Matthew Bernhard, Obinna Okorie, Wei-Ju Tseng, Mengcun Chen, Julia Danon, Mingshu Cui, Elisabeth Lashbrooks, Yanmei Yang, Bin Wang
{"title":"在雄性小鼠体内,ucOcn 和 cOcn 的比例发生了新陈代谢变化,转向骨吸收,导致了年龄依赖性骨质流失。","authors":"Matthew Bernhard, Obinna Okorie, Wei-Ju Tseng, Mengcun Chen, Julia Danon, Mingshu Cui, Elisabeth Lashbrooks, Yanmei Yang, Bin Wang","doi":"10.1152/ajpendo.00294.2024","DOIUrl":null,"url":null,"abstract":"<p><p>The study of the senile osteoporosis in men still lags significantly behind in women. The changes of protein molecule levels and their relationships with bone loss remain poorly understood. In the present study, we used C57BL/6J male mice at ages from 3 to 24 months to delineate the mechanisms of aging effects on bone loss. We employed the micro-computed tomography, mechanical testing, histomorphometry assays, and detection of serum levels of undercarboxylated osteocalcin (ucOcn) and carboxylated osteocalcin (cOcn) to assess bone mass changes and their relationships with ratios of ucOcn to cOcn in mice from different age groups. The results showed that mouse trabecular bone mass reduced gradually with age while cortical bone loss and mechanical property changes mostly occurred in advanced age. Our findings further demonstrated that the increase in osteoclast activity and the decrease in osteoblast function were significantly corelated with blood levels of ucOcn and cOcn, respectively. The dynamic metabolic changes of ucOcn to cOcn ratio were correlated with age-dependent bone loss in mice. In summary, metabolic shifts in ratio of ucOcn to cOcn towards bone resorption from young adult to elderly mice contribute to the pathogenesis of age-related bone loss. Simultaneously monitoring blood ratios of ucOcn to cOcn may be useful to predict the status of bone mass <i>in vivo</i>.</p>","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":" ","pages":""},"PeriodicalIF":4.2000,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Metabolic shifts in ratio of ucOcn to cOcn towards bone resorption contribute to age-dependent bone loss in male mice.\",\"authors\":\"Matthew Bernhard, Obinna Okorie, Wei-Ju Tseng, Mengcun Chen, Julia Danon, Mingshu Cui, Elisabeth Lashbrooks, Yanmei Yang, Bin Wang\",\"doi\":\"10.1152/ajpendo.00294.2024\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The study of the senile osteoporosis in men still lags significantly behind in women. The changes of protein molecule levels and their relationships with bone loss remain poorly understood. In the present study, we used C57BL/6J male mice at ages from 3 to 24 months to delineate the mechanisms of aging effects on bone loss. We employed the micro-computed tomography, mechanical testing, histomorphometry assays, and detection of serum levels of undercarboxylated osteocalcin (ucOcn) and carboxylated osteocalcin (cOcn) to assess bone mass changes and their relationships with ratios of ucOcn to cOcn in mice from different age groups. The results showed that mouse trabecular bone mass reduced gradually with age while cortical bone loss and mechanical property changes mostly occurred in advanced age. Our findings further demonstrated that the increase in osteoclast activity and the decrease in osteoblast function were significantly corelated with blood levels of ucOcn and cOcn, respectively. The dynamic metabolic changes of ucOcn to cOcn ratio were correlated with age-dependent bone loss in mice. In summary, metabolic shifts in ratio of ucOcn to cOcn towards bone resorption from young adult to elderly mice contribute to the pathogenesis of age-related bone loss. Simultaneously monitoring blood ratios of ucOcn to cOcn may be useful to predict the status of bone mass <i>in vivo</i>.</p>\",\"PeriodicalId\":7594,\"journal\":{\"name\":\"American journal of physiology. Endocrinology and metabolism\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":4.2000,\"publicationDate\":\"2024-10-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"American journal of physiology. 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Metabolic shifts in ratio of ucOcn to cOcn towards bone resorption contribute to age-dependent bone loss in male mice.
The study of the senile osteoporosis in men still lags significantly behind in women. The changes of protein molecule levels and their relationships with bone loss remain poorly understood. In the present study, we used C57BL/6J male mice at ages from 3 to 24 months to delineate the mechanisms of aging effects on bone loss. We employed the micro-computed tomography, mechanical testing, histomorphometry assays, and detection of serum levels of undercarboxylated osteocalcin (ucOcn) and carboxylated osteocalcin (cOcn) to assess bone mass changes and their relationships with ratios of ucOcn to cOcn in mice from different age groups. The results showed that mouse trabecular bone mass reduced gradually with age while cortical bone loss and mechanical property changes mostly occurred in advanced age. Our findings further demonstrated that the increase in osteoclast activity and the decrease in osteoblast function were significantly corelated with blood levels of ucOcn and cOcn, respectively. The dynamic metabolic changes of ucOcn to cOcn ratio were correlated with age-dependent bone loss in mice. In summary, metabolic shifts in ratio of ucOcn to cOcn towards bone resorption from young adult to elderly mice contribute to the pathogenesis of age-related bone loss. Simultaneously monitoring blood ratios of ucOcn to cOcn may be useful to predict the status of bone mass in vivo.
期刊介绍:
The American Journal of Physiology-Endocrinology and Metabolism publishes original, mechanistic studies on the physiology of endocrine and metabolic systems. Physiological, cellular, and molecular studies in whole animals or humans will be considered. Specific themes include, but are not limited to, mechanisms of hormone and growth factor action; hormonal and nutritional regulation of metabolism, inflammation, microbiome and energy balance; integrative organ cross talk; paracrine and autocrine control of endocrine cells; function and activation of hormone receptors; endocrine or metabolic control of channels, transporters, and membrane function; temporal analysis of hormone secretion and metabolism; and mathematical/kinetic modeling of metabolism. Novel molecular, immunological, or biophysical studies of hormone action are also welcome.