Liraglutide promotes angiogenesis in adipose tissue via suppression of adipocyte-derived IL-6.

Accumulating evidence suggests that Liraglutide is a favorable treatment for obese people. Obesity induces cellular senescence and accumulated senescent adipocytes in adipose tissue. However, the role of Liraglutide in adipose tissue (AT) senescence and the underlying mechanisms remain obscure. In this study, we found that HFD induces adipocyte senescence and impaired angiogenesis in AT. The deleterious effects provoked unhealthy adipose tissue remodeling and metabolic disturbance. In contrast, treatment of Liraglutide promoted weight reduction, alleviated adipose tissue senescence, and improved angiogenesis in AT. Notably, we demonstrated that Liraglutide promotes angiogenesis in AT dependent on adipocyte-derived IL-6. These findings revealed distinctive roles of Liraglutide in the regulation of adipocyte senescence and provide a therapeutic potential to obesity-associated metabolic disorders.

Senescent T Cell Induces Brown Adipose Tissue "Whitening" Via Secreting IFN-γ.

Aging-associated chronic inflammation is a key contributing factor to a cluster of chronic metabolic disorders, such as cardiovascular disease, obesity, and type 2 diabetes. Immune cells particularly T cells accumulate in adipose tissue with advancing age, and there exists a cross talk between T cell and preadipocyte, contributing to age-related adipose tissue remodeling. Here, we compared the difference in morphology and function of adipose tissue between young (3-month-old) and old (18-month-old) mice and showed the phenomenon of brown adipose tissue (BAT) "whitening" in old mice. Flow cytometry analysis suggested an increased proportion of T cells in BAT of old mice comparing with the young and exhibited senescent characteristics. We take advantage of coculture system to demonstrate directly that senescent T cells inhibited brown adipocyte differentiation of preadipocytes in adipose tissue. Mechanistically, both in vitro and in vivo studies suggested that senescent T cells produced and released a higher level of IFN-γ, which plays a critical role in inhibition of preadipocyte-to-brown adipocyte differentiation. Taken together, the data indicate that senescent T cell-derived IFN-γ is a key regulator in brown adipocyte differentiation.