The stress-activated c-Jun amino-terminal kinase (JNK) plays a pivotal role in metabolic conditions such as obesity, insulin resistance, and type 2 diabetes. Intricate tissue-specific tweaking of JNK activity in preclinical models of metabolic diseases reveals a complex interplay among local and systemic effects on carbohydrate and lipid metabolism. Synthesis of these entangled effects illustrates that for JNK inhibitors to have therapeutic impact, they must function in multiple cell types to modulate JNK activity.
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Vallerie et al. (2010) studied this question.
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