The gravitostat is purported to function as a leptin-independent, osteocyte-dependent mechanism for regulation of energy balance. If correct, reduced activation of gravitostat signaling caused by prolonged sitting may contribute to obesity. The gravitostat concept is supported by reduced body mass in rodents following surgical implantation of weighted capsules.
View Article and Find Full Text PDFThe rodent hindlimb unloading (HU) model was developed in the 1980s to make it possible to study mechanisms, responses, and treatments for the adverse consequences of spaceflight. Decades before development of the HU model, weightlessness was predicted to yield deficits in the principal tissues responsible for structure and movement on Earth, primarily muscle and bone. Indeed, results from early spaceflight and HU experiments confirmed the expected sensitivity of the musculoskeletal system to gravity loading.
View Article and Find Full Text PDFAstronauts are exposed to radiation during space travel under conditions of dramatically reduced weightbearing activity. However, we know little about how gravity-dependent loading affects tissue sensitivity to radiation. We hypothesize gravity-dependent loading and irradiation share common molecular signaling pathways in bone cell progenitors that are sensitive to stress-induced reactive oxygen species (ROS), species capable of impacting skeletal health.
View Article and Find Full Text PDFJ Musculoskelet Neuronal Interact
June 2007
Animals have been a critical component of the spaceflight program since its inception. The Russians orbited a dog one month after the Sputnik satellite was launched. The dog mission spurred U.
View Article and Find Full Text PDFUnlabelled: HLU suppressed bone formation and resulted in bone loss in the tibial metaphysis of 6-month-old male rats. A human therapeutic dose of intermittent PTH (1 microg/kg/day) prevented the skeletal changes associated with HLU.
Introduction: Skeletal unloading of skeletally mature rats results in trabecular thinning in the proximal tibial metaphysis, which is in part caused by a decrease in bone formation.