Effect of dietary boron on mineral, estrogen, and testosterone metabolism in postmenopausal women

A study was done to examine the effects of aluminum, magnesium, and boron on major mineral metabolism in postmenopausal women. This communication describes some of the effects of dietary boron on 12 women between the ages of 48 and 82 housed in a metabolic unit. A boron supplement of 3 mg/day markedly affected several indices of mineral metabolism of seven women consuming a low-magnesium diet and five women consuming a diet adequate in magnesium; the women had consumed a conventional diet supplying about 0.25 mg boron/day for 119 days. Boron supplementation markedly reduced the urinary excretion of calcium and magnesium; the depression seemed more marked when dietary magnesium was low. Boron supplementation depressed the urinary excretion of phosphorus by the low-magnesium, but not by the adequate-magnesium, women. Boron supplementation markedly elevated the serum concentrations of 17 beta-estradiol and testosterone; the elevation seemed more marked when dietary magnesium was low. Neither high dietary aluminum (1000 mg/day) nor an interaction between boron and aluminum affected the variables presented. The findings suggest that supplementation of a low-boron diet with an amount of boron commonly found in diets high in fruits and vegetables induces changes in postmenopausal women consistent with the prevention of calcium loss and bone demineralization.     

Effect of various chloride salts on the utilization of phosphorus, calcium, and magnesium

Only part of the effect of dietary protein on urinary calcium excretion can be ascribed to sulfur amino acids. We hypothesized that chloride, another factor often associated with isolated proteins, and another amino acid, lysine, affect utilization of calcium. The effects of supplemental dietary chloride, inorganic or organic, on calcium, phosphorus, and magnesium utilization were studied in two rat studies. Weanling Sprague-Dawley rats were fed semi-purified diets that contained moderate (1.8 mg Cl/g diet) or supplemental (15.5 mg Cl/g diet) chloride as sodium chloride, potassium chloride, or lysine monohydrochloride with or without calcium carbonate for 56 or 119 days. Rats fed supplemental sodium chloride or potassium chloride had higher urinary phosphorus excretion, more efficient phosphorus absorption, but unchanged tissue phosphorus levels after 7 and 16 weeks of dietary treatment as compared to rats fed moderate chloride. Rats fed supplemental sodium chloride or potassium chloride excreted more calcium in urine at 7 weeks and absorbed calcium less efficiently at 16 weeks. Tissue calcium concentrations were unaffected, but total tibia magnesium and plasma magnesium concentrations were lower in rats fed supplemental sodium chloride or potassium chloride than those fed moderate chloride. Lysine chloride with or without additional calcium elevated urinary calcium excretion even more than sodium chloride and potassium chloride ingestion. Rats fed lysine chloride with supplemental calcium had smaller apparent absorption and urinary losses of phosphorus and magnesium after 16 weeks and lower tibia and plasma magnesium concentrations than rats fed lysine chloride.     

Studies of the interaction between boron and calcium,and its modification by magnesium and potassium,in rats

Two experiments were performed to confirm that boron interacts with calcium, and that this interaction can be modified by dietary magnesium and potassium in the rat. Upon manipulating the dietary variables listed above, it was found that under certain conditions, boron and calcium deprivation similarly affected several variables; for example, they both could be made to elevate plasma alkaline phosphatase activity and to depress femur calcium concentration. Under some dietary conditions, both boron and calcium deprivation affected some variables related to blood or iron metabolism. However, the effects of dietary boron and calcium on spleen weight/body weight ratio, hematocrit, and femur iron concentration generally were not similar. Femur copper, magnesium, phosphorus, and zinc also were affected by an interaction between boron and calcium under some dietary conditions. The findings show that there is a relationship between boron and calcium, but they do not clearly indicate the nature of the relationship. However, the data suggest that boron and calcium act on similar systems in the rat.     

Magnesium and methionine deprivation affect the response of rats to boron deprivation

A series of nine experiments were done to obtain further evidence that boron might be involved in major mineral metabolism (Ca, P, and Mg), thus indicating that boron is an essential nutrient for animals. Eight factorially arranged experiments of 6–10 wk durations were done with weanling Sprague-Dawley male rats. One factorially arranged experiment was done with weanling spontaneously hypertensive rats. The variables in each experiment were dietary boron supplements of 0 and 3 μg/g, and dietary magnesium supplements of either 200 (Experiments 1–3) or 100 (Experiments 4–9) and 400 μg/g. In Experiments 7 and 9, a third variable was dietary manganese supplements of 25 and 50 μg/g. Methionine status was varied throughout the series of experiments by supplementing the casein-based diet with methionine and arginine. Findings were obtained indicating that the severity of magnesium deprivation and the methionine status of the rat strongly influence the extent and nature of the interaction between magnesium and boron, and the response to boron deprivation. When magnesium deprivation was severe enough to cause typical signs of deficiency, a significant interaction between boron and magnesium was found. Generally, the interaction was characterized by the deprivation of one of the elements making the deficiency signs of the other more marked. The interaction was most evident when the diet was not supplemented with methionine and especially when the diet contained luxuriant arginine. Signs of boron deprivation were also more marked and consistent when the diet contained marginal methionine and luxuriant arginine. Among the signs of boron deprivation exhibited by rats fed marginal methionine were depressed growth and bone magnesium concentration, and elevated spleen wt/body wt and kidney wt/body wt ratios. Because the boron supplement of 3 μg/g did not make the dietary intake of this element unusual, it seems likely that the response of the rats to dietary boron in the present study were manifestations of physiological, not pharmacological, actions, and support the hypothesis that boron is an essential nutrient for the rat. Mentions of a trademark or proprietary product does not consitute a guarantee or warranty of the product by the US Department of Agriculture and does not imply its approval to the exclusion of other products that may also be suitable.     

The Effects of Probenecid and Thiazides and Their Combination on the Urinary Excretion of Electrolytes and on Acid-base Equilibrium

The effects of commonly used therapeutic doses of hydrochlorothiazide and probenecid, given singly and in combination, on the urinary excretion of monovalent and divalent ions and on acid-base equilibrium were studied in four patients with idiopathic hypercalciuria.Probenecid had no effect on the urinary excretion of monovalent ions but resulted in a sustained increase in the urinary excretion of calcium, magnesium and citrate and a temporary increase in the urinary excretion of ammonium, in addition to its well-known effects on uric acid metabolism. A temporary fall in serum phosphorus levels was also observed.Probenecid also modified the response to hydrochlorothiazide in that the urinary excretion of calcium, magnesium and citrate was greater during combined therapy than when hydrochlorothiazide was administered alone. Probenecid prevented or abolished the increase in serum uric acid levels associated with the use of thiazide but did not modify the effects of hydrochlorothiazide on the urinary excretion of sodium, chloride, potassiu, phosphorus, ammonium, titratable acid and bicarbonate.     

Effects of calcium deprivation and orchidectomy on bone composition in the rat.

The effects of calcium deprivation and of orchidectomy, separately and combined, on body growth and bone composition have been examined in mature male rats. Calcium deprivation had no significant effect on the rate of body growth but femoral bone weight, bone ash weight and total calcium and phosphorus contents of the femora were reduced while the water content increased. However, there were no significant changes in the ratio of bone weight to body weight, in the amounts of calcium or phosphorus per unit weight of bone, or in the ratio of calcium to phosphorus in the bone. Orchidectomy reduced the rate of body growth, the mean weight of the femora and the ratio of bone weight to body weight. There was a 60% decrease in bone water and a 30--35% reduction in the calcium and phosphorus content of the femora but the amounts of ash, calcium and phosphorus per unit weight of bone fell by only 6--10%. The combination of orchidectomy and calcium deprivation had no greater effect on body weight, bone weight or bone composition than had orchidectomy alone. It is concluded that calcium deprivation and orchidectomy both cause osteoporosis in mature rats but the effects of orchidectomy are more severe than those of calcium deprivation and there appears to be some demineralization of the bone remaining after orchidectomy.     

Excess calcium increases bone zinc concentration without affecting zinc absorption in rats

We examined zinc (Zn) metabolism in rats given diets containing excess calcium (Ca). Rats were given phytate-free diet containing 5 g Ca/kg (control), 12.5 g Ca/kg, or 25 g Ca/kg for 4 wk in Experiment 1. The dietary treatment did not affect Zn concentration in the plasma, testis, kidney, spleen and liver; however, Zn concentration in the femur and its cortex was significantly higher in rats given diet containing 25 g Ca/kg than in other rats. Rats were given phytate-free diet containing 5 g Ca /kg or 25 g Ca /kg for 4 wk in Experiment 2. After 12-h food deprivation, rats were given a diet extrinsically labeled by 67Zn with dysprosium as a fecal marker for 4 h. Feces were collected from 1 d before administration of the labeled diet to 5 d after administration. Excess Ca did not affect the true absorption of Zn and its endogenous excretion but increased femoral Zn. These results suggest that excess Ca improves Zn bioavailability without affecting Zn absorption when diets do not contain phytate.     

Dietary silicon and arginine affect mineral element composition of rat femur and vertebra

Both arginine and silicon affect collagen formation and bone mineralization. Thus, an experiment was designed to determine if dietary arginine would alter the effect of dietary silicon on bone mineralization and vice versa. Male weanling Sprague-Dawley rats were assigned to groups of 12 in a 2×2 factorially arranged experiment. Supplemented to a ground corn/casein basal diet containing 2.3 μg Si/g and adequate arginine were silicon as sodium metasilicate at 0 or 35 μg/g diet and arginine at 0 or 5 mg/g diet. The rats were fed ad libitum deionized water and their respective diets for 8 wk. Body weight, liver weight/body weight ratio, and plasma silicon were decreased, and plasma alkaline phosphatase activity was increased by silicon deprivation. Silicon deprivation also decreased femoral calcium, copper, potassium, and zinc concentrations, but increased the femoral manganese concentration. Arginine supplementation decreased femoral molybdenum concentration but increased the femoral manganese concentration. Vertebral concentrations of phosphorus, sodium, potassium, copper, manganese, and zinc were decreased by silicon deprivation. Arginine supplementation increased vertebral concentrations of sodium, potassium, manganese, zinc, and iron. The arginine effects were more marked in the silicon-deprived animals, especially in the vertebra. Germanium concentrations of the femur and vertebra were affected by an interaction between silicon and arginine; the concentrations were decreased by silicon deprivation in those animals not fed supplemental arginine. The change in germanium is consistent with a previous finding by us suggesting that this element may be physiologically important, especially as related to bone DNA concentrations. The femoral and vertebral mineral findings support the contention that silicon has a physiological role in bone formation and that arginine intake can affect that role. The U.S. Department of Agriculture, Agricultural Research Service, Northern Plains Area is an equal opportunity/affirmative action employer, and all agency services are available without discrimination. Mention of a trademark or proprietary product does not constitute a guarantee or warranty of the product by the U.S. Department of Agriculture and does not imply its approval to the exclusion of other products that may be suitable.     

Effect of dietary nickel deprivation on vision,olfaction, and taste in rats

Early studies on dietary nickel deprivation found decreased reproduction rate in pigs and decreased insemination and conception rates in goats. Studies from our laboratory demonstrated that nickel deprivation impaired male reproductive function of rats. A physiological amount of nickel modulates the function of cyclic nucleotide-gated cation channels (CNG channels) in vitro. Thus, because CNG channels have important roles in spermatozoa function, it was speculated that the impairment of reproduction by nickel deprivation was through an effect on CNG channels. Because CNG channels are found in retinal photoreceptor, olfactory receptor, and taste receptor cells, we hypothesized that nickel deprivation would also alter light/dark preference, odor preference to female rat urine, and taste preference/aversion in rats. In the light/dark Y-maze, nickel deprivation significantly decreased time spent in the dark arm by rats. The number of sniffs to estrous female urine was significantly increased only in nickel-supplemented rats. The number of licks at the saccharin bottle was significantly decreased by dietary nickel deprivation. These findings suggest that nickel has a biological role in the special senses: vision, olfaction and taste.     

Effects of boric acid supplementation on bone histomorphometry,metabolism, and biomechanical properties in aged female F-344 rats

Postmenopausal women may benefit from dietary interventions in order to increase bone strength and prevent fractures. Dietary boron (B) may be beneficial for optimal calcium metabolism and, as a consequence, optimal bone metabolism. The present study evaluated the effects of boron, in the form of boric acid, with or without 17β-estradiol (E₂) supplementation (via subcutaneous implant), in ovariectomized (OVX) aged 13-mo-old F-344 rats. Boric acid was administered by gavage at a subtoxic dose (8.7 mg B/kg/d) for 40 d. Results indicate that serum level of minerals as well as osteocalcin (a marker of bone resorption) are dependent to a greater extent on the hormonal status of the animals than on boron supplementation. Boron treatment increased the E₂-induced elevation of urinary calcium and magnesium. Bone mineral density (BMD) of the L5 vertebra and proximal femur was highest in the E₂-treated groups; no increase in BMD was conferred by boron treatment. By histomorphometry of the proximal tibial metaphysis, osteoblastic, osteoid, and eroded surfaces were significantly suppressed by E₂ treatment, but not by boron treatment. In biomechanical testing of femur and vertebra, neither E₂ nor boron treatment significantly increased bone strength. At the levels given, boron alone provided no protection against OVX-induced osteopenia. In addition, combination therapy (B + E₂) provided no additional benefits over those of 17β-estradiol treatment alone in this aged rat model.     

Diethyl maleate,an in vivo chemical depletor of glutathione,affects the response of male and female rats to arsenic deprivation

An experiment was performed to determine the effect of diethyl maleate (DEM), and in vivo depletor of glutathione, on the response of male and female rats to arsenic deprivation. A 2×2×2 factorially arranged experiment used groups of six weanling Sprague-Dawley rats. Dietary variables were arsenic at 0 or 0.5 μg/g and DEM at 0 or 0.25%; the third variable was gender. Animals were fed for 10 wk a casein-ground corn based diet that contained amounts of calcium, phosphorus, and magnesium similar to the AIN-76 diet. DEM supplementation increased blood arsenic in both male and female rats; female rats had the greatest amount of arsenic in whole blood. Although female rats in general had a lower concentration of glutathione in liver, those fed no supplemental DEM, regardless of their arsenic status, had the lowest amounts. Compared to males, female rats had a lower activity of liver glutathione S-transferase (GST). Arsenic deprivation decreased, and DEM supplementation increased liver GST activity in both male and female rats. Lung GST activity was also increased by DEM supplementation in male, but not female, rats. The most striking finding of the study was that compared to males, females had extremely elevated kidney calcium concentrations, and that the elevation was exacerbated by arsenic deprivation. DEM supplementation also exacerbated the accumulation of calcium in the kidney of the female rats. The response of the rat to both DEM and arsenic was, for many variables, dependent on gender. This gender dependence may be explained by the differences in methionine metabolism between male and female rats. Thus, arsenic deprivation apparently can manifest itself differently depending on gender.     

Dietary vitamin B12, sulfur amino acids,and odd-chain fatty acids affect the response of rats to nickel deprivation

An experiment was performed to ascertain whether changing the dietary intake of two substances, cystine and margaric acid (heptadecanoic acid), that affect the flux through pathways involving the two vitamin B₁₂-depednent enzymes, methionine synthase and methylmalonyl-CoA mutase, would affect the interaction between nickel and vitamin B₁₂. Rats were assigned to treatment groups of six in a fully crossed, four-factorial arrangement. The independent variables, or factors, were: per kg of fresh diet, nickel analyzed at 25 and 850 μg; vitamin B₁₂ supplements of 0 and 50 μg; margaric acid supplements of 0 and 5 g; andl-cystine supplements of 0 and 12 g. The diet without cystine was marginally deficient in sulfur amino acids. Nickel affected growth, liver wt/body wt ratio (LB/BW), and a number of variables associated with iron, calcium, zinc, copper, and magnesium metabolism. Most of the effects of nickel were modified by the vitamin B₁₂ status of the rat. In numerous cases, the interaction between nickel and vitamin B₁₂ was dependent on, or altered by, the cystine or margaric acid content of the diet. Thus, the findings showed that the extent and the direction of changes in numerous variables in response to nickel deprivation varied greatly with changes in diet composition. These variables include those previously reported to be affected by nickel deprivation, including growth and the distribution or functioning of iron, calcium, zinc, copper, and magnesium. The findings also support the hypothesis that nickel has a biological function in a metabolic pathway in which vitamin B₁₂ is important.     

Iron accumulation in tissues of magnesium-deficient rats with dietary iron overload

The mineral imbalances in magnesium-deficient rats with dietary iron overload were studied. Forty-four male Wister rats were divided into six groups and fed six diets, two by three, fully crossed: magnesium adequate or deficient, and iron deficient, adequate, or excess. The concentrations of iron, magnesium, calcium, and phosphorus in tissues of the rats were measured. The results were as follows: (1) The excess iron intake reinforced the iron accumulation in liver and spleen of magnesium deficient rats; (2) The saturation of iron binding capacity was enormously elevated in the magnesium deficient rats fed excess iron; and (3) Dietary iron deprivation diminished the degree of calcium deposition in kidney of magnesium deficient rats. These results suggest that magnesium-deprived-rats have abnormal iron metabolism losing homeostatic regulation of plasma iron, and magnesium deficient rats with dietary iron overload may be used as an experimental hemochromatosis model.     

High dietary aluminum affects the response of rats to silicon deprivation

Antagonistic interactions between silicon and aluminum occur in living organisms. Thus, an experiment was performed to ascertain whether high dietary aluminum would accentuate the signs of silicon deprivation in rats and conversely whether silicon deprivation would accentuate the response to high dietary aluminum. The experiment was factorially arranged with two variables: silicon as sodium metasilicate, 0 or 40 μg/g diet, and aluminum as aluminum citrate, 0 or 500 μg/g diet. After 9 wk, body weights and plasma urea nitrogen were higher and plasma concentrations of threonine, serine, glycine, cystine, and methionine were lower in silicon-adequate than silicon-deprived rats. High dietary aluminum significantly decreased plasma phenylalanine. An interaction between aluminum and silicon affected plasma triglyceride, cholesterol, and phosphorus concentrations. High dietary aluminum decreased these variables when silicon was absent from the diet, but increased them when silicon was present. Skull iron and silicon concentrations were decreased and iron and zinc concentrations in the femur were increased by the addition of 500 μg Al/g diet. High dietary aluminum decreased tibia density in silicon-adequate rats, but increased tibial density in silicon-deprived rats. The findings indicate that in rats, high dietary aluminum can affect the response to silicon deprivation and dietary silicon can affect the response to high dietary aluminum.     

Interactions among nickel,copper, and iron in rats

In two fully crossed, three-way, two by three by three, factorially arranged experiments, female weanling rats were fed a basal diet supplemented with iron at 15 and 45 μg/g, nickel at 0, 5, and 50 μg/g and copper at 0, 0.5, and 5 μg/g (Expt. 1) or 0, 0.25, and 12 μg/g (Expt. 2). Expt. 1 was terminated at 11 weeks, and Expt. 2 at 8 weeks because, at those times, some rats fed no supplemental copper and the high level of nickel began to lose weight, or die from heart rupture. The experiments showed that nickel interacted with copper and this interaction was influenced by dietary iron. If copper deficiency was neither very severe or mild, copper deficiency signs of elevated levels of total lipids and lipid phosphorus in liver and plasma, and cholesterol in plasma, were made more severe by supplemental dietary nickel. Rats in which nickel supplementation exacerbated copper deficiency did not exhibit a depressed level of copper in liver and plasma. Also, although iron deprivation enhanced the interaction between nickel and copper, iron deprivation did not significantly depress the level of copper in liver and plasma. The findings confirmed that, in rats, a complex relationship exists between nickel, copper, and iron, thus indicating that both the iron and copper status of experimental animals must be controlled before data about nickel nutriture and metabolism can be compared among studies.     

Silicon deprivation decreases collagen formation in wounds and bone,and ornithine transaminase enzyme activity in liver

We have shown that silicon (Si) deprivation decreases the collagen concentration in bone of 9-wk-old rats. Finding that Si deprivation also affects collagen at different stages in bone development, collagen-forming enzymes, or collagen deposition in other tissues would have implications that Si is important for both wound healing and bone formation. Therefore, 42 rats in experiment 1 and 24 rats in experiment 2 were fed a basal diet containing 2 or 2.6 μg Si/g, respectively, based on ground corn and casein, and supplemented with either 0 or 10 μg Si/g as sodium metasilicate. At 3 wk, the femur was removed from 18 of the 42 rats in experiment 1 for hydroxyproline analysis. A polyvinyl sponge was implanted beneath the skin of the upper back of each of the 24 remaining rats. Sixteen hours before termination and 2 wk after the sponge had been implanted, each rat was given an oral dose of ¹⁴C-proline (1.8 μCi/100 g body wt). The total amount of hydroxyproline was significantly lower in the tibia and sponges taken from Si-deficient animals than Si-supplemented rats. The disintegrations per minute of ¹⁴C-proline were significantly higher in sponge extracts from Si-deficient rats than Si-supplemented rats. Additional evidence of aberrations in proline metabolism with Si deprivation was that liver ornithine aminotransferase was significantly decreased in Si-deprived animals in experiment 2. Findings of an increased accumulation of ¹⁴C-proline and decreased total hydroxyproline in implanted sponges and decreased activity of a key enzyme in proline synthesis (liver ornithine aminotransferase) in Si-deprived animals indicates an aberration in the formation of collagen from proline in sites other than bone that is corrected by Si. This suggests that Si is a nutrient of concern in wound healing as well as bone formation. The U.S. Department of Agriculture, Agricultural Research Service, Northern Plains Area is an equal opportunity/affirmative action employer, and all agency services are available without discrimination. Mention of a trademark or proprietary product does not constitute a guarantee or warranty of the product by the US Department of Agriculture and does not imply its approval to the exclusion of other products that may be suitable.     

Tissue manganese levels and liver pyruvate carboxylase activity in magnesium-deficient rats

To investigate the manganese status in magnesium deficiency, 40 male Wistar rats, 3 wk old, were divided into two groups and fed a magnesium deficient diet or a normal synthetic diet for 2 wk. Dietary magnesium depletion decreased magnesium levels in brain, spinal cord, lung, spleen, kidney, testis, bone, blood, and plasma, while it elevated the magnesium level in liver. In magnesium-depleted rats, calcium concentration was increased in lung, liver, spleen, kidney, and testis, while it was decreased in tibia. In magnesium-depleted rats, manganese concentration was decreased in plasma and all tissues except adrenal glands and blood. Dietary magnesium depletion diminished pyruvate carboxylase (EC 6.4.1.1) activity in the crude mitochondrial fraction of liver. Positive correlation was found between the liver manganese concentration and the pyruvate carboxylase activity. In the magnesium-depleted rats, glucose was decreased while plasma lipids (triglycerides, phospholipids, and total cholesterol) were increased. These results suggest that dietary magnesium deficiency changes manganese metabolism in rats.     

Selected indicators of calcium-phosphate metabolism in patients with diabetes mellitus

The changes in blood serum concentrations of calcium, magnesium, inorganic phosphate, total activity of alkaline phosphatase and the activity of its bone fraction, as well as urinary excretion of calcium, phosphate, hydroxyproline and oxalate have been measured in 31 patients with insulin-dependent (type I) diabetes, in 31 patients with non-insulin-dependent (type II) diabetes and in 29 healthy subjects in the condition of low-calcium diet. The elevated urinary excretion of calcium, phosphate, hydroxyproline and oxalate, lowered blood serum level of magnesium, and increased total and bone fraction activities of alkaline phosphatase were found in diabetic patients. The urinary excretion of calcium and hydroxyproline, and the activity of bone fraction alkaline phosphatase were significantly higher in patients with type II diabetes than in those with type I diabetes. It was concluded that there is a significant relation between the state of metabolic normalization of diabetes and the degree of biochemical aberrations concerning calcium-phosphate metabolism.     

Citrus bioactive compounds improve bone quality and plasma antioxidant activity in orchidectomized rats

BackgroundsWe reported that citrus consumption improves bone quality in orchidectomized male rats. In the present study, effects of feeding citrus bioactive compounds and crude extract on bone quality in orchidectomized rats were evaluated.MethodsSeventy 90-days-old male rats were randomly assigned to five groups for 60 days of feeding study. The treatment groups were SHAM-control, orchidectomy (ORX), ORX+crude extract, ORX+limonin, and ORX+naringin. At termination, animals were euthanized, blood was collected for the plasma antioxidant status. Bone resorption and bone formation markers in the blood and urine were evaluated. Bone quality in the femur and the 5th lumbar and the total calcium concentration in the bones and excreta were evaluated.ResultsOrchidectomy lowered (p<0.05) plasma antioxidant capacity, bone quality, and bone calcium; elevated (p<0.05) TRAP, deoxypyridinoline (DPD), and calcium excretion; and did not change the plasma IGF-I in comparison to the SHAM group. The citrus crude extract or the purified bioactive compounds increased (p<0.05) the plasma antioxidant status, plasma IGF-I, and bone density, preserved (p<0.05) the concentration of calcium in the femur and in the 5th lumbar, and numerically improved bone strength. The crude extract and the bioactive compounds decreased (p<0.05) fecal excretion of calcium, numerically lowered the urinary excretion of calcium, and suppressed (p<0.05) the plasma TRAP activity without affecting (p>0.1) urinary excretion of DPD in comparison to the ORX group.ConclusionsPotential benefit of the citrus crude extract and its bioactive compounds on bone quality appears to preserve bone calcium concentration and increase antioxidant status.     

Dietary fat composition modifies the effect of boron on bone characteristics and plasma lipids in rats

Female and male rats weighing about 170 g and 200 g, respectively, were fed diets (approximately 70 microg boron/kg) in a factorial arrangement with supplemental boron at 0 (deficient) and 3 (adequate) mg/kg and canola oil or palm oil at 75 g/kg of diet as variables. After 5 weeks, six females in each treatment were bred. Dams and pups continued on their respective dietary treatments through gestation, lactation and post-weaning. Thirteen weeks after weaning, plasma and bones were collected from 12 male and 12 female offspring in each treatment. Boron supplementation increased femur strength measured by the breaking variable bending moment; tibial calcium and phosphorus concentrations; and plasma alkaline phosphatase. Femur breaking stress was greatest in boron-supplemented rats fed canola oil, and lowest in boron-deprived females fed canola oil; this group also exhibited the lowest femur bending moment. Minerals associated with bone organic matrix, zinc and potassium, were increased by boron supplementation in tibia. Plasma phospholipids were decreased by boron deprivation in females, but not males. Plasma cholesterol was decreased in boron-supplemented males by replacing canola oil with palm oil. The findings suggest that a diet high in omega-3 alpha-linolenic acid promotes femur strength best when the dietary boron is adequate.