Weight loss can increase bone mass, or become a new anti-osteoporosis treatment strategy

it is well known that adipose tissue can affect bone growth, it is commonly understood that obesity tends to increase bone mass. There is now evidence of a metabolic relationship between adipose tissue and bones. More significantly, understanding the mechanisms by which the products of fat cells control bone cells may lead to new anti-osteoporosis treatment strategies.On October 6, 2020, the Steven L. Teitelbaum team at the University of Washington School of Medicine published an article in the international academic journal Cell-Metabolism entitled "Ablation of Fat Cells in Adult Mice Induces Massive Bone Gain", revealing that the elimination of fat cells in adult mice can induce significant bone growth.The team has previously demonstrated that significant bone mass increases can be observed by expressing diphtheria toxin subjects (DTRs) in fat, resulting in the loss of white (WAT) and brown adipose tissue (BAT). However, this system induces fat consumption to occur only during embryonic development. To overcome this limitation, the team built a more therapeuticly relevant model that induced fat ablation in adult mice. To do this, the team mated mice that expressed primate diphtheria toxin ligands (DTRs) with mice that expressed liposin (ADQ)-Cre. As a result, DT dosing completely eliminates WAT and BAT from these DTRADQ mice and melts bone marrow fat cells.To test this hypothesis, the team paired mice carrying primate DTR (DTR-STOPfl/fl) with mice expressing ADQ-Cre (DTRADQ mice) to give 2 The DT of the DTRADQ mice (DT/DTRADQ mice) in the months-old actually eliminated WAT-BAT, leading to the disappearance of serum lipids and elevated levels of serum lactic acid dehydrogenase (LDH), which represents almost complete ablation of the outer fat bank. After 10 days of dosing, it was found that the bone essentially occupied thethe whole cortial gap from the end of the dry bone to the backbone. A large number of new bone substates can be observed within 3-4 days of DT being given, at which point bone marrow fat cells are no longer visible and there are no signs of bone marrow necroticity.The researchers then conducted a mechanism study of their results, which showed that this fat cell knock-out-mediated bone mass enhancement phenomenon reflected the elimination of the activation of the bone morphological protein (BMP) receptor after its inhibitor, which was associated with simultaneous surface growth factor (EGF) receptor signaling. DTRADQ-induced bone sclerosis is not caused by the elimination of surrounding fat cells, but may eliminate bone marrow fat cells that express ADQ.Osteoporosis manifests it as an increase in the activity of bone-breaking cells relative to osteoblasts. Treatments include anti-absorption or bone-promoting drugs. However, anti-absorption agent-induced bone mass can lead to atypical fractures, possibly because it does not occur in the context of drug-induced bone anabolic metabolism and therefore requires the stimulation of bone-forming agents, while anabolic drugs targeting BMP inhibitors (with short-term EGF-induced activity) may be a means of significantly increasing bone mass to prevent or reverse pathological bone loss. (Biological Discovery):1. Ablation of F at Cells in Adult Mice Massive Bone Gain