Abstract
In obesity, adipose tissue macrophages (ATMs) are abundant immune cells in the adipose tissue and are known as inducers of metabolic inflammation that may lead to insulin resistance and immune disorders associated with obesity. However, much less is known about the ontogeny and physiological functions of ATMs in lean adipose tissue. ATMs are present at birth and actively participate in the synthesis of mediators that induce lipolysis, mitobiogenesis, and thermogenesis in adipocytes. Later in life ATMs limit the thermogenic competence of the adipocytes and favor lipid storage. ATMs respond to lipid overload of adipocytes in obesity with a sequence of pro-inflammatory events, including inflammasome activation and pyroptosis, as well as stimulation of nuclear factor kappa B and interferon regulatory factors that evoke an uncontrolled inflammation. ATMs are life-long constituents of the adipose tissue and hence signals that control ATM development and ATM-adipocyte interactions determine adipose tissue health.
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