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. Author manuscript; available in PMC: 2017 Oct 1.
Published in final edited form as: Trends Endocrinol Metab. 2016 Jul 20;27(10):706–718. doi: 10.1016/j.tem.2016.06.001

Figure 3. Liver-centric metabolic functions of CaMKK2.

Figure 3

In the liver, ablation of CaMKK2 impacts the metabolic flexibility of numerous pathways as indicated by the asterisks (*). Loss of CaMKK2 in response to high fat diet feeding reduces levels of free fatty acids (FFAs), triglyercides (TGs) and very low-density lipoproteins (VLDL) as well as low densitiy lipoproteins and cholesterol (not depicted) [52]. Consistent with these observations, hepatic-specific ablation of CaMKK2 is sufficient to confer improved insulin sensitivity [33]. Primary hepatocytes devoid of CaMKK2 show increased de novo lipogenesis along with increased β-oxidation [33]. In the context of hepatic cancer, CaMKK2 is essential for driving mTOR/S6K signaling to promote protein synthesis that increases cancer cell proliferation [35].