Animals ; Bone and Bones ; metabolism ; Energy Metabolism ; physiology ; Humans ; Osteocalcin ; metabolism

The prevailing model of osteology is that bones constantly undergo a remodeling process, and that the differentiation and functions of osteoblasts are partially regulated by leptin through different central hypothalamic pathways. The finding that bone remodeling is regulated by leptin suggested possible endocrinal effects of bones on energy metabolism. Recently, a reciprocal relationship between bones and energy metabolism was determined whereby leptin influences osteoblast functions and, in turn, the osteoblast-derived protein osteocalcin influences energy metabolism. The metabolic effects of bones are caused by the release of osteocalcin into the circulation in an uncarboxylated form due to incomplete gamma-carboxylation. In this regard, the Esp gene encoding osteotesticular protein tyrosine phosphatase is particularly interesting because it may regulate gamma-carboxylation of osteocalcin. Novel metabolic roles of osteocalcin have been identified, including increased insulin secretion and sensitivity, increased energy expenditure, fat mass reduction, and mitochondrial proliferation and functional enhancement. To date, only a positive correlation between osteocalcin and energy metabolism in humans has been detected, leaving causal effects unresolved. Further research topics include: identification of the osteocalcin receptor; the nature of osteocalcin regulation in other pathways regulating metabolism; crosstalk between nutrition, osteocalcin, and energy metabolism; and potential applications in the treatment of metabolic diseases.
Bone Remodeling/physiology ; Bone and Bones/*metabolism ; *Energy Metabolism ; Humans ; Leptin/metabolism ; Osteocalcin/genetics/*metabolism

Animals ; Bone and Bones ; metabolism ; physiology ; Endocrine System ; metabolism ; physiology ; Female ; Humans ; Male ; Osteocalcin ; metabolism

OBJECTIVETo study the mechanism of new bone formation and remodeling of distraction osteogenesis (DO) by analysis of the expression of osteopontin (OPN) and osteocalcin (OC).

METHODSRhesus were operated to reconstruct the animal model of cleft palate (CP). The CP was closed by DO in experimental group(n = 21). After consolidation of 1, 2, 4, 6, 8, 12, 24 weeks, every 3 animals were killed to collect the specimens, respectively. The OPN and OC and their mRNA were detected quantitatively by Real-time RT-PCR and ELISA, respectively. The animals in control group (n = 2) and sham group (n = 2) were used as control.

RESULTSThe mRNA expression of OPN increased since 2nd week of consolidation and reached the peak at 4th week (7.59 +/- 0.37). The mRNA expression of OC was up-regulated since 4th week, and reach the peak at 6th week (7.94 +/- 0.31). Then they decreased to about the level in sham group at 24th week (P > 0.05). The OPN and OC were highly expressed during 4 to 6 weeks of consolidation. During 8 to 12 weeks, they decreased like their mRNA expression.

CONCLUSIONThe intramembraneous new bone formation after DO can reconstruct the bone defect of CP. The new formed bone can be remodeled to be quite normal bone tissue.

Animals ; Cleft Palate ; metabolism ; surgery ; Macaca mulatta ; Osteocalcin ; metabolism ; Osteogenesis, Distraction ; Osteopontin ; metabolism

OBJECTIVETo evaluate the biological effects of nano-hydroxyapatite/polyamide 66(nHA-PA66) on the growth and activity of osteoblast.

METHODSMTT assay was used to determine the growth of osteoblast, enzymatic measure was used to determine the activity of ALP and quantitative RT-PCR (QRT-PCR) to evaluate the changes of osteoclacin mRNA expression in osteoblasts treated by DMEM eluate of nHA-PA66.

RESULTSOsteoblasts of different test groups demonstrated relative proliferation rate ranging from 98% - 106% without dose-dependent effect. The ALP activity and osteocalcin mRNA expression were similar in test and control groups (P > 0.05).

CONCLUSIONnHA-PA66 has no negative effects on the osteoblast and its osteoblast-compatibility is proved.

Durapatite ; pharmacology ; Nylons ; pharmacology ; Osteoblasts ; drug effects ; Osteocalcin ; metabolism ; RNA, Messenger ; metabolism

Bone remodeling requires a large amount of energy, and is regulated by various hormones. Leptin, produced by adipocytes, is a well-known regulator of energy balance and is also involved in controlling bone mass through interaction with the central nervous system. Serotonin, downstream of leptin, is also emerging as a candidate for controlling energy balance and bone metabolism. Currently, bone is also considered to be an endocrine regulator of energy metabolism. Osteocalcin, secreted from osteoblasts, is known to be a key regulator of glucose and fat metabolism. In this review, we describe a novel concept that asserts that there exists a biological link between bone and energy metabolism, and we summarize what is currently known about the relationship between bone and energy metabolism.
Adipocytes ; Bone Remodeling ; Central Nervous System ; Energy Metabolism* ; Glucose ; Leptin ; Metabolism ; Neurotransmitter Agents ; Osteoblasts ; Osteocalcin ; Serotonin

OBJECTIVES: To investigate the patterns of biochemical bone markers, such as urinary deoxypyridinoline (DPD), N-telopeptide of type I collagen (NTX), and serum osteocalcin (OC), bone-specific alkaline pbosphatase (BSAP) in postmenopansal women with hormone replacement therapy (HRT). Materials and METHOD: From July 1997 to January 1998, total 239 postmenopausal women were emolled in the present study, and 198 healthy premenopausal women with regular menstruation were served as control. The postmenopausal women were pouped into the HRT group and the non-HRT group. The women in the HRT poup have received estrogen with continuous or cyclic progestin therapy far more tban 6 months. The biochemical bone markers of all women were assayed. Results were analysed with Students t-test. RESULTS: The urinary DPD of the non-HRT group was sigaificantly higher than both the HRT poup and the premenopausal group(5.51 +/- 2.47 vs. 3.36 +/- 1.02 and 4.01 +/- 3.86 nM/mM, p < 0.05, repectively). The urinary NTX of the non-HRT group was also higher in comparison to the HRT group and the premenopausal group(48.71 +/- 11.54 vs. 33.70 +/- 17.43 and 33.70 +/- 17.43 nM BCE/mmol, p < 0.05, repectively). However, there were no significant differences in the concentrations of serum BSAP and OC among the three poups. CONCLUSION: The urinary DPD and NTX were more sensitive indicators of bone metabolism tban serum BSAP and OC in postmenopausal women undergoing HRT.
Collagen Type I ; Estrogens ; Female ; Hormone Replacement Therapy* ; Humans ; Menstruation ; Metabolism ; Osteocalcin

OBJECTIVE: To determine the effect of hormone replacement therapy on bone mineral density and biochemical marker of bone metabolism in postmenopausal women receiving hormone replacement therapy. METHOD: We have treated two groups of menopausal women for 4 years; Group 1 received Conjugated Equine Estrogen 0.625 mg (Premarin(R)); Group 2 received Cyclic combined therapy, estrogen and progestin, (Premarin(R) 0.625 mg per day, Provera(R) 10mg per day for 12days), Group 1 was hysterectomized women, received Conjugated Equine Estrogen 0.625 mg per day. We compared the change of bone marker, osteocalcin and bone mineral density during therapy. RESULT: The data demonstrated a beneficial effect in bone marker, osteocalcin decreased in two groups from the baseline values. And hormone replacement therapy shows the beneficial effect in bone mineral densities. Spine BMD increased in two groups by 3.67%, 3.04% after 4years. Femur BMD increased in two groups by 5.34%, 5.25% from the initial value after 4 years. CONCLUSION: Our study results suggest that single estrogen therapy and cyclic combined therapy have benificial effect on increased BMD and decreased bone marker, osteocalcin. Their effects were not signigicantly different between two groups.
Biomarkers* ; Bone Density* ; Estrogens ; Female ; Femur ; Hormone Replacement Therapy* ; Humans ; Metabolism* ; Osteocalcin ; Spine

BACKGROUND: In this study, we examined the influence of exercise loading characteristics on bone metabolic responses and bone morphology in the growth phase and adulthood. METHODS: Running exercise (RUN) and jumping exercise (JUM) were used for the exercise loading in 28-day-old male Wistar rats. Bone metabolism was measured by blood osteocalcin (OC) and tartrate-resistant acid phosphatase (TRACP) levels. For bone morphology, the maximum bone length, bone weight, and bone strength of the femur and tibia were measured. RESULTS: A pre- and post-exercise loading comparison in the growth phase showed significantly increased OC levels in the RUN and JUM groups and significantly decreased TRACP levels in the JUM group. On the other hand, a pre- and post-exercise loading comparison in adulthood showed significantly decreased TRACP levels in the RUN and JUM groups. Femur lengths were significantly shorter in the RUN and JUM groups than in the control (CON) group, while bone weight was significantly greater in the JUM group than in the CON group. CONCLUSIONS: Exercise loading activates OC levels in the growth phase and suppresses TRACP levels in adulthood. On the other hand, these results suggest that excessive exercise loading may suppress bone length.
Acid Phosphatase ; Femur ; Hand ; Humans ; Male ; Metabolism* ; Osteoblasts ; Osteocalcin ; Osteoclasts ; Osteogenesis* ; Rats, Wistar ; Running ; Tibia

BACKGROUND: Biochemical markers have been proposed as sensitive indicators of high bone turnover and for monitoring response to osteoporosis treatment. We conducted a retrospective study to investigate the pattern of biochemical markers of bone metabolism (urinary deoxypryridinoline(D PYD), serum osteocalcin) across menopausal transition in women. METHODS: We measured the urinary excretion of D PYD, serum osteocalcin and BMD in 44 premenopausal and age matched 44 postmenopausal women who visited a tertiary hospital from May 1, 1997 to July 31, 1997. Each values between premenopausal and postmenopausal women were anaysed with paired t-tests. Pearson's correlation coefficients were performed to assess the relationships between the three values. RESULTS: Urinary excretion of D-PYD in postmenopausal women (12.103+/-2.27 nM/mM creatinine) was higher than in premenopausal women (9.322+/-2.53 nM/mM creatinine) (P<0.05). Serum osteocalcin in postmenopausal women (12.8698+/-3.1 ng/ml) was higher than in premenopausal women (9.0949+/-2.7 ng/ml) (P<0.01). BMD in postmenopausal women (0.9979+/-0.1863 g/cm2) was lower than in postmenopausal women (1.1845+/-0.1591 g/cm2) (P<0.01). The serum osteocalcin level was positively correlated with D-PYD (r=0.547, p<0.01). Urine excretion of D-PYD was negatively correlated with BMD (r= 0.36, p<0.01). Serum osteocalcin was negatively correlated with BMD (r= 0.427, P<0.01). CONCLUSION: Urinary D-PYD excretion and serum osteocalcin were increased, but BMD was decreased significantly in postmenopausal women. Urinary D-PYD, serum osteocalcin, and BMD were significantly correlated with each other in women.
Biomarkers ; Bone Density ; Female ; Humans ; Menopause ; Metabolism ; Osteocalcin* ; Osteoporosis ; Retrospective Studies ; Tertiary Care Centers