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. Author manuscript; available in PMC: 2016 Jun 1.
Published in final edited form as: Bone. 2015 Feb 25;75:120–127. doi: 10.1016/j.bone.2015.01.021

Figure 4. Model: Pharmacological inhibition of CaMKK2 reverses age-associated bone loss in WT mice while its genetic loss attenuates it.

Figure 4

From 12 to 32 weeks of age, male WT mice suffer a significant decline in trabecular bone volume, microarchitecture, strength as well as cortical bone strength. Acute inhibition of CaMKK2 in the 32 week old mice through a 6 week treatment with STO-609 stimulates new bone formation in these mice and significantly increases trabecular bone volume, microarchitecture, strength as well as mid-shaft geometry and cortical bone strength to levels observed in 12 week old WT mice. Moreover, regardless of age, the Camkk2−/− mice possess significantly elevated bone mass and strength compared to age-matched WT mice. Whereas they undergo age-associated bone loss albeit smaller and often non-significant; the trabecular bone volume, microarchitecture, strength as well as cortical bone strength values are still significantly higher in 32 week old Camkk2−/− mice than age-matched WT mice, implying that the chronic absence of CaMKK2 attenuates the deleterious effects of age on bone.