Effect of green tea and Tai Chi on bone health in postmenopausal osteopenic women: a 6-month randomized placebo-controlled trial.

UNLABELLED: Postmenopausal women with osteopenia received green tea polyphenols (GTP) supplement and/or Tai Chi exercise for 6 months. Bone turnover biomarkers, calcium metabolism, and muscle strength were measured. This study showed that GTP supplementation and Tai Chi exercise increased bone formation biomarkers and improved bone turnover rate. Tai Chi exercise increased serum parathyroid hormone. GTP supplementation, Tai Chi exercise, and the combination of the two all improved muscle strength in postmenopausal women with osteopenia. INTRODUCTION: This study evaluated the effect of GTP supplementation and Tai Chi (TC) exercise on serum markers of bone turnover (bone-specific alkaline phosphatase, BAP, and tartrate-resistant acid phosphatase, TRAP), calcium metabolism, and muscle strength in postmenopausal osteopenic women. METHODS: One hundred and seventy-one postmenopausal osteopenic women were randomly assigned to four groups: (1) placebo (500 mg starch/day), (2) GTP (500 mg GTP/day), (3) placebo + TC (placebo plus TC training at 60 min/session, three sessions/week), and (4) GTP + TC (GTP plus TC training). Overnight fasting blood and urine samples were collected at baseline, 1, 3, and 6 months for biomarker analyses. Muscle strength was evaluated at baseline, 3, and 6 months. One hundred and fifty subjects completed the 6-month study. RESULTS: Significant increases in BAP level due to GTP intake (at 1 month) and TC (at 3 months) were observed. Significant increases in the change of BAP/TRAP ratio due to GTP (at 3 months) and TC (at 6 months) were also observed. Significant main effect of TC on the elevation in serum parathyroid hormone level was observed at 1 and 3 months. At 6 months, muscle strength significantly improved due to GTP, TC, and GTP + TC interventions. Neither GTP nor TC affected serum TRAP, serum and urinary calcium, and inorganic phosphate. CONCLUSION: In summary, GTP supplementation and TC exercise increased BAP and improved BAP/TRAP ratio. TC exercise increased serum parathyroid hormone. GTP supplementation, TC exercise, and the combination of the two all improved muscle strength in postmenopausal women with osteopenia.

Green tea polyphenols attenuate deterioration of bone microarchitecture in female rats with systemic chronic inflammation.

UNLABELLED: Green tea polyphenols (GTP) are promising agents for preventing bone loss. GTP supplementation sustained microarchitecture and improved bone quality via a decrease in inflammation. Findings suggest a significant role for GTP in skeletal health of patients with chronic inflammation. INTRODUCTION: This study evaluated whether GTP can restore bone microstructure along with a molecular mechanism in rats with chronic inflammation. A 2 [placebo vs. lipopolysaccharide (LPS)]× 2 [no GTP vs. 0.5% GTP (w/v) in drinking water] factorial design was employed. METHODS: Female rats were assigned to four groups: placebo, LPS, placebo + GTP, and LPS + GTP for 12 weeks. Efficacy was evaluated by examining changes in bone microarchitecture using histomorphometric and microcomputed tomographic analyses and by bone strength using the three-point bending test. A possible mechanism was studied by assessing the difference in tumor necrosis factor-α (TNF-α) expression in tibia using immunohistochemistry. RESULTS: LPS lowered trabecular volume fraction, thickness, and bone formation in proximal tibia while increasing osteoclast number and surface perimeter in proximal tibia and eroded surface in endocortical tibial shafts. GTP increased trabecular volume fraction and number in both femur and tibia and periosteal bone formation rate in tibial shafts while decreasing trabecular separation in proximal tibia and eroded surface in endocortical tibial shafts. There was an interaction between LPS and GTP in trabecular number, separation, bone formation, and osteoclast number in proximal tibia, and trabecular thickness and number in femur. GTP improved the strength of femur, while suppressing TNF-α expression in tibia. CONCLUSION: In conclusion, GTP supplementation mitigated deterioration of bone microarchitecture and improved bone integrity in rats with chronic inflammation by suppressing bone erosion and modulating cancellous and endocortical bone compartments, resulting in a larger net bone volume. Such a protective role of GTP may be due to a suppression of TNF-α.

Synergistic effects of green tea polyphenols and alphacalcidol on chronic inflammation-induced bone loss in female rats.

UNLABELLED: Studies suggest that green tea polyphenols (GTP) or alphacalcidol is promising agent for preventing bone loss. Findings that GTP supplementation plus alphacalcidol administration increased bone mass via a decrease of oxidative stress and inflammation suggest a significant role of GTP plus alphacalcidol in bone health of patients with chronic inflammation. INTRODUCTION: Studies have suggested that green tea polyphenols (GTP) or alphacalcidol are promising dietary supplements for preventing bone loss in women. However, the mechanism(s) related to the possible osteo-protective role of GTP plus D(3) in chronic inflammation-induced bone loss is not well understood. METHODS: This study evaluated bioavailability, efficacy, and related mechanisms of GTP in combination with alphacalcidol in conserving bone loss in rats with chronic inflammation. A 12-week study of 2 (no GTP vs. 0.5% GTP in drinking water) × 2 (no alphacalcidol vs. 0.05 µg/kg alphacalcidol, 5×/week) factorial design in lipopolysaccharide-administered female rats was performed. In addition, a group receiving placebo administration was used to compare with a group receiving lipopolysaccharide administration only to evaluate the effect of lipopolysaccharide. RESULTS: Lipopolysaccharide administration resulted in lower values for bone mass, but higher values for serum tartrate-resistant acid phosphatase (TRAP), urinary 8-hydroxy-2'-deoxyguanosine, and mRNA expression of tumor necrosis factor-α and cyclooxygenase-2 in spleen. GTP supplementation increased urinary epigallocatechin and epicatechin concentrations. Both GTP supplementation and alphacalcidol administration resulted in a significant increase in bone mass, but a significant decrease in serum TRAP levels, urinary 8-hydroxydeoxyguanosine levels, and mRNA expression of tumor necrosis factor-α and cyclooxygenase-2 in spleen. A synergistic effect of GTP and alphacalcidol was observed in these parameters. Neither GTP nor alphacalcidol affected femoral bone area or serum osteocalcin. CONCLUSION: We conclude that a bone-protective role of GTP plus alphacalcidol during chronic inflammation bone loss may be due to a reduction of oxidative stress damage and inflammation.

Premenopausal bone mass is related to physical activity.

The relationship between physical activity and bone mass was investigated in 24 healthy, white, premenopausal women (mean age [+/- SE], 39.0 +/- 1.39 years). Physical activity was determined by a sensor that measures movement of the trunk, and bone mineral levels were determined by means of single- and dual-photon absorptiometry and neutron activation analysis. Total physical activity levels were related both to bone mineral density of the spine (r = .41) and to total body calcium levels (r = .51). There was no significant relationship between the bone density of the distal portion of the radius and activity (r = .20). Nonparametric analysis and stepwise multiple regression analysis revealed negative correlations between cigarette smoking and bone density of the spine and radius. These data suggest that the level of physical activity in sedentary white women may be a determinant of peak total skeletal mass and bone density of the spine.

Determinants of bone mass in postmenopausal women.

Eighty white women, mean age 52 years, within one to six years postmenopausal, were studied to examine the relationship of various factors to bone mass. Forty-four of the women had annual measurements of bone mass, so that the rate of bone loss could be determined. Bone mass was measured by total body neutron activation analysis and photon absorptiometry of the distal radius (total body calcium [TBCa] and bone mineral content [BMC], respectively). Breast-feeding and pregnancy were noted to be associated with higher bone mass; those with lower BMC and/or TBCa tended to have higher serum alkaline phosphatase levels, lower testosterone levels, and more years since the cessation of menses. The rate of bone loss from the radius was greater in those with higher parathyroid hormone levels; those with reduced dietary intake of calcium and lower 25-hydroxyvitamin D levels had a greater rate of loss of TBCa.

Combined vitamin D parathyroid defect in thalassemia major.

A 17-year-old girl with thalassemia major experienced tetany. The serum calcium level was 5.5 mg/dL, and the phosphorus level was 6.3 mg/dL. Serum levels of parathyroid hormone (PTH) and 25-hydroxyvitamin D (25-OHD) were subnormal at 125 pg/mL and 8.1 ng/mL, respectively, As a result of these findings, serum 25-OHD and PTH levels were measured in an additional 12 patients with thalassemia major. Low levels of both 25-OHD and PTH were found frequently. An increase in serum 25-OHD levels was noted in each of four patients who were examined after iron chelation therapy.

Differential effect of caffeine administration on calcium and vitamin D metabolism in young and adult rats.

Since coffee drinking may lead to a worsening of calcium balance in humans, we studied the serial changes of serum calcium, PTH, 1,25-dihydroxyvitamin D (1,25(OH)2D) and calcium balance in young and adult rats after daily administration of caffeine for 4 weeks. In the young rats, there was an increase in urinary calcium and endogenous fecal calcium excretion after four days of caffeine administration that persisted for the duration of the experiment. Serum calcium decreased on the fourth day of caffeine administration and then returned to control levels. In contrast, the serum PTH and 1,25(OH)2D remained unchanged initially, but increased after 2 weeks of caffeine administration. The intestinal absorption coefficient of calcium remained unchanged, instead of declining gradually as observed in the young control group. This finding suggests that the intestinal absorption of calcium was stimulated by the increase in 1,25(OH)2D production after chronic administration of caffeine. In the adult rat group, an increase in the urinary calcium and endogenous fecal calcium excretion and serum levels of PTH was found after caffeine administration. However, the serum 1,25(OH)2D levels and intestinal absorption coefficient of calcium remained the same as in the adult control group. A decrease in the net balance of calcium occurred as a result of increased calcium excretion. The current study, using an animal model, supports the suggestion that chronic administration of caffeine could lead to negative calcium balance when there is an impaired ability to increase the efficiency of calcium absorption. Such a situation exists in elderly human subjects, since they have a reduced capacity to synthesize 1,25(OH)2D.

Effect of deconditioning on cortical and cancellous bone growth in the exercise trained young rats.

Exercise enhances bone growth and increases peak bone mass. The aim of this study was to determine whether or not 4 weeks of deconditioning after 8 weeks of exercise in growing rats would result in a decrease in bone gain or reverse the benefits of exercise. Fifty 4-week-old female Sprague-Dawley rats were randomized by a stratified weight method into 5 groups with 10 rats in each group: 8 weeks exercise (8EX), 8 weeks sedentary control (8S), 12 weeks exercise (12EX), 8 weeks exercise followed by 4 weeks sedentary (8EX4S), and 12 weeks sedentary control (12S). The exercise consisted of running on a treadmill with a 5 degrees slope at 24 m/minute for 1 h/day and 5 days/week. After each period of exercise, cancellous and cortical bone histomorphometry were performed on double fluorescent labeled 5-microm-thick sections of the proximal tibia and 40-microm-thick sections of the tibial shaft, respectively. Eight and 12 weeks of exercise resulted in a significant increase in the body weight and gastrocnemius muscle weight by two-way analysis of variance (ANOVA). The femoral wet weight (mg; mean +/- SD; 8EX, 781 +/- 45.1 vs. 8S, 713 +/- 40.5; p < 0.05; 12EX, 892 +/- 41.6 vs. 12S, 807 +/- 19.8; p < 0.05) was significantly higher in the exercise group than that in the respective control groups. The femoral wet weight and bone volume (BV) of the 8EX4S group (818 +/- 46.2 mg and 531 +/- 31.2 microl, respectively) were significantly lower than those of the 12EX group (p < 0.05) and did not differ significantly from those of the 12S groups. The cancellous BV was significantly higher in the 8EX and 12EX groups than that in the respective sedentary groups (p < 0.05). The cortical bone area of the tibial shaft was also significantly higher in the 12EX than that in the 12S group (p < 0.05). The increase in the cancellous BV or cortical bone area was caused by an increase in the mineral apposition rate (MAR), without a significant effect in the labeled perimeter. The bone formation rate (BFR; microm3/microm2 per day) in the cancellous bone (12EX, 27.9 +/- 7.74 vs. 12S, 15.4 +/- 4.56; p < 0.05) or periosteal surface (12EX, 127.6 +/- 27.7 vs. 12S, 79.5 +/- 18.6; p < 0.05) was significantly higher in the exercised groups than that in the respective control group (p < 0.05). Again, deconditioning resulted in a decrease in the cancellous BFR, BV, periosteal BFR, and cortical bone area to levels not significantly different from the 12S group. In conclusion, our findings showed that exercised growing rats, when deconditioned, lost the benefits gained through exercise and their bone parameters were reduced to levels not different from the sedentary control. Thus, continued exercise is required to maintain high bone mass.

Additive effect of treadmill exercise and 17 beta-estradiol replacement on prevention of tibial bone loss in adult ovariectomized rat.

The effects of 17 beta-estradiol (E2) and treadmill exercise on tibial bone mass, tibial uptake of 45Ca, and proximal tibia osteoblast and osteoclast cell number were determined in adult ovariectomized rats. Female rats aged 10 months were ovariectomized and divided into five groups: (1) sham-operated; (2) ovariectomized; (3) ovariectomized, given 10 micrograms E2 biweekly; (4) ovariectomized, trained to exercise on a treadmill daily; and (5) ovariectomized, given E2 and exercised. E2 and/or exercise interventions were started 2 months following surgery and continued for 4 months. The calcium content of the tibial metaphysis and diaphysis and the proximal cancellous bone (BV/TV) were lower in the ovariectomized than in the sham-operated controls 6 months after ovariectomy. This lower bone content was associated with a greater bone uptake of 45Ca and a greater number of osteoblasts and osteoclasts in the proximal tibia compared to the control rats. The metaphyseal calcium content was higher and the 45Ca uptake and osteoblast and osteoclast number were lower in the E2-treated rats than in the nontreated rats. In the exercised group, higher diaphyseal calcium content and proximal cancellous bone were associated with lower bone resorption parameters without a significant effect on bone formation. This study demonstrates that E2 primarily influences tibial cancellous bone of the ovariectomized rat and a positive adaptation to exercise occurs in both cancellous and cortical bone. Under estrogen deficiency, E2 replacement suppresses increased bone formation and resorption; exercise suppresses mainly bone resorption. The effects of E2 replacement and exercise training are independent and additive.

Effect of ovariectomy on cancellous bone in the hypophysectomized rat.

This experiment studied the effects of hypophysectomy (HX) and ovariectomy (OV) on cancellous bone in the proximal tibia and distal 5th lumbar vertebra by dynamic histomorphometry. Forty-eight female Sprague-Dawley rats, 3 months of age, were divided into age-matched control, HX, OV, and HX + OV (HO) groups. Ten rats were sacrificed at 3 months of age as baseline controls, and the rest of the animals were sacrificed 5 weeks after the surgery. While the age-matched controls, and the OV rats significantly increased in body weight compared with the baseline control rats, cancellous bone volumes in the proximal tibia and distal 5th lumbar vertebra increased in the age-matched controls and decreased in the OV rats. In the HX and HO rats, body weight equaled baseline control values, and their cancellous bone volumes were decreased with a poorer trabecular architecture in both bone sites. In all HX, OV, and HO rats, uterine weight and serum estradiol were significantly decreased. OV significantly increased longitudinal bone growth and the tissue- and surface-based bone formation and bone resorption parameters in both the proximal tibia and 5th lumbar vertebra (p < 0.05). HX alone or HO significantly decreased longitudinal bone growth and the tissue-based bone formation rate without significantly affecting surface-based bone formation and bone resorption parameters when compared with the age-matched controls. No significant differences were detected in any variables between the HX alone and HO rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of exercise on cancellous bone of the aged female rat.

Dual-energy x-ray absorptiometry and dynamic histomorphometry were used to examine the effect of treadmill exercise on the bone density and cancellous bone formation and resorption in the proximal tibia and fifth lumbar vertebra (L5) of the aged female rat. Female rats aged 14 months were divided into four groups: 8 controls and 10 exercised for a 9 week study and 8 controls and 9 exercised for a 16 week study. Exercise consisted of running on a flat-bed treadmill, 17 m/minute, 1 h/day, 5 days/week. Tibial metaphysis and L5 vertebral density of each rat were measured in the 16 week study by DXA at weeks 0, 9, and 16. Compared to the control group, a significant increase in bone density in both metaphyseal tibia and L5 vertebra was apparent at 16 weeks after exercise training (P = 0.046 and 0.025, respectively, by two-way ANOVA). Histomorphometric analysis showed that the trabecular bone eroded surface and the ratio of eroded to mineralizing surface in tibial metaphysis were significantly lower in the exercised than in the respective control group in both the 9 and 16 week studies. In L5 vertebra, these decreases by exercise were apparent only in the 16 week study. A significant increase in the bone formation rate was apparent in the cancellous bone of the tibia but not of the vertebra after 16 weeks of exercise (P < 0.05). The trabecular architecture (bone number and separation) of the L5 vertebra in the exercised rats did not differ from that of the controls in either study.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of hypophysectomy and 1,25-dihydroxyvitamin D on duodenal calcium absorption.

Intestinal active and passive transport of calcium were studied in hypophysectomized (HX) and intact rats using the in vivo duodenal loop technique. In the vitamin D-supplemented condition, hypophysectomy resulted in a decrease in serum 1,25-dihydroxyvitamin D [1,25-(OH)2D]. Hypophysectomy prevented a gain in body weight and decreased intestinal mucosal weight and total calcium absorption. When the data were expressed per unit mucosal wet weight, duodenal active calcium transport was not different in the HX and intact groups, but passive transport was persistently decreased by hypophysectomy. Administration of bovine GH to the HX rats did not change the mucosal mass, but enhanced both active and passive duodenal transport to calcium. Vitamin D depletion for 6 weeks decreased serum 25-hydroxy-vitamin D and 1,25-(OH)2D levels in both intact and HX rats to about the same level. After bovine GH and 1,25-(OH)2D3 replacement, the calcium absorption studies suggest that 1) 1,25-(OH)2D3 enhances intestinal calcium passive transport as well as active transport in intact and HX rats; 2) GH enhances both active and passive transport of calcium in the presence of sufficient quantities of 1,25-(OH)2D; 3) this latter effect is independent of the metabolism of vitamin D; and 4) a decrease in mucosal mass is one of the factors that results in decreased calcium absorption after hypophysectomy.

Vitamin D supplementation in postmenopausal black women.

Black women have lower levels of serum 25-hydroxyvitamin D (25OHD) with higher serum PTH levels than white women. Correction of these alterations in the vitamin D-endocrine system could lead to less bone loss in postmenopausal women and, consequently, preservation of bone mass. Ten healthy postmenopausal black women were given 20 microg vitamin D3 daily for 3 months. At the end of the study, mean serum 25OHD levels had increased from 24 to 63 nmol/L. Serum intact PTH and nephrogenous cAMP declined significantly, and there was a 21% drop in the fasting urinary N-telopeptide of type I collagen. Vitamin D3 supplementation raises serum 25OHD levels in postmenopausal black women, decreases secondary hyperparathyroidism, and reduces bone turnover. These findings should spur further investigation of the use of vitamin D supplementation in the prevention of osteoporosis in this population.

Effect of hypophysectomy on intestinal phosphate absorption in rats.

Intestinal active and passive transport of phosphate (Pi) was studied in hypophysectomized (HX) and intact rats using the in situ intestinal loop technique. Hypophysectomy resulted in a significant reduction of total Pi absorption under active transport conditions. However, when transport data were expressed on the basis of mucosal mass, the reduction was not apparent. Under passive transport conditions, net Pi absorption was lower in the HX rats even after correction for the decrease of mucosal mass. Administration of bovine growth hormone (bGH) did not change the intestinal Pi absorption in the HX rats. These results indicate that a decrease in mucosal mass following hypophysectomy is one of the factors that causes a decrease of intestinal Pi absorption.

Differential effect of treadmill exercise on three cancellous bone sites in the young growing rat.

The aim of the present study was to examine cancellous bone changes induced by exercise on three different skeletal sites, the lumbar vertebra, the proximal, and the distal tibia, in the young growing rat. Forty 4-week-old female Sprague-Dawley rats were randomized into 4 groups of 10 animals each; 8 weeks exercise (8EX), 8 weeks sedentary control (8CON), 12 weeks exercise (12EX), and 12 weeks sedentary control (12CON). The exercise regimen consisted of treadmill running at 24 m/min 1 hr per day 5 days a week. After each period of exercise, the proximal and distal tibial metaphyses (PTM and DTM, respectively) and the fifth lumbar (L5) vertebral body were processed for histomorphometry of the cancellous bone (secondary spongiosa) and cortical periosteum. Eight and twelve weeks of exercise significantly increased the mineral apposition rate and bone formation rate in the PTM and DTM, and 12 weeks of exercise significantly increased the labeled perimeter in the DTM, compared with the age-matched controls. Eight and twelve weeks of exercise significantly increased cancellous bone volume in the PTM (mean +/- standard deviation, 8EX; 19.1 +/- 2.9% vs 8CON; 14.3 +/- 3.1%, P < 0.05 and 12EX; 18.8 +/- 3.5% vs 12CON; 15.2 +/- 3.3%, P < 0.05), and 12 weeks exercise significantly increased cancellous bone volume in the DTM, compared with age-matched control (12EX; 32.5 +/- 7.7%, 12CON; 22.2 +/- 4.8%, P < 0.05). The increase in cancellous bone volume by 12 weeks exercise was higher in the DTM than that in the PTM (43.4% and 24.0%, respectively). On the other hand, the exercise did not significantly affect cancellous bone volume and bone formation in the L5 vertebral body, although the cortical periosteal bone formation rate and the L5 vertebral bone mass were increased. These findings suggest that cancellous bone adaptation to treadmill exercise is site specific, and the effect may be influenced by factors such as mechanical loading and metaphyseal bone architecture in the young growing rat.

Effect of hypophysectomy on the occupied and unoccupied binding sites for 1,25-dihydroxyvitamin D3 in rat intestine.

It is not known why the intestinal active transport of calcium per unit of mucosal mass is not affected by hypophysectomy (HX) even though serum 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] and intestinal calcium-binding protein are decreased. In order to study the effect of HX on the quantity of intestinal receptor of 1,25(OH)2D3 and its binding characteristics, the intestinal total occupied and unoccupied binding sites for 1,25(OH)2D3 were measured, by the use of the mercurial reagent mersalyl, in the intestine of HX and age-matched control rats. In addition, the effect of bovine growth hormone (bGH) replacement on the quantity of both binding states was examined in the HX rats. Results of Scatchard analysis and sucrose density gradients showed that the 3.5S receptor of the HX rat intestine was not distinguishable from that seen in the intact rat intestinal cytosol. Under vitamin D-supplemented conditions, HX was shown to reduce the levels of occupied receptors when the data were expressed on the basis of cytosolic protein. The reduced occupied sites could, in fact, have resulted from the reduction in plasma 1,25(OH)2D3 levels. No synthesis rates were determined. The unoccupied and total binding sites for 1,25(OH)2D3 per length of intestine were lower in the HX group than in the intact group. Administration of bGH resulted in an increase of endogenously occupied binding sites without affecting the total binding activity. Under vitamin D-depleted (-D) conditions, the total binding activity (intestinal) for 1,25(OH)2D3 was increased in the intact but not in the -DHX rats. Administration of bGH to the -DHX rat resulted in no effect on the binding levels of 1,25(OH)2D3 receptor.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of 17 beta-estradiol administration on cortical and cancellous bone of ovariectomized rats with and without hypophysectomy.

Pituitary hormones are essential for bone growth and bone turnover. Hypophysectomy (HX) diminishes mitogenesis and abolishes the high bone turnover rate induced by ovariectomy (OV). It is not known whether the suppressive effect of estrogen on bone resorption is diminished or abolished by HX. The present study investigates the effects of 17 beta-estradiol (E2) (20 micrograms/wk) on cortical and cancellous bone mass and bone turnover as measured by histomorphometry in HX + OV (HO) rats. Sprague-Dawley rats at 2 months of age were OV or HO and the experiment was performed over a 6 week period. Hypophysectomy + OV (HO) resulted in a cessation of periosteal bone formation, and longitudinal bone growth and a decrease in cancellous bone volume. The tibial dry weight and tibial density were significantly lower in the HO than in the intact or OV groups. Administration of E2 to HO rats partially prevented cancellous bone loss, whereas the same dosage of E2 fully prevented cancellous bone loss in rats with OV alone. Nevertheless, cancellous bone volume was higher in the HO + E2 than in the HO-alone groups. Estradiol administration in HO rats did not suppress cancellous bone formation rate or the eroded surface as much as it did in the OV rats. The suppressive effect of E2 on periosteal bone formation rate and mineral apposition rate was also diminished in HO rats. However, factorial ANOVA showed that the effects of E2 on increasing cancellous bone volume and decreasing periosteal bone formation rate and mineral apposition rate were still significant in the HO rats. Tibial dry weight and tibial density did not differ between HO and HO + E2 groups. In conclusion, we have demonstrated that the estrogen-induced effects of preventing cancellous bone loss, of suppressing bone formation, and resorption as seen in OV rats was diminished but not abolished in HO rats.

RETRACTED: Comparative effects of vitamin K and vitamin D supplementation on prevention of osteopenia in calcium-deficient young rats.

The aim of this study was to clarify the difference in the effects of vitamin K and vitamin D supplementation on the development of osteopenia in young rats under mild calcium deficiency. Sixty female Sprague-Dawley rats, 6 weeks of age, were randomized by stratified weight method into six groups with 10 rats in each group: baseline control, 0.5% (normal) calcium diet, 0.1% (low) calcium diet, 0.1% calcium diet + vitamin K (30 mg/100 g, food intake), 0.1% calcium diet + vitamin D (25 microg/100 g, food intake), and 0.1% calcium diet + K + D. After 10 weeks of feeding, serum calcium, 25-hydroxyvitamin D(3) [25 (OH) D(3)], 1,25-dihydroxyvitamin D(3) [1,25 (OH)(2) D(3)], and parathyroid hormone (PTH) levels were measured, and intestinal calcium absorption and renal calcium reabsorption were evaluated. Bone histomorphometric analyses were performed on cortical bone of the tibial shaft and cancellous bone of the proximal tibia. Calcium deficiency induced hypocalcemia, increased serum PTH and 1,25 (OH)(2) D(3) levels with decreased serum 25 (OH) D(3) level, stimulated intestinal calcium absorption and renal calcium reabsorption, and reduced maturation-related cortical bone gain as a result of decreased periosteal bone gain and enlarged marrow cavity but did not significantly influence maturation-related cancellous bone gain. Vitamin K supplementation in calcium-deficient rats stimulated renal calcium reabsorption, retarded the abnormal elevation of serum PTH level, increased maturation-related cancellous bone gain, and retarded the reduction in maturation-related cortical bone gain. On the other hand, vitamin D supplementation in calcium-deficient rats stimulated intestinal calcium absorption via increased serum 1,25 (OH)(2) D(3) level with prevention of the abnormal elevation of serum PTH level, prevented hypocalcemia, reduced the maturation-related cancellous bone gain, and prevented the reduction in periosteal bone gain and enhanced enlargement of the marrow cavity with no significant effect on the reduction in maturation-related cortical bone gain. However, no synergistic effect of vitamin K and vitamin D on intestinal calcium absorption, renal calcium reabsorption, and cancellous and cortical bone mass was found. This study shows the differential effects of vitamin K and vitamin D supplementation on the development of osteopenia in young rats under mild calcium deficiency. Vitamin K supplementation stimulates renal calcium reabsorption, increases maturation-related cancellous bone gain, and retards the reduction in maturation-related cortical bone gain, whereas vitamin D supplementation stimulates intestinal calcium absorption and prevents the reduction in maturation-related periosteal bone gain by inducing accumulation of calcium from cancellous and endocortical bone.

Ovariectomy-induced high turnover in cortical bone is dependent on pituitary hormone in rats.

The aim of this study is to examine the interrelationship of pituitary and ovarian hormone deficiency on the regulation of bone growth and bone formation rate. 48 female rats, at 3 months of age, were divided into age-matched intact control, hypophysectomized (HX), ovariectomized (OV), and HX + OV groups. Ten rats were killed at 3 months of age as baseline controls, and the rest of the animals were killed 5 weeks after surgery. Serum levels of osteocalcin and dynamic histomorphometry on the periosteal surface of the tibial shaft and fifth lumbar vertebrae were measured to evaluate systemic and local bone turnover. Tibial and fourth lumbar vertebral bone area, bone mineral content, and bone density were measured by dual-energy X-ray absorptiometry (DXA). Our results confirmed that OV increased and HX suppressed systemic and periosteal bone formation parameters in both bone sites, OV increased and HX suppressed the gain in bone size and bone mass. When OV rats were HX, the serum levels of osteocalcin and periosteal bone formation parameters of the tibial shaft and the fifth lumbar vertebrae were, however, depressed and did not differ from that of the HX alone. DXA results show that the effect of OV on bone size and bone mass is also abolished by HX. In conclusion, we have demonstrated that OV increases tibial and lumbar vertebral bone formation and bone growth and this effect is pituitary hormone dependent.