Altered thermogenesis and impaired bone remodeling in Misty mice.

摘要: Fat mass may be modulated by the number of brown-like adipocytes in white adipose tissue (WAT) humans and rodents. Bone remodeling is dependent on systemic energy metabolism and, with age, bone becomes uncoupled brown (BAT) function declines. To test interaction between BAT bone, we employed Misty (m/m) mice, which were reported deficient BAT. We found that mice have accelerated age-related trabecular loss impaired fat (including reduced temperature, lower expression Pgc1a, less sympathetic innervation compared to wild-type (+/ +)). Despite function, had normal core body suggesting heat produced from other sources. Indeed, upon acute cold exposure (4°C for 6 hours), inguinal WAT compensated dysfunction increasing Acadl, Dio2, thermogenic genes. Interestingly, also decreased Runx2 increased Rankl but only was wild-type. Browning under control nervous system (SNS) if present at room could impact metabolism. whether SNS activity responsible loss, treated β-blocker, propranolol. As predicted, propranolol slowed volume/total volume (BV/TV) distal femur without affecting Finally, mutation (a truncation DOCK7) has a significant cell-autonomous role. DOCK7 whole osteoblasts. Primary osteoblast differentiation calvaria impaired, demonstrating novel role remodeling. multifaceted effects mutation, shown leads altered first time negatively affects