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Article summary:

1. Ksr2, an obesity gene, negatively regulates femoral bone mass in two genetic backgrounds.

2. Ksr2 influences adipocyte differentiation at the expense of osteoblasts in the bone marrow.

3. Despite gains in appendicular bone mass observed in the absence of Ksr2, bone strength and fracture healing response remain compromised in these mice.

Article analysis:

The article is generally reliable and trustworthy as it provides a detailed overview of the research conducted on Ksr2, an obesity gene, and its effects on trabecular bone volume and bone marrow adiposity. The authors provide evidence for their claims by citing relevant studies and experiments conducted on mice with global Ksr2 null mutations. Furthermore, they discuss potential mechanisms behind their findings and provide insights into how Ksr2 can regulate bone formation autonomously.

However, there are some points that could be improved upon to make the article more comprehensive. For instance, while the authors discuss potential mechanisms behind their findings, they do not explore any counterarguments or alternative explanations for their results. Additionally, they do not mention any possible risks associated with deleting Ksr2 or any other potential implications of their findings that could be explored further in future studies. Finally, while the authors present both sides of the argument equally when discussing their results, they do not provide any evidence to support their claims or explore any unexplored counterarguments which could have strengthened their conclusions further.