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In the lean, healthy state, adipose tissue (AT) has critical roles in maintaining organismal homeostasis. Paramount among the various roles of AT is the regulation of whole body metabolism. While adipocytes per se are key players in metabolic homeostasis, for example, by storing nutrients and releasing soluble factors, work over the last decade has revealed that AT-resident immune cells have a profound impact on AT function. Obesity is a risk factor for numerous conditions, including cardiovascular disease, type 2 diabetes, cancer, osteoarthritis, sleep apnoea and infertility. Obesity is also a major risk factor for the development of non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH), an effect that is primarily attributable to increased hepatic lipid accumulation and inflammation. During the development of obesity, the AT expands and the AT-resident immune cell profile is dramatically altered,1 ultimately initiating AT inflammation and altered whole body metabolism. Most prominent among these changes is the marked recruitment of CD11c+ inflammatory macrophages to visceral (v)AT. By producing a range of secreted factors, obese, inflamed AT, primarily via inflammatory macrophages, has effects on multiple tissues, including initiating myelopoiesis within the bone marrow and stimulating hepatic glucose production. However, while the role of AT inflammatory macrophages in altered metabolic homeostasis is well established, whether AT macrophages (ATMs) directly cause hepatic inflammation during the development of NASH is unknown.
In Gut, Bijnen and colleagues show that macrophages recruited to obese vAT contribute to innate immune cell recruitment in the liver, …
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