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Results. The role of leptin in bone preserves bone mineral density (BMD) through increased OPG levels leading to bind RANKL, resulting in reducing osteoclast activity. The estrogen role on bone is also mediated by RANKL and OPG.
Leptin increased adipogenesis and reduced osteogenesis by activating Jak2/Stat3 signaling in bone marrow stromal cells. A high-fat diet increased adipogenesis and reduced osteogenesis in limb bones from wild-type mice, but not from Prx1-Cre;Lepr(fl/fl) mice.
Taken as a whole, leptins function in the body pertains to regulating the balance between food intake and energy expenditure. The classic primary physiologic role of leptin is to serve as a marker of long-term energy stores for the central nervous system (CNS).
Our studies show that leptin is equipotent in the control of body weight and bone mass and that circulating leptin, at low or high concentrations, regulates bone mass. Furthermore, available evidence suggests that this function of leptin is, like its other functions, conserved between mouse and human.
The role of leptin in bone preserves bone mineral density (BMD) through increased OPG levels leading to bind RANKL, resulting in reducing osteoclast activity. The estrogen role on bone is also mediated by RANKL and OPG.
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Abstract. Objective: Leptin is a peptide hormone that mainly regulates food intake and energy expenditure of human body. A close correlation between serum leptin levels and the percentage of body fat stores is well known. Nonalcoholic steatohepatitis (NASH) is a common disorder which causes serum liver enzyme elevation
In general, normal ranges for leptin levels include: Adults assigned female at birth: 0.5 - 15.2 nanograms per milliliter (ng/mL). Adults assigned male at birth: 0.5 - 12.5 ng/mL.
Leptin increased proliferation of isolated fetal rat osteoblasts in bone and inhibited osteoclastogenesis in bone marrow, leading to new bone formation, higher bone density and reduction in fracture risk [80].

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