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Brain JNK and metabolic disease
Rubén Nogueiras1,2,3, Guadalupe Sabio4
1Department of Physiology, Center for Research in Molecular Medicine and Chronic Diseases (CIMUS), University of Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain.
Diabetologia
|November 17, 2020
Summary
Nutrient overload causes hypothalamic stress, activating stress-activated c-Jun N-terminal kinases (JNKs). These JNKs play complex roles in energy balance, influencing obesity and related diseases.
Area of Science:
- Neuroscience
- Metabolic Research
- Cellular Stress Response
Background:
- Obesity is a global epidemic linked to organ stress and diseases like type 2 diabetes.
- Overnutrition rapidly induces hypothalamic stress, central insulin, and leptin resistance.
- Stress-activated c-Jun N-terminal kinases (JNKs) are activated by nutrient overload in the brain.
Purpose of the Study:
- To review recent findings on JNK regulation and effects in the hypothalamus.
- To highlight the role of JNKs in energy and glucose homeostasis.
- To discuss the complex and opposing roles of JNK1 and JNK3 in hypothalamic neurons.
Main Methods:
- Review of recent scientific literature on JNKs and hypothalamic function.
- Focus on JNK1, JNK2, and JNK3 signaling pathways.
- Analysis of JNK roles in agouti gene-related protein (AgRP) neurons.
Main Results:
- JNK1 activation in AgRP neurons promotes feeding, weight gain, and impairs insulin/leptin signaling.
- JNK3 deletion in AgRP neurons yields similar effects to JNK1 activation, indicating opposing roles.
- JNK1 inhibits the hypothalamic-pituitary-thyroid axis, reducing energy expenditure and promoting obesity.
Conclusions:
- JNK kinases play intricate roles in hypothalamic control of energy balance.
- Opposing functions of JNK1 and JNK3, and the unknown role of JNK2, highlight JNK pathway complexity.
- Further research is needed to elucidate specific JNK functions in neuronal and non-neuronal cells for understanding energy balance regulation.
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