ABSTRACT
As the most important tissues of the motor system, skeleton and skeletal muscles are closely related to each other. The concept of bone-muscle units has been proposed for a long time, and they are linked closely by mechanical loading generated by exercise. Skeleton provides mechanical support attachments for skeletal muscle force, and contraction of skeletal muscle drives body movement. During the process of body movement, acting as an intermediate medium between the mechanical load and bone, skeletal muscles regulate metabolic activity of the bone through endocrine factors and mechanical stimulation, which is closely related to continuous bone remodeling and maintains good structure and function of the bone. This review focuses on recent research progress of skeletal muscle affecting bone remodeling by applying mechanical stimulation to the bone, which will provide some new ideas for prevention and treatment of bone metabolism diseases.
ABSTRACT
Brown adipose tissue (BAT) increases energy consumption by directly dissipating stored energy in the form of heat through the role of uncoupling protein (UCP1). Recent studies have found that brown adipocytes may also regulate metabolism through autocrine, paracrine, and endocrine mechanisms. A growing body of evidences have shown that the BAT has a close relationship with bone metabolism, in which BAT secretes a variety of factors to regulate bone metabolism, while bone also secretes a variety of bioactive substances to control BAT function. In addition, BAT may indirectly participate in bone metabolism through muscle-mediated regulation or SNS activity and improvement of body metabolism, thus forming a BAT-skeletal axis. In this paper, we try to explain the relationship between brown adipose tissue and bone, and to discuss their interactive mechanisms.
ABSTRACT
Endocrine-disrupting chemicals (EDCs) are exogenous substances that alter the structure or function of the endocrine system. 4-Tert-octylphenol (OP) is one of the most representative EDCs and has estrogenic effects. In this study, we examined the effects of ethinyl estradiol (EE) and OP on the pituitary gland, placenta, and uterus of pregnant rats. Expression levels of human chorionic gonadotropin (hCG), oxytocin (OT), and contraction-associated proteins (CAPs) were determined, and uterine contractile activity was measured by uterine contraction assay. EE and OP both increased mRNA expression of OT and hCG in the pituitary gland but not the placenta. Since OT and hCG control uterine contraction, we next examined CAP expression in the uterus. Expression of 15-hydroxyprostaglandin-dehydrogenase (PGDH) was upregulated by OP, whereas expression of other CAPs was unaffected. To clarify the effect of OP on uterine contraction in pregnant rats, uterine contraction assay was performed. The 17beta-Estradiol (E2) did not affect contraction of primary uterine cells harvested from pregnant rats in a 3D collagen gel model. However, OP showed different effects from E2 by significantly reducing contraction activity. In summary, we demonstrated that OP interferes with regulation of OT and hCG in the pituitary gland as well as PGDH in the uterus, thereby reducing uterine contraction activity. This result differs from the action of endogenous E2. Collectively, these findings suggest that exposure to EDCs such as OP during pregnancycan reduce uterine contractile ability, which may result in contraction-associated adverse effects such as metratonia, bradytocia, and uterine leiomyomata.
Subject(s)
Animals , Rats , Chorionic Gonadotropin , Collagen , Endocrine System , Estradiol , Estrogens , Ethinyl Estradiol , Oxytocin , Pituitary Gland , Placenta , RNA, Messenger , Uterine Contraction , UterusABSTRACT
The etiology of benign prostatic hyperplasia( BPH) is multifactorial, but it is recognized that two important factors necessary for the induction of BPH in men are the testis(endocrine control) and the aging. From January 1991 to June 1992, we measured 6 hormonal factors in the serum of 129 men who were diagnosed as benign prostatic hyperplasia pathologically to determine whether endocrine factors influence the volume of benign prostatic hyperplasia. These hormonal levels were correlated with the prostatic volume measured by transrectal ultrasound(TRUS). There was no significant correlation for age with total prostatic volume(r=0.06, p=0.31l). With age there was a significant increase in serum testosterone(r=0.25, p=0.003), LH(r=0.42, p=0.000) and cortisol(r=0.25, p=0.016). The prostatic volume measured by prostatic ultrasound was correlated positively with estradiol(r=0.34, p=0.002) and cortisol(r=0.28. p =0.008). Also the prostatic volume was correlated with resected weight of prostate(r=0.38, p=0.000). We suggested that serum estrogen and cortisol levels may be the factors in persistent stimulation of benign prostatic hyperplasia.