PRJNA413726
Reduced ER stress-mediated autophagy is required for leptin alleviating inflammation in adipose tissue
Metabolic disorders, especially obesity and diabetes, become the most important public health concern in worldwide. The pathophysiology seems to be largely attributable to endoplasmic reticulum (ER) stress, inflammation and cytokines resistance (e.g. leptin resistance and insulin resistance) in adipose tissue. Therefore, dynamic improvement of these disorders in adipose tissue provides an effective therapeutic strategy to alleviate severe systemic metabolic disorders. In this study, we investigated the effects of leptin on autophagy and inflammation of adipose tissue. We show that leptin alleviates ER stress-induced inflammation through the Atf4/Atg5-mediated autophagy in mice adipocytes. Thus, our study has revealed the mechanistic link between leptin, autophagy and ER stress, providing novel insights into the pharmacologically therapeutic target for obesity and inflammation.