Depletion of JunB increases adipocyte thermogenic capacity and ameliorates diet-induced insulin resistance.

Adipose tissue is a crucial metabolic organ in the human body. It stores and exerts distinct physiological functions in different body regions. Fat not only serves as a cushion and insulator but also stores energy and conveys endocrine signals within the body. There is a growing recognition that adipose tissue is an organ that is misunderstood and underestimated in contribution to human health and disease progression by regulating its size and functionality. In mammals, the adipose tissue reservoir consists of three functionally distinct types of fat: white adipose tissue (WAT), brown adipose tissue (BAT), and beige or inducible brown adipose tissue (iWAT), which exhibits thermogenic capabilities intermediate between the other two. Fat in different depots exhibits considerable differences in origin, characteristics, and functions. They vary not only in adipocyte lineage, properties, thermogenesis, and endocrine functions but also in their immunological functions. In a recent study published in Nature Metabolism, Zhang et al. investigated the role of JunB in the thermogenic capacity of adipocytes and its significance in obesity and metabolic disorders. The study revealed that JunB expression in BAT coexists with both low and high thermogenic adipocytes, indicating a fundamental feature of heterogeneity and plasticity within BAT. In summary, this article demonstrates that research targeting JunB holds promise for improving diet-induced obesity and insulin resistance, offering new avenues for treating metabolic disorders.