Role of the mixed-lineage protein kinase pathway in the metabolic stress response to obesity

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Abstract

Saturated free fatty acid (FFA) is implicated in the metabolic response to obesity. Invitro studies indicate that FFA signaling may be mediated by the mixed-lineage protein kinase (MLK) pathway that activates cJun NH2-terminal kinase (JNK). Here, we examined the role of the MLK pathway invivo using a mouse model of diet-induced obesity. The ubiquitously expressed MLK2 and MLK3 protein kinases have partially redundant functions. We therefore compared wild-type and compound mutant mice that lack expression of MLK2 and MLK3. MLK deficiency protected mice against high-fat-diet-induced insulin resistance and obesity. Reduced JNK activation and increased energy expenditure contribute to the metabolic effects of MLK deficiency. These data confirm that the MLK pathway plays a critical role in the metabolic response to obesity

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Kant, S., Barrett, T., Vertii, A., Noh, Y. H., Jung, D. Y., Kim, J. K., & Davis, R. J. (2013). Role of the mixed-lineage protein kinase pathway in the metabolic stress response to obesity. Cell Reports, 4(4), 681–688. https://doi.org/10.1016/j.celrep.2013.07.019

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