Effects of Soy Phytoestrogens and New Zealand Functional Foods on Bone Health.

New Zealand is a rich source of food components that may have bioactivity on bone. Docosahexaenoic acid (DHA) from fish oil has been shown to maintain bone in ovariectomised (OVX) rats. Kiwifruit, a source of fibre and carotenoids, may also affect bone via a prebiotic as well as direct cell-based mechanisms. We aimed to 1) ascertain the effects of DHA on two cell models, including interactions with soy isoflavones; 2) and investigate the specific effects of carotenoids from kiwifruit as well as whole kiwifruit in cell-based and rodent models as well as in a human study. RAW 264.7 mouse monocytes or mouse bone marrow was used to generate osteoclasts (OC). Cells were exposed to the agents between 5 and 21 d and formation and activity of OC measured, including molecular markers. DHA inhibited OC formation in both cell models, including expression of cathepsin K, NFATc1 as well as actin ring formation. Combination with isoflavones enhanced these effects. In OVX rats and mice fed with kiwifruit for 8 wk, green kiwifruit reduced the rate of bone loss after OVX, and in mice it reduced C-telopeptide of Type 1 collagen (CTX) levels and RANKL expression while in menopausal women, green kiwifruit affected blood lipids and bone markers positively.

Onset of nephrocalcinosis depends on dietary phosphorus concentration in male rats fed a magnesium-deficient diet.

Although a magnesium (Mg)-deficient diet is generally known to induce nephrocalcinosis, our previous study observed that despite the administration of a Mg-deficient diet, the kidney calcium (Ca) and phosphorus (P) concentrations were not increased in male rats. We speculated that this result was due to the P concentration of the experimental diet based on the AIN-93G formula used in the previous study. In the present study, male rats were fed modified AIN-93G diets containing the two different Mg concentrations [0.5 g per kg diet (normal-Mg) or Mg-free (Mg-deficient)] and three different P concentrations [3 (3-P), 5 (5-P) or 7 (7-P) g per kg diet]. By histological examination of the kidney, nephrocalcinosis was not observed in rats fed on the Mg-deficient diet containing 3-P While nephrocalcinosis appeared in rats fed on the Mg-deficient diet containing 5-P and 7-P The degree of nephrocalcinosis was severe in rats fed on the Mg-deficient diet containing 7-P compared with rats fed on the Mg-deficient diet containing 5-P These results demonstrated that the Mg-deficient diet based on AIN-93G formula dose not induce nephrocalcinosis and that the Mg-deficient diet based on AIN-93G formula with increased dietary P concentrations induces nephrocalcinosis in male rats. We suggest that the onset of nephrocalcinosis could depend on the dietary P concentration in male rats fed on a Mg-deficient diet.

Effect of dietary magnesium supplementation on bone loss in rats fed a high phosphorus diet.

The purpose of this study was to investigate the effect of dietary magnesium (Mg) supplementation on bone loss in rats fed a high phosphorus (P) diet. Weanling Wistar strain rats were randomly divided into four dietary groups of 6 rats each and fed their respective diets; a diet containing 0.3% P and 0.05% Mg (C), a diet containing 1.5% P and 0.05% Mg (HP), a diet containing 0.3% P and 0.15% Mg (HMg), or a diet containing 1.5% P and 0.15% Mg (HPMg), for 21 days. Compared to the C and HMg groups, serum parathyroid hormone (PTH) concentration was significantly higher in the HP and HPMg groups. Serum osteocalcin concentration and urinary excretion of C-terminal telopeptides of type I collagen (CTx), markers of bone turnover, were significantly higher in the HP and HPMg groups than in the C and HMg groups. Dietary Mg supplementation had no significant effects on serum PTH and osteocalcin concentrations, while urinary excretion of CTx was significantly lower in the HPMg group than in the HP group. These results suggested that dietary Mg supplementation suppressed bone resorption due to high P diet.

Effects of high calcium intake on bone metabolism in magnesium-deficient rats.

We examined the effects of high calcium (Ca) intake on bone metabolism in magnesium (Mg)-deficient rats. Male Wistar rats were divided into three groups, with each group having a similar mean body weight, and fed a control diet (control group), a Mg-deficient diet (Mg-deficient group) or a Mg-deficient Ca-supplemented diet (Mg-deficient Ca-supplemented group) for 14 d. Femoral Ca content was significantly lower in the Mg-deficient Ca-supplemented group than in the control group and Mg-deficient group. Femoral Mg content was significantly lower in the Mg-deficient group and Mg-deficient Ca-supplemented group than in the control group. Furthermore, femoral Mg content was significantly lower in the Mg-deficient Ca-supplemented group than in the Mg-deficient group. Serum osteocalcin levels (a biochemical marker of bone formation) were significantly lower in the two Mg-deficient groups than in the control group. As a biochemical marker of bone resorption, urinary deoxypyridinoline excretion was significantly higher in the Mg-deficient Ca-supplemented group than in the control group and Mg-deficient group. The results in the present study suggest that high Ca intake had no preventive effect on alteration of bone metabolism in Mg-deficient rats.

An in situ hybridization study on interleukin-1 beta mRNA induced by transient forebrain ischemia in the rat brain.

Expression of interleukin-1 beta (IL-1 beta) mRNA in the rat brain after transient forebrain ischemia was investigated by in situ hybridization histochemistry. Thirty min after the start of recirculation, IL-1 beta mRNA was induced in the several brain regions, including the olfactory bulb, cerebral cortex, hippocampus, striatum and thalamus where neuronal degeneration was reported to be observed after transient forebrain ischemia. The hybridization signals were observed both on the glial cells and around the vascular walls.

Molecular cloning and in situ hybridization histochemistry for rat mu-opioid receptor.

We cloned a cDNA for the rat mu-opioid receptor from a rat thalamus cDNA library. The deduced amino-acid sequence of rat mu-opioid receptor consists of 398 residues with the features shared by the members of the G-protein coupled receptor family, and is 59% and 60% identical with those of rat kappa-opioid and mouse delta-opioid receptors, respectively. Northern blot analysis showed that expression of mu-opioid receptor mRNA was intensive in the thalamus, striatum, hypothalamus and pons-medulla, moderate in the hippocampus and midbrain, and slight in the cerebral cortex and cerebellum. More detailed distribution of the mRNA in the rat brain was examined using the in situ hybridization technique. Intense expression of mu-opioid receptor mRNA was observed in the internal granular and glomerular layers of the olfactory bulb, caudate putamen, nucleus accumbens, medial septum, diagonal band, medial preoptic area, several nuclei of thalamus, amygdala, interpeduncular nucleus, medial raphe nucleus, inferior colliculus, parabrachial nucleus, locus coeruleus, nucleus solitary tract and ambiguus nucleus. Furthermore, mu-opioid receptor mRNA was moderately expressed in the hippocampus, globus pallidus, ventral pallidus, arcuate hypothalamic nucleus, supramammillary nucleus, superior colliculus, periacqueductal gray, and several nuclei of lower brain stem, including raphe magnus nucleus, reticular gigantocellular nucleus and lateral paragigantocellular nucleus.