Adipose tissue (AT)
inflammation is strongly associated with
obesity-induced
insulin resistance. When subjected to metabolic stress, adipocytes become inflamed and secrete a plethora of
cytokines and
chemokines, which recruit circulating immune cells to AT. Although
sirtuin 6 (Sirt6) is known to control genomic stabilization, aging, and cellular metabolism, it is now understood to also play a pivotal role in the regulation of AT
inflammation. Sirt6
protein levels are reduced in the AT of obese humans and animals and increased by
weight loss. In this review, we summarize the potential mechanism of AT
inflammation caused by impaired action of Sirt6 from the immune cells' point of view. We first describe the properties and functions of immune cells in obese AT, with an emphasis on discrete macrophage subpopulations which are central to AT
inflammation. We then highlight data that links Sirt6 to functional phenotypes of AT
inflammation. Importantly, we discuss in detail the effects of Sirt6 deficiency in adipocytes, macrophages, and eosinophils on
insulin resistance or AT browning. In our closing perspectives, we discuss emerging issues in this field that require further investigation.