Emerging Concept of Adipogenesis Regulation by the Renin–Angiotensin System

Abstract

The renin–angiotensin system (RAS) has been the focus of attention not only for its classical action through circulating RAS but also its local actions in tissues such as the brain,1 liver,2 lung,3 and adipose tissue.4 The roles of the local RAS in adipose tissue have recently been highlighted, because obesity is one of the major risks for the metabolic syndrome with hypertension and glucose intolerance. However, there have been inconsistent reports on the role of the adipose tissue RAS. The role of local RAS in adipogenesis has been discussed but is not well elucidated. In this issue of Hypertension , Matsushita et al5 examined the role of local RAS during adipocyte differentiation using human mesenchymal stem cells (MSCs) instead of preadipocytes in an elegant fashion. They reported the influence of RAS on MSCs as follows (Figure 1): (1) Comparison of the expression of RAS components between MSCs and differentiated adipocytes revealed that mRNA of renin and the angiotensin II (Ang II) type-2 (AT2) receptor were highly expressed, and Ang II concentration was significantly increased in differentiated adipocytes; (2) administration of Ang II with or without an Ang II type-1 (AT1) receptor blocker (ARB), valsartan, in MSC during adipogenesis showed that Ang II inhibited adipogenesis, and AT2 receptor activation by valsartan further inhibited it; and (3) moreover, treatment with valsartan alone also inhibited adipocyte differentiation. These results suggest that the local RAS, especially AT2 receptor signaling, has a crucial role in adipogenesis. Figure 1. Effect of endogenous RAS on adipocyte differentiation from MSCs. RAS-related genes are expressed in MSCs, and Ang II secretion is increased during …