.03-0.75 mmol.kg(-1).day(-1) for 7 days. Acute NaCl administration increased PV (+6.3-8.9%) and plasma sodium concentration (~2%) and decreased plasma protein concentration (-6.4-8.1%). Plasma ANG II and aldosterone concentrations decreased transiently. Potassium excretion increased substantially. Sodium excretion, arterial blood pressure, glomerular filtration rate, urine flow, plasma potassium, and plasma renin activity did not change. The results indicate that sodium excretion is controlled by neurohumoral mechanisms that are quite resistant to acute changes in plasma volume and colloid osmotic pressure and are not down-regulated within 2 h. With previous data, we demonstrate that RAAS variables are log-linearly related to sodium intake over a >250-fold range in sodium intake, defining dietary sodium function lines that are simple measures of the sodium sensitivity of the RAAS. The dietary function line for plasma ANG II concentration increases from theoretical zero at a daily sodium intake of 17 mmol Na/kg (intercept) with a slope of 16 pM increase per decade of decrease in dietary sodium intake.     

Ammonia excretion increased and urea excretion decreased in urine of a new world nectarivorous bat with decreased nitrogen intake

We determined the effect of water and nitrogen intake on nitrogenous waste composition in the nectarivorous Pallas's long-tongued bat Glossophaga soricina (Phyllostomidae) to test the hypothesis that bats reduce excretion of urea nitrogen and increase the excretion of ammonia nitrogen as nitrogen intake decreases and water intake decreases. Because changes in urine nitrogen composition are expected only in animals whose natural diets are low in nitrogen and high in water content, we also measured maintenance nitrogen requirements (MNR). We hypothesized that, similar to other plant-eating vertebrates, nectarivorous bats have low MNR. Our nitrogen excretion hypothesis was partly proved correct. There was an increase in the proportion of N excreted as ammonia and a decrease in the proportion excreted as urea in low-nitrogen diets. The proportion of N excreted as ammonia and urea was independent of water intake. Most individuals were ureotelic (n = 28), and only a few were ureo-ammonotelic (n = 3) or ammonotelic (n = 2). According to our nitrogen requirement hypothesis, apparent MNR (60 mg kg(-0.75) d(-1)) and truly digestible MNR (54 mg N kg(-0.75) d(-1)) were low. A decrease in urea excretion in low-nitrogen diets may result from urea recycling from liver to the gut functioning as a nitrogen salvage system in nectarivorous bats. This mechanism probably contributes to the low MNR found in Pallas's long-tongued bats.     

Effect of low-protein corn and soybean meal-based diets on nitrogen utilization,litter quality,and water consumption in broiler chicken production: insight from meta-analysis

The growing demand for high-value animal protein must be met using sustainable means that optimize the utilization of nutrients, especially nitrogen (N) so that excreta do not over-fertilize fields and end up causing soil acidification, waterway eutrophication and greenhouse gas emissions. Malodorous N compounds can cause respiratory diseases and poor growth in livestock. The increasing availability of feed-grade amino acids makes it possible to formulate low-protein diets for broilers and thereby reduce N excretion. However, published studies of the effects of such diets on broiler growth performance have been based on reducing CP contents gradually in a variety of ways that have given inconsistent results. Since the amount of published data is now large, a meta-analysis was performed in order to categorize diet formulation strategies and quantify their impact on N balance, water consumption, litter moisture, plasma uric acid. This showed that lowering the CP content of broiler diets generally means replacing some soybean meal with corn and hence increasing the starch content. However, since soybean meal is also a source of potassium, this reduces electrolyte balance. Lowering the CP content from 19% to 17% is associated with a 29% reduction of N excretion in broilers aged 0–21 d, and a 7% increase in N efficiency (N retention/N intake). Reducing the CP content from 19% to 17% decreases daily water consumption by 20.6 mL/bird, litter moisture by 2.2% and plasma uric acid by 0.56 mg/dL. This meta-analysis improves our understanding of the low-protein strategy and allows us to quantify its impact on N balance, litter quality and uric acid. It shows that managing N excretion is wholly beneficial and reduces litter wetness.     

Serum Cholesterol-Decreasing Effect of Heat-Moisture-Treated High-Amylose Cornstarch in Cholesterol-Loaded Rats

Rats were fed on a diet containing cholesterol (Chol) at a level corresponding to the standard Chol intake in humans, and the influence of heat-moisture-treated high-amylose cornstarch (HHA) on their serum Chol level was investigated. HHA decreased the serum level of Chol in rats fed on the diet containing 0.1% Chol, which corresponds to a Chol intake in humans of 800 mg/d, although the liver levels of Chol increased in these rats. HHA did not influence the fecal excretion of Chol/bile acids. It is possible that the decrease in serum Chol level in the rats fed on the high-Chol diet can be attributed to the promotion of Chol uptake in the liver.     

Serum cholesterol-decreasing effect of heat-moisture-treated high-amylose cornstarch in cholesterol-loaded rats

Rats were fed on a diet containing cholesterol (Chol) at a level corresponding to the standard Chol intake in humans, and the influence of heat-moisture-treated high-amylose cornstarch (HHA) on their serum Chol level was investigated. HHA decreased the serum level of Chol in rats fed on the diet containing 0.1% Chol, which corresponds to a Chol intake in humans of 800 mg/d, although the liver levels of Chol increased in these rats. HHA did not influence the fecal excretion of Chol/bile acids. It is possible that the decrease in serum Chol level in the rats fed on the high-Chol diet can be attributed to the promotion of Chol uptake in the liver.     

Effect of ascorbic acid and green tea on endogenous formation of N-nitrosodimethylamine and N-nitrosopiperidine in humans.

Many constituents present in the human diet may inhibit endogenous formation of N-nitroso compounds (NOC). Studies with human volunteers showed inhibiting effects of intake of ascorbic acid and green tea consumption on nitrosation using the N-nitrosoproline test. The aim of the present study was to evaluate the effects of ascorbic acid and green tea on urinary excretion of carcinogenic N-nitrosodimethylamine (NDMA) and N-nitrosopiperidine (NPIP) in humans. Twenty-five healthy female volunteers consumed a fish meal rich in amines as nitrosatable precursors in combination with intake of nitrate-containing drinking water at the Acceptable Daily Intake level during 7 consecutive days. During 1 week before and after nitrate intake a diet low in nitrate was consumed. Using the same protocol, the effect of two different doses of ascorbic acid (250 mg and 1 g/day) and two different doses of green tea (2 g and 4 g/day) on formation of NDMA and NPIP was studied. Mean nitrate excretion in urine significantly increased from control (76+/-24) to 167+/-25 mg/24 h. Intake of nitrate and fish resulted in a significant increase in mean urinary excretion of NDMA compared with the control weeks: 871+/-430 and 640+/-277 ng/24 h during days 1-3 and 4-7, respectively, compared with 385+/-196 ng/24 h (p<0.0002). Excretion of NPIP in urine was not related to nitrate intake and composition of the diet. Intake of 250 mg and 1 g of ascorbic acid per day resulted in a significant decrease in urinary NDMA excretion during days 4-7 (p=0.0001), but not during days 1-3. Also, consumption of four cups of green tea per day (2 g) significantly decreased excretion of NDMA during days 4-7 (p=0.0035), but not during days 1-3. Surprisingly, consumption of eight cups of green tea per day (4 g) significantly increased NDMA excretion during days 4-7 (p=0.0001), again not during days 1-3. This increase is probably a result of catalytic effects of tea polyphenols on nitrosation, or of another, yet unknown, mechanism. These results suggest that intake of ascorbic acid and moderate consumption of green tea can reduce endogenous NDMA formation.     

Biotin biochemistry and human requirements

Human biotin turnover and requirements can be estimated on the basis of (1) concentrations of biotin and metabolites in body fluids, (2) activities of biotin-dependent carboxylases, and (3) the urinary excretion of organic acids that are formed at increased rates if carboxylase activities are reduced. Recent studies suggest that the urinary excretions of biotin and its metabolite bisnorbiotin, activities of propionyl-CoA carboxylase and beta-methylcrotonyl-CoA carboxylase in lymphocytes, and urinary excretion of 3-hydroxyisovaleric acid are good indicators of marginal biotin deficiency. On the basis of studies using these indicators of biotin deficiency, an adequate intake of 30 microg (123 nmoles) of biotin per day is currently recommended for adults. The dietary biotin intake in Western populations has been estimated to be 35 to 70 microg/d (143-287 nmol/d). Recent studies suggest that humans absorb biotin nearly completely. Conditions that may increase biotin requirements in humans include pregnancy, lactation, and therapy with anticonvulsants or lipoic acid.     

Comparison of Risk Assessments of Boron: Alternate Approaches to Chemical-Specific Adjustment Factors

Health risk assessments of boron (B) have been performed in recent years by seven well-respected regulatory and scientific organizations, including the Institute for Evaluating Health Risks, European Centre for Ecotoxicology and Toxicology of Chemicals, International Programme on Chemical Safety, World Health Organization, National Academy of Sciences Food and Nutrition Board, U.K. Expert Group of Vitamins and Minerals (draft) and U.S. Environmental Protection Agency (draft). Of interest, all of these risk assessments employed chemical-specific adjustment factors, resulting in total uncertainty factors in the range of 25–62 and estimates of tolerable intake levels ranging from 10 to 24 mg B/day. These risk assessments are particularly instructive because they all used the same critical developmental toxicity study and the same NOAEL (10 mg B/kg/day). Therefore, the primary differences among these risk assessments reside in the choice of chemical-specific adjustment factors. It is generally agreed that renal clearance is the primary determinant of B pharmacokinetic variability, both within and among species. However, the methods used to select chemical-specific adjustment factors for pharmacokinetics vary among B risk assessments. Several have estimated intraspecies pharmacokinetic variability based on glomerular filtration rates (GFR) in pregnant women. Based on the results of renal clearance studies of B, the use of GFR is scientifically appropriate to estimate the intraspecies pharmacokinetic variability in B renal clearance. B homeostasis in humans appears to be primarily regulated by the kidney, and at typical low doses in humans, there is evidence of tubular reabsorption of B in the kidneys. Human studies indicate that urinary B excretion is a sensitive indicator of recent dietary intake. The major source of B exposure in humans is consumption of fruits, vegetables, nuts and legumes, which are naturally rich in B. Human dietary consumption of B is below the estimated tolerable intake levels established in these recent risk assessments. Considering the growing evidence of the nutritional role of B, it is important to consider both the benefits and risks of B consumption. By legitimately reducing the uncertainty factor for toxicity, the margin of safety is effectively increased to protect against the possibility of insufficient dietary intake. Risk assessments of B provide valuable lessons regarding how chemical-specific adjustment factors may be selected.     

Effect of sodium intake on fasting and postprandial levels of atrial natriuretic factor in humans

The effect of chronic dietary sodium intake on fasting and postprandial plasma atrial natriuretic factor (ANF) levels was examined in 2 studies of normal humans. In Study I, 3 separate groups of normals (n = 8 for each) received diets of either low (L), normal (N) or high (H) daily sodium intake for 7 days. Twenty-four h urines for sodium were obtained on days 6 and 7. Urine sodium excretion for each group was (L) 13.1 +/- 3.7, (N) 150.1 +/- 19.4 and (H) 271.3 +/- 33.6 mEq/day. On the completion of day 7, fasting plasma ANF showed no change with alteration in sodium intake. In contrast, when blood samples were obtained postprandially, significant increases in plasma ANF were observed in the group maintained on high sodium diet. In Study II, a continuous group of normals (n = 8) received the 3 sodium controlled diets for 7 days sequentially (L/N/H). No significant changes in fasting levels of ANF were detected between L/N/H sodium diets. In conclusion, these studies show that the maintenance of sodium balance during chronic changes in sodium intake can occur despite no significant increase in plasma ANF under normal steady state conditions. However, plasma ANF is significantly elevated during chronic high sodium intake, when measured postprandially.     

Effect of Roux-en-Y Gastric Bypass Surgery on Bile Acid Metabolism in Normal and Obese Diabetic Rats

In addition to classic functions of facilitating hepatobiliary secretion and intestinal absorption of lipophilic nutrients, bile acids (BA) are also endocrine factors and regulate glucose and lipid metabolism. Recent data indicate that antiobesity bariatric procedures e.g. Roux-en-Y gastric bypass surgery (RYGB), which also remit diabetes, increase plasma BAs in humans, leading to the hypothesis that BAs may play a role in diabetes resolution following surgery. To investigate the effect of RYGB on BA physiology and its relationship with glucose homeostasis, we undertook RYGB and SHAM surgery in Zucker diabetic fatty (ZDF) and normoglycemic Sprague Dawley (SD) rats and measured plasma and fecal BA levels, as well as plasma glucose, insulin, Glucagon like peptide 1 (GLP-1) and Peptide YY (PYY), 2 days before and 3, 7, 14 and 28 days after surgery. RYGB decreased body weight and increased plasma GLP-1 in both SD and ZDF rats while decreasing plasma insulin and glucose in ZDF rats starting from the first week. Compared to SHAM groups, both SD-RYGB and ZDF-RYGB groups started to have increases in plasma total BAs in the second week, which might not contribute to early post-surgery metabolic changes. While there was no significant difference in fecal BA excretion between SD-RYGB and SD-SHAM groups, the ZDF-RYGB group had a transient 4.2-fold increase (P<0.001) in 24-hour fecal BA excretion on post-operative day 3 compared to ZDF-SHAM, which paralleled a significant increase in plasma PYY. Ratios of plasma and fecal cholic acid/chenodeoxycholic acid derived BAs were decreased in RYGB groups. In addition, tissue mRNA expression analysis suggested early intestinal BA reabsorption and potentially reduced hepatic cholic acid production in RYGB groups. In summary, we present novel data on RYGB-mediated changes in BA metabolism to further understand the role of BAs in RYGB-induced metabolic effects in humans.     

Dietary calcium and blood lead levels in women

Nutritional factors are known to influence metabolism and toxicity of several metals in animal experiments, but relevant human data are scarce and inconclusive. In this work, we tested the hypothesis that dietary calcium influences lead metabolism in humans. Blood lead concentrations were used as indicators of lead exposure and metabolism. Two groups of peasant women living in similar conditions in two different regions in Yugoslavia (100 in each) were chosen as subjects for this purpose. In region A, the dietary calcium intake was about 940 mg, and in region B about two times lower, i.e., 450 mg/day. The average blood lead concentration was significantly lower in women from region A (69 micrograms/L) than from region B (83 micrograms/L). Our results support the assumption that adequate calcium intake might be one of the preventive measures for decreasing lead absorption. This new evidence, sought for some time by nutritionists and toxicologists, needs further international confirmation.     

The justification for providing dietary guidance for the nutritional intake of boron

Because a biochemical function has not been defined for boron (B), its nutritional essentiality has not been firmly established. Nonetheless, dietary guidance should be formulated for B, because it has demonstrated beneficial, if not essential, effects in both animals and humans. Intakes of B commonly found with diets abundant in fruits, vegetables, legumes, pulses, and nuts have effects construed to be beneficial in macromineral, energy, nitrogen, and reactive oxygen metabolism, in addition to enhancing the response to estrogen therapy and improving psychomotor skills and cognitive processes of attention and memory. Perhaps the best-documented beneficial effect of B is on calcium (Ca) metabolism or utilization, and thus, bone calcification and maintenance. The paradigm emerging for the provision of dietary guidance that includes consideration of the total health effects of a nutrient, not just the prevention of a deficiency disease, has resulted in dietary guidance for chromium (Cr) and fluoride; both of these elements have beneficial effects in humans, but neither has a defined biochemical function. Knowledge of B nutritional effects in humans equals or is superior to that of Cr and fluoride; thus, establishing a dietary reference intake for B is justified. An analysis of both human and animal data suggests that an acceptable safe range of population mean intakes of B for adults could well be 1–13 mg/d. Recent findings indicate that a significant number of people do not consistently consume more than 1 mg B/d; this suggests that B could be a practical nutritional or clinical concern.     

Gut sensing of dietary K⁺ intake increases renal K⁺excretion

Dietary K(+) intake may increase renal K(+) excretion via increasing plasma [K(+)] and/or activating a mechanism independent of plasma [K(+)]. We evaluated these mechanisms during normal dietary K(+) intake. After an overnight fast, [K(+)] and renal K(+) excretion were measured in rats fed either 0% K(+) or the normal 1% K(+) diet. In a third group, rats were fed with the 0% K(+) diet, and KCl was infused to match plasma [K(+)] profile to that of the 1% K(+) diet group. The 1% K(+) feeding significantly increased renal K(+) excretion, associated with slight increases in plasma [K(+)], whereas the 0% K(+) diet decreased K(+) excretion, associated with decreases in plasma [K(+)]. In the KCl-infused 0% K(+) diet group, renal K(+) excretion was significantly less than that of the 1% K(+) group, despite matched plasma [K(+)] profiles. We also examined whether dietary K(+) alters plasma profiles of gut peptides, such as guanylin, uroguanylin, glucagon-like peptide 1, and glucose-dependent insulinotropic polypeptide, pituitary peptides, such as AVP, α-MSH, and γ-MSH, or aldosterone. Our data do not support a role for these hormones in the stimulation of renal K(+) excretion during normal K(+) intake. In conclusion, postprandial increases in renal K(+) excretion cannot be fully accounted for by changes in plasma [K(+)] and that gut sensing of dietary K(+) is an important component of the regulation of renal K(+) excretion. Our studies on gut and pituitary peptide hormones suggest that there may be previously unknown humoral factors that stimulate renal K(+) excretion during dietary K(+) intake.     

High intakes of tin lower iron status in rats

The effects of relatively low (1, 10, and 50 mg/kg) and high (100 and 200 mg/kg) dietary concentrations of tin (added as stannous chloride) on iron status of rats were determined. After feeding the diets for 28 d, feed intake and body weights were not significantly affected. Iron concentrations in plasma, spleen, and tibia as well as percentage transferrin saturation were decreased in rats fed the diets supplemented with 100 or 200 mg tin/kg. In rats fed the diet containing 200 mg tin/kg, group mean hemoglobin, hematocrit, and red blood cell count were slightly lowered but total iron binding capacity was not affected. Iron status was not influenced by dietary tin concentrations lower than 100 mg/kg. If these results can be extrapolated to humans, then it may be concluded that tin concentrations in the human diet, which range from 2 to 76 mg/kg dry diet, do not influence iron status in humans.     

Manganese,copper, and zinc in cerebrospinal fluid from patients with multiple sclerosis

The concentrations of manganese, copper, and zinc in cerebrospinal fluid (CSF) from patients with multiple sclerosis (MS) and patients with no known neurological disease (control group) were measured. Manganese and copper levels were determined by two different analytical methods: atomic absorption spectrometry (AAS) and high-resolution inductively coupled plasma-mass spectrometry (HR-ICP-MS), whereas zinc levels were determined by HR-ICP-MS only. Manganese levels (mean±SEM) were significantly decreased in the CSF of MS patients (1.07±0.13 μg/L, ICP-MS; 1.08±0.11 μg/L, AAS) compared to the levels in the control group (1.78±0.26 μg/L, ICP-MS; 1.51±0.17 μg/L, AAS). Copper levels were significantly elevated in the CSF of MS patients (10.90±1.11 μg/L; ICP-MS, 11.53±0.83 μg/L, AAS) compared to the levels in the control group (8.67±0.49 μg/L, ICP-MS; 9.10±0.62 μg/L, AAS). There were no significant differences between the CSF zinc levels of MS and control patients. The physiological basis for the differences in manganese and copper concentrations between MS patients and controls is unknown, but could be related to alterations in the manganese-containing enzyme glutamine synthetase and the copper-containing enzyme cytochrome oxidase.