The Effects of Annatto Tocotrienol on Body Composition and Serum Adiponectin, Leptin and Glucose Level in a Rat Model of Androgen Deficiency Induced by Buserelin

@#Androgen ablation therapy using gonadotropin-releasing hormone agonists is reported to be associated with metabolic abnormalities. Annatto tocotrienol (AnTT) is reported to reduce the expression of genes related to adipogenesis but the mechanism remains elusive. This study sought to determine the effects of annatto tocotrienol on body composition (lean and fat mass), serum adiponectin, leptin, and glucose levels in male rats treated with buserelin, a testosterone ablation agent. Three-month-old male Sprague Dawley rats (n=32) were randomly divided into four groups. The normal control (n=8) was given corn oil orally daily and normal saline subcutaneously daily. The remaining groups were injected with buserelin subcutaneously (75µg/kg/day). The buserelin group (n=8) was given corn oil orally, while the treatment groups were supplemented orally with AnTT at 60 or 100 mg/kg (n = 8/group). After treatment of 12 weeks, rats were euthanized. Dual-energy x-ray absorptiometry was performed to determine the lean and fat mass of the rats. Blood was collected for the evaluation of adiponectin, leptin and glucose levels. After 12 weeks, the lean mass, fat mass, adiponectin and leptin levels for all groups increased significantly compared to their respective baseline levels irrespective of their treatment (P<0.05). All groups, except rats receiving AnTT at 60 mg/kg, experienced a significant increase in glucose level after 3 months (P<0.05). Androgen ablation and AnTT do not influence body composition, adiponectin and leptin levels in male rats. However, annatto tocotrienol at 60 mg/kg may improve glucose metabolism.

Protective Effects of Palm Tocotrienol Against Glucocorticoid Induced Osteoporosis via Regulation of Gene Expressions

Long term glucocorticoids administration induces oxidative stress which leads to alteration of bone structure and strength. Palm oil is rich in tocotrienol, an antioxidant. It can be used for the prevention of oxidative stress related diseases. The main objective of this study was to determine the mechanism of palm tocotrienol in maintaining the bone structure and strength in glucocorticoid-induced osteoporosis. Thirty two adult male Sprague-Dawley rats, aged 3 months, weighing 300-320 g rats were used in this study. Sixteen rats undergone adrenalectomy and were administered with 120μg/kg/day intramuscular injection of dexamethasone. Eight rats were supplemented with oral palm tocotrienol 60 mg/kg/day (Adrx+Dex+PTT) and the other eight rats were given oral vehicle palm olein 0.1 ml/kg/day (Adrx+Dex). Eight rats underwent sham procedure and were given vehicle palm olein 0.05 ml/kg/day by intramuscularly and oral 0.1 ml/kg/day (Sham). The rats were euthanized after two months of treatments. Eight rats were euthanized after acclimatic action without receiving any treatment (Baseline). The right femurs were used for bone biomechanical strength and histomorphometry analysis while the left for gene expression and oxidative stress enzymes activities. The results indicated that long-term glucocorticoid treatment significantly increased bone resorption marker, CTX (6060.7 ± 410 pg/ml) and decreased bone structure and strength. Osteoblast and osteoclast related genes expressions indicated an increase in bone turnover. Supplementation of palm tocotrienol had maintained serum resorption (2619.4 + 209 pg/ml) marker level and preserved bone structure and strength. Gene expression analysis showed decrease in bone resorption. The findings suggested that palm tocotrienol has potential benefits against glucocorticoid-induced osteoporosis by regulating osteoblast and osteoclast related gene expression

Quantification of Bone Histomorphometric Parameters Using the Weibel Technique in Animals

Bone histomorphometric measurements are required to understand the efficacy of treatment on bone remodelling. Previous studies used the Weibel technique as a quantitative stereological method to determine bone cellular and dynamic changes. However, there was no description on how this technique was applied. This studyaimed to provide a full picture about the utilization of the Weibel technique to measure static and dynamic bone histomorphometric indices. Technical expertise, processing of bone samples, randomization of the trabecular sections and an adequate number of analysed images for each section are required to achieve reliable results with a low possibility of errors.

Total testosterone and sex hormone-binding globulin are significantly associated with metabolic syndrome in middle-aged and elderly men.

Testosterone and sex hormone-binding globulin (SHBG) have been shown to be associated with metabolic syndrome (MS) in men. This study aimed at validating these relationships in a group of middle-aged and elderly men and assessing their strength of association to MS. A cross-sectional study of 332 Malaysian men aged 40 years and above was conducted. The blood of subject was collected under fasting condition for determination of testosterone, SHBG, glucose and lipid levels. Their medical history, smoking and alcohol consumption status, waist circumference (WC), body mass index (BMI) and blood pressure (BP) were recorded. All testosterone and SHBG levels were significantly reduced in MS subjects compared to non-MS subjects (p<0.05). Testosterone and SHBG were correlated significantly with most of the MS indicators without adjustments. In multiple regression analysis, the triglyceride level was the only MS indicator that was significantly, inversely and independently associated with all testosterone measurements and SHBG (p<0.05). Waist circumference was significantly and negatively associated with SHBG level (p<0.05) though not independent of BMI. Total testosterone and SHBG were significantly and inversely associated with the presence of MS. Testosterone and SHBG are potential intervention targets for the prevention of MS in men.

Piper sarmentosum is comparable to glycyrrhizic acid in reducing visceral fat deposition in adrenalectomised rats given dexamethasone.

OBJECTIVES: Visceral obesity may be due to the dysregulation of cortisol production or metabolism that lead to metabolic disease. In adipose tissue, the enzyme 11beta-hydroxysteroid dehydrogenase type 1 regulates cortisol metabolism (11beta-HSD1). A previous study showed an increase in the visceral fat deposition in adrenalectomised rats given intramuscular dexamethasone. Glycyrrhizic acid (GCA) has been shown to reduce fat deposition because it is a known potent inhibitor of the 11beta-HSD1 enzyme. Piper sarmentosum (PS) is an edible medicinal plant commonly used in Asia as traditional medicine for treating diabetes, hypertension and joint pains. In this study, we determined the effects of PS extract on the disposition and morphology of perirenal adipocytes of adrenalectomised rats given intramuscular dexamethasone. MATERIALS AND METHODS: A total of 21 male Spraque Dawley rats were adrenalectomised and given intramuscular dexamethasone, 120 µg/kg/day. These rats were further divided into three groups: adrenalectomised control (ADR+Dexa; n=7), GCA-treated (ADR+Dexa+GCA; dose=240 mg/kg/day; n=7) and PS-treated (ADR+Dexa+PS; dose=125 mg/kg/day; n=7) groups. The various treatments were given via gastric gavage following 2 weeks of adrenalectomy. RESULTS: Treatment with PS extract for 8 weeks showed decreased deposition of perirenal adipocytes which was similar to the GCA-treated group. However, PS-treated rats had thinner adipocyte membrane compared with that of the GCA-treated group. CONCLUSION: In conclusion, PS extract decreased perirenal fat deposition and reduced the diameter of the adipocyte membrane. However, the mechanisms of action needed further study.

The Anti-Inflammatory, Phytoestrogenic, and Antioxidative Role of Labisia pumila in Prevention of Postmenopausal Osteoporosis.

Osteoporosis is characterized by skeletal degeneration with low bone mass and destruction of microarchitecture of bone tissue which is attributed to various factors including inflammation. Women are more likely to develop osteoporosis than men due to reduction in estrogen during menopause which leads to decline in bone-formation and increase in bone-resorption activity. Estrogen is able to suppress production of proinflammatory cytokines such as IL-1, IL-6, IL-7, and TNF-α. This is why these cytokines are elevated in postmenopausal women. Studies have shown that estrogen reduction is able to stimulate focal inflammation in bone. Labisia pumila (LP) which is known to exert phytoestrogenic effect can be used as an alternative to ERT which can produce positive effects on bone without causing side effects. LP contains antioxidant as well as exerting anti-inflammatory effect which can act as free radical scavenger, thus inhibiting TNF-α production and COX-2 expression which leads to decline in RANKL expression, resulting in reduction in osteoclast activity which consequently reduces bone loss. Hence, it is the phytoestrogenic, anti-inflammatory, and antioxidative properties that make LP an effective agent against osteoporosis.

Effect of 11ß-HSD1 dehydrogenase activity on bone histomorphometry of glucocorticoid-induced osteoporotic male Sprague-Dawley rats.

INTRODUCTION: Glucocorticoids cause osteoporosis by decreasing bone formation and increasing bone resorption activity. Glucocorticoid action in bones depends on the activity of 11-beta-hydroxysteroid dehydrogenase type 1 (11ß-HSD1) enzyme, which plays an important role in regulating corticosteroids. 11ß-HSD1 is expressed by human and rat osteoblasts. We aimed to investigate the relationship between 11ß-HSD1 dehydrogenase activity and bone histomorphometric changes in glucocorticoid-induced osteoporotic bone in rats. METHODS: A total of 30 male Sprague-Dawley rats (aged three months, weighing 200-250 g) were divided into three groups of ten each. Group 1 rats were the baseline control, which were sacrificed untreated at the beginning of the study. Group 2 rats underwent sham operation and were administered with vehicle olive oil intramuscularly at 0.05 ml/kg. Group 3 rats were adrenalectomised and administered with an intramuscular injection of dexamethasone 120 µg/kg body weight/day. The treatment was started two weeks after the operation, for a duration of two months. Plasma osteocalcin, plasma pyrodinoline, plasma corticosterone and 11ß-HSD1 were measured, and bone histomorphometry analysis was performed. RESULTS: Dexamethasone treatment caused an increase in plasma corticosterone level, together with a significant reduction in 11ß-HSD1 dehydrogenase activity of the bone, along with a higher plasma level of the bone resorption marker, pyridinoline. Dexamethasone treatment also caused a reduction in trabecular volume, number and thickness, and an increase in trabecular separation. CONCLUSION: Long-term glucocorticoid treatment reduces the 11ß-HSD1 dehydrogenase activity in the bone, which can otherwise lead to bone loss due to the increased level of active glucocorticoids.

Low dose of tocotrienols protects osteoblasts against oxidative stress.

AIMS: Vitamin E is an antioxidant that may protect bone against oxidative stress-induced osteoporosis. This in vitro study was conducted to determine the protective effects of a-tocopherol and γ-tocotrienol on osteoblasts, the bone forming cells, against oxidative stress. MATERIALS AND METHODS: Toxicity tests were carried out on hydrogen peroxide (H(2)O(2)), a-tocopherol and γ-tocotrienol and their inhibitory concentration 50 (IC(50)) on osteoblasts were determined if any. Osteoblast cultures were then pretreated with different concentrations of a-tocopherol or γ-tocotrienol for 24 hours before incubated with the IC50 of H(2)O(2) for 2 hours. Cell viability was determined by using MTS assay to compare the protective effects of both vitamin E on osteoblast exposed to H(2)O(2). RESULTS: The IC(50) after 2 hours and 24 hours incubation time for H(2)O(2) were 490 µM and 280 µM respectively. γ-Tocotrienol was found to be toxic to osteoblasts with the IC(50) of 290 µM after 24 hours incubation time while a-tocopherol was not toxic to osteoblasts at any doses. However, γ-tocotrienol was able to protect osteoblasts from H(2)O(2) toxicity at low concentration (1 µM), whereras a-tocopherol was not able to offer protection against H2O2 toxicity. CONCLUSIONS: γ-tocotrienol was found to be toxic to osteoblasts at high concentrations but at much lower concentration, it has better antioxidant activity than a-tocopherol to protect osteoblasts from oxidative stress.

Effects of vitamin E on receptor activator of nuclear factor kappa B ligand (RANKL) and osteoprotegerin (OPG) in rats treated with nicotine.

Vitamin E is found to reverse the effects of nicotine on bone and this study aimed to determine its mechanism. Male Sprague Dawley rats were divided into four groups and treated for 3 months: Group 1 was the control group (RC). Groups 2 (N), 3 (N+TT) and 4 (N+ATF) received nicotine 7 mg/kg throughout the treatment period. In addition, groups 3 and 4 received tocotrienol 60 mg/kg and alpha-tocopherol 60 mg/kg respectively during months 2 and 3. Parameters measured were serum osteoprotegerin (OPG), serum receptor activator of nuclear factor kappa B ligand (RANKL), femoral and lumbar bone calcium content and body weight. Nicotine did not affect OPG or RANKL levels but reduced bone calcium content suggesting the calcium loss is not due to increase osteoclastogenesis. OPG was increased in N+ATF while RANKL was slightly increased in N+TT. Both vitamin E supplements restored bone calcium loss induced by nicotine. Nicotine impaired weight gain in all treatment groups starting week 4 however, N+TT group was comparable to RC from week 6 onwards. Bone protective effects of ATF, but not TT, may be partly due to inhibition of osteoclastogenesis.

Effects of Palm Tocotrienols on Oxidative Stress and Bone Strength in Ovariectomised Rats

Oxidative stress has been associated with postmenopausal osteoporosis which pre-disposes to risk of fracture. Palm tocotrienol is a potent antioxidant and has the poten-tial to be used for treatment of post-menopausal osteoporosis. The aim of the study is to determine if palm tocotrienol supplementation could alleviate oxidative stress in ovariectomised rat model and improve its bone strength. The rats were divided into four groups: (i) sham-operated group (SHAM) (ii) ovariectomised-control group (OVX) (iii) ovariectomised and given 60mg/kg α-tocopherol by oral gavage (OVX + ATF) (iv) ovariectomised and given 60mg/kg palm tocotrienols by oral gavage (OVX + PTT). After eight weeks of treatment, blood samples were taken to measure oxidative status (MDA, SOD and GPX) while the femurs were biomechanically tested for strength and resistance to fracture. Ovariectomy was shown to induce oxidative stress as shown by the raised MDA levels and reduced GPX activity. Palm tocotrienols seemed to offer protection against the ovariectomy-induced oxidative stress as shown by the suppression of MDA levels and raised GPX and SOD activities in the OVX+PTT group. In comparison, α-tocopherol was only able to raise the SOD but not as high as palm tocotrienols. The biomechanical tests have shown that ovariectomy has not af-fected the bone strength significantly after eight weeks. Palm tocotrienols supplemen-tation for eight weeks was effective in preventing oxidative stress in a post-meno-pausal rat.

Effects of vitamin E supplementation on bone metabolism in nicotine-treated rats.

INTRODUCTION: Nicotine has been shown to exert negative effects on bone. This study determined whether vitamin E supplementation is able to repair the nicotine-induced adverse effects in bone. METHODS: 24 male rats were divided into three groups. The fi rst group was the baseline control and killed untreated at the beginning of the study. Groups 2 and 3 received nicotine at 7 mg per kg for three months but during the second and third months, group 2 was supplemented with alpha-tocopherol (N+ATF) while group 3 was given palm tocotrienol mixture (N+TT). Serum interleukin-1 (IL-1), serum interleukin-6 (IL-6), serum osteocalcin, urine deoxypyridinoline (DPD) and bone calcium content were measured. RESULTS: Palm tocotrienol mixture was able to prevent the increment of IL-1 and IL- 6 due to nicotine treatment. No changes were seen in the osteocalcin levels, but the N+ATF group had lower urine DPD levels after treatment. However, bone-remodelling index revealed no significant changes. No significant differences were seen in the femoral bone calcium content results, although the fourth lumbar bone calcium content was reduced in both groups with 66.5 percent reduction in the N+ATF group and 59.6 percent reduction in the N+TT group. CONCLUSION: Palm tocotrienol mixture was better than alpha-tocopherol in reversing the effects of nicotine on IL-1 and IL-6. Both forms of vitamin E were not able to restore the nicotine-induced bone calcium loss, but the N+ATF group suffered a greater loss. Tocotrienol seemed to be superior to alpha-tocopherol in combating against the adverse effect of nicotine.

Reheating of soy oil is detrimental to bone metabolism in oestrogen deficient rats.

INTRODUCTION: The short-term and long- term effects of heated soy oil on bone metabolism in ovariectomised Sprague-Dawley rats were studied. METHODS: Three-month-old female rats, were divided into five groups: normal control (NC); ovariectomised control (OVXC); ovariectomised and fed rat chow with added fresh soybean oil (SOF) or once-heated soy oil (SO1) or five-times-heated soy oil (SO5). Short-term parameters measured after one month were serum interleukin-6 (IL-6) and osteocalcin. Long-term parameters measured after six months were the structural bone histomorphometrical parameters. Vitamin E content in the soy oil subjected to the different heating treatments were also measured. RESULTS: Rats in the SO5 group had higher levels of IL-6 after one month compared to the other four groups. Osteocalcin levels in the SO1 and SO5 groups remained high after treatment, while those in the NC and SOF groups declined. After six months, bone mass declined in the SO5 group. Vitamin E assay in the oils showed that levels of alpha-tocopherol decreased after heating the oil once and five times, while levels of gamma- and delta-tocopherols only declined after heating five times. CONCLUSION: Repeated heating of soy oil destroyed the tocopherols causing raised serum IL-6 and osteocalcin levels, leading to increased bone resorption and osteoporosis in the long term.

The effects of repeatedly heated frying oil and high cholesterol diet on the bone in ovariectomised rats.

The use of repeatedly heated frying oils and intake of high cholesterol diet have been linked to bone damage. The aim of this study is to determine the combined effects of taking repeatedly heated frying oils (palm or soy oil) and high cholesterol diet on the dynamic histomorphometric parameters of bone. Ovariectomised rats were used as animal model of post-menopausal osteoporosis. After six months of treatment, Double-labeled Surface (dLS/BS), Mineralising surface (MS/BS) and Bone Formation Rate (BFR/BS) of ovariectomised rats (OvxC) were significantly reduced compared to the normal control group. Additions of fresh or once-heated palm or soy oil into high cholesterol diet seem to have improved the dynamic parameters towards the normal control values. However, when these oils were repeatedly heated, the protective effects were lost and the dynamic parameters except MS/BS dropped back towards the ovariectomised-control values.

The effects of repeatedly heated frying oil and high cholesterol diet on the bone in ovariectomised rats

The use of repeatedly heated frying oils and intake of high cholesterol diet have been linked to bone damage. The aim of this study is to determine the combined effects of taking repeatedly heated frying oils (palm or soy oil) and high cholesterol diet on the dynamic histomorphometric parameters of bone. Ovariectomised rats were used as animal model of post-menopausal osteoporosis. After six months of treatment, Double-labeled Surface (dLS/BS), Mineralising surface (MS/BS) and Bone Formation Rate (BFR/BS) of ovariectomised rats (OvxC) were significantly reduced compared to the normal control group. Additions of fresh or once-heated palm or soy oil into high cholesterol diet seem to have improved the dynamic parameters towards the normal control values. However, when these oils were repeatedly heated, the protective effects were lost and the dynamic parameters except MS/BS dropped back towards the ovariectomised-control values.

Tocotrienol offers better protection than tocopherol from free radical-induced damage of rat bone.

1. Free radicals generated by ferric nitrilotriacetate (FeNTA) can activate osteoclastic activity and this is associated with elevation of the bone resorbing cytokines interleukin (IL)-1 and IL-6. In the present study, we investigated the effects of 2 mg/kg FeNTA (2 mg iron/kg) on the levels of serum IL-1 and IL-6 with or without supplementation with a palm oil tocotrienol mixture or alpha-tocopherol acetate in Wistar rats. 2. The FeNTA was found to elevate levels of IL-1 and IL-6. Only the palm oil tocotrienol mixture at doses of 60 and 100 mg/kg was able to prevent FeNTA-induced increases in IL-1 (P < 0.01). Both the palm oil tocotrienol mixture and alpha-tocopherol acetate, at doses of 30, 60 and 100 mg/kg, were able to reduce FeNTA-induced increases in IL-6 (P < 0.05). Therefore, the palm oil tocotrienol mixture was better than pure alpha-tocopherol acetate in protecting bone against FeNTA (free radical)-induced elevation of bone-resorbing cytokines. 3. Supplementation with the palm oil tocotrienol mixture or alpha-tocopherol acetate at 100 mg/kg restored the reduction in serum osteocalcin levels due to ageing, as seen in the saline (control) group (P < 0.05). All doses of the palm oil tocotrienol mixture decreased urine deoxypyridinoline cross-link (DPD) significantly compared with the control group, whereas a trend for decreased urine DPD was only seen for doses of 60 mg/kg onwards of alpha-tocopherol acetate (P < 0.05). 4. Bone histomorphometric analyses have shown that FeNTA injections significantly lowered mean osteoblast number (P < 0.001) and the bone formation rate (P < 0.001), but raised osteoclast number (P < 0.05) and the ratio of eroded surface/bone surface (P < 0.001) compared with the saline (control) group. Supplementation with 100 mg/kg palm oil tocotrienol mixture was able to prevent all these FeNTA-induced changes, but a similar dose of alpha-tocopherol acetate was found to be effective only for mean osteoclast number. Injections of FeNTA were also shown to reduce trabecular bone volume (P < 0.001) and trabecular thickness (P < 0.05), whereas only supplementation with 100 mg/kg palm oil tocotrienol mixture was able to prevent these FeNTA-induced changes.

Effects of tocopherols and tocotrienols on body composition and bone calcium content in adrenalectomized rats replaced with dexamethasone.

Long-term glucocorticoid treatment is associated with severe side effects, such as obesity and osteoporosis. A palm oil-derived vitamin E mixture had been shown previously to be protective against osteoporosis in rats given 120 microg/kg dexamethasone daily for 12 weeks. In this study we determined the effects of two isomers of vitamin E (i.e., palm oil-derived gamma-tocotrienol and the commercially available alpha-tocopherol, 60 mg/kg of body weight/day) on body composition and bone calcium content in adrenalectomized rats replaced with two doses of dexamethasone, 120 microg/kg and 240 microg/kg daily. Treatment period was 8 weeks. gamma-Tocotrienol (60 mg/kg of body weight/day) was found to reduce body fat mass and increase the fourth lumbar vertebra bone calcium content in these rats, while alpha-tocopherol (60 mg/kg of body weight/day) was ineffective. Therefore, in conclusion, palm oil-derived gamma-tocotrienol has the potential to be utilized as a prophylactic agent in prevention of the side effects of long-term glucocorticoid use.

Vitamin E deficiency reduced lumbar bone calcium content in female rats.

Vitamin E deficiency has been found to impair bone calcification. This study was done to determine the effects of vitamin E deficiency and supplementation on parathyroid hormone, i.e. the hormone involved in bone regulation. Female Sprague-Dawley rats were divided into 4 groups: 1) normal rat chow (RC), 2) vitamin E deficiency (VED), vitamin E deficient rats supplemented with 3) 60 mg/kg alpha-tocotrienol (ATT) and 4) 60 mg/kg (alpha-tocopherol (ATF). Treatment was carried out for 3 months. Vitamin E deficiency caused hypocalcaemia during the first month of the treatment period, increased the parathyroid hormone level in the second month and decreased the bone calcium content in the 4th lumbar bone at the end of the treatment. Vitamin E supplementation (ATT and ATF) failed to improve these conditions. The bone formation marker, osteocalcin, and the bone resorption marker, deoxypyridinoline did not change throughout the study period. In conclusion vitamin E deficiency impaired bone calcium homeostasis with subsequent secondary hyperparathyroidism and vertebral bone loss. Replacing the vitamin E with pure ATF or pure ATT alone failed to correct the changes seen.

Palm vitamin eprotects bone against dexamethasone-induced osteoporosis in male rats.

The aim of this study was to determine the effects of palm oil-derived vitamin E on glucocorticoid-induced osteoporosis. Three-month old male Wistar rats were adrenalectomised to remove circulating glucocorticoids. The animals were then administered with Dexamethasone 120 µg/kg body weight/day. Treatment with palm vitamin E 60 mg/kg body weight/day was given simultaneously. The results showed that palm vitamin E prevented the loss in regional and whole body bone mineral density seen in the Dexamethasone treated animals. Palm vitamin E improved femoral length and calcium content in the Dexamethasone treated animals. The results confirmed that palm oil-derived vitamin E was effective in preventing glucocorticoid-induced osteoporosis.

Palm vitamin E is comparable to alpha-tocopherol in maintaining bone mineral density in ovariectomised female rats.

Vitamin E has been shown to affect bone metabolism. In this study we determined the effects of palm vitamin E and alpha-tocopherol on bone metabolism. Sprague-Dawley female rats fed with normal rat chow were divided into 4 groups and supplemented with either palm vitamin E 30 mg/kg rat weight, palm vitamin E 60 mg/kg rat weight or alpha-tocopherol 30 mg/kg rat weight. One group was not supplemented. Half of these rats were ovariectomised before supplementation was given for 10 months. As expected, bone mineral density of the ovariectomised rats fed on normal rat chow diet was lower compared to the intact rats. However, these changes were not seen in the supplemented group of rats. Both intact and ovariectomised rats supplemented with palm vitamin E 30 mg/kg rat weight had a lower bone calcium content in both femoral and vertebral bones whilst rats fed palm vitamin E 60 mg/kg rat weight or alpha-tocopherol 30 mg/kg rat weight were able to maintain bone calcium content. Alkaline phosphatase activity was elevated in ovariectomised rats supplemented with palm vitamin E 30 mg/kg rat weight and alpha-tocopherol 30 mg/kg rat weight compared to the intact rats. Alpha-tocopherol also reduced the activity of tartrate-resistant acid phosphatase post-ovariectomy. These findings indicate that both palm vitamin E and alpha-tocopherol maintained bone mineral density in ovariectomised rats but caused conflicting effects on bone calcium content. Further study is needed in order to determine the mechanisms involved.

Palm vitamin E improves bone metabolism and survival rate in thyrotoxic rats.

The effects of vitamin E derived from palm oil on bone turnover in thyrotoxic rats were studied. Palm vitamin E reduced bone resorption to a greater extent than bone formation in thyrotoxic rats, suggesting a net reduction in bone loss. The action of palm vitamin E is probably due to its antioxidant properties. Survival rates were also significantly increased in thyrotoxic rats given palm vitamin E, suggesting the role of free radicals in the overall morbidity and mortality in thyrotoxicosis.