SSTR2 Mediates the Inhibitory Effect of SST/CST on Lipolysis in Chicken Adipose Tissue

Simple Summary The chicken is one of the model organisms of birds and is important for the poultry industry. Chickens have many unique metabolic characteristics, and the metabolic regulatory mechanisms for these characteristics remain poorly understood. For example, somatostatin has been reported to have an anti-lipolytic effect but its mediator remains to be identified. In our study, we found that somatostatin receptor 2 (SSTR2) is highly expressed in chicken adipose tissue, and SSTR2 antagonists can block the anti-lipolytic effect of somatostatin, supporting that this effect is mediated by SSTR2. At the same time, we found that SST28 can stimulate the proliferation of chicken preadipocytes, and this proliferation effect may be mediated by SSTR2 through the MAPK/ERK signaling pathway. The present study identified the primary mediator responsible for the anti-lipolytic effect of somatostatin in chickens, thereby reinforcing its significant role in adipose metabolism.Abstract Somatostatin shows an anti-lipolytic effect in both chickens and ducks. However, its molecular mediator remains to be identified. Here, we report that somatostatin type 2 receptor (SSTR2) is expressed at a high level in chicken adipose tissue. In cultured chicken adipose tissue, the inhibition of glucagon-stimulated lipolysis by somatostatin was blocked by an SSTR2 antagonist (CYN-154086), supporting an SSTR2-mediated anti-lipolytic effect. Furthermore, a significant pro-proliferative effect was detected in SST28-treated immortalized chicken preadipocytes (ICP-1), and this cell proliferative effect may be mediated through the MAPK/ERK signaling pathway activated by SSTR2. In summary, our results demonstrate that SSTR2 may regulate adipose tissue development by affecting the number and volume of adipocytes in chickens.