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. Author manuscript; available in PMC: 2018 Dec 1.
Published in final edited form as: Trends Endocrinol Metab. 2017 Nov 8;28(12):868–878. doi: 10.1016/j.tem.2017.10.007

Figure 1.

Figure 1

Growth factor receptors, cytokine receptors and free fatty acids can stimulate the activity of ERK, JNK and p38 MAPK in the liver. ERK is activated through the Ras-Raf-MEK cascade and can influence gluconeogenesis by phosphorylating Foxo1. Stress conditions such as in obesity can lead to increased cytokine activity and increased free fatty acid levels can generate reactive oxygen species resulting in the activation of p38 MAPKs and JNKs which, can lead to dysregulation of hepatic gluconeogenesis and fatty acid synthesis. In the liver, JNK2 appears to be mainly responsible for the regulation of insulin sensitivity. Whilst the activity of JNK1/2 maintains NCor1 expression which inhibits PPARα-dependent inhibition of FGF21 leading to reduced fatty acid oxidation.