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Brain JNK and metabolic disease – published online 16/11/2020

Rubén Nogueiras, Guadalupe Sabio

Obesity has become a global epidemic. In recent years, major efforts have been made to define the role played by the central nervous system (CNS) in this disease. Several CNS circuits are altered in obese individuals, and these changes can induce uncontrolled hunger and/or decreased energy expenditure, the latter being associated with physical inactivity, reduced baseline metabolism and poor thermogenic capacity. c-Jun N-terminal kinases (JNKs) in the hypothalamus are among the signalling molecules activated during obesity that may contribute to deleterious molecular adaptations. In this issue, Nogueiras and Sabio (https://doi.org/10.1007/s00125-020-05327-w) review recent findings that reveal opposing pro- and anti-obesogenic actions of JNK family members in the CNS—more precisely the hypothalamus—with regard to the control of food intake and energy expenditure. The authors also discuss the future potential of these kinases as targets in the treatment of obesity. The figures from this review are available as a downloadable slideset

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