The quantity and activation state as well as metabolic phenotype of ATMs impact the development of obesity-induced metabolic diseases. Lipid-rich CD11c + ATMs appear earlier in VAT than SAT in response to ectopic lipid accumulation as adipocytes reach maximal lipid storage capacity. Resident ATMs have lower levels of apoptosis and rapid proliferation during early phases of WAT expansion with a high-fat diet (HFD).
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The number of tissue-infiltrating macrophages is higher in superficial adipose tissue than deep adipose tissue, suggesting accessibility to skin microorganisms might promote macrophage infiltration in SAT. It seems that ATMs develop from circulating monocytes accumulating in adipose tissue, self-renew from various tissue-resident macrophages, or proliferate in situ driven by monocyte chemotactic protein 1 (MCP-1), which is an important process for macrophages accumulating in VAT in obesity. Macrophages are key modulators of energy metabolism and mitochondrial function in adipocytes. Īdipose tissue macrophages (ATMs) are pivotal players in obesity-associated inflammation and metabolic diseases. Macrophages exploit protective and pathogenic roles in anti-infection defense, antitumor immunity, metabolic disease development, and even obesity. On the other hand, alternatively activated M2 or anti-inflammatory and immunoregulatory macrophages produce anti-inflammatory cytokines such as IL-10 and TGF-β, contribute to tissue repair, remodeling, and vasculogenesis, and maintain homeostasis. Classically activated M1 or proinflammatory macrophages produce proinflammatory cytokines such as interleukin-1β (IL-1β), IL-6, IL-12, IL-23, and TNF-α, in response to infection and stress. Macrophages are heterogeneous, and their phenotype and functions are regulated by the surrounding microenvironment.
Adipose tissue is not only the body’s energy reservoir to insulate against the cold and protect vital organs but also an essential endocrine organ, especially white adipose tissue, which is the main source of endocrine signals. Overall, the understanding of protective and pathogenic roles of ATMs in adipose tissue can potentially provide strategies to prevent and treat obesity-related metabolic disorders.Īdipose tissue can be divided into white adipose tissue (WAT) and brown adipose tissue (BAT) the percentage of WAT is up to 5 to 50% of body weight including subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT), and the percentage of BAT decreases with age. In particular, the interplay between ATMs and adipocytes in energy metabolism, glycolysis, OXPHOS, iron handing and even interactions with the nervous system have been reviewed. Here, this review focuses on macrophage metabolism linked to functional phenotypes with an emphasis on macrophage polarization in adipose tissue physiological and pathophysiological processes. Macrophage polarization is accompanied by metabolic shifting between glycolysis and mitochondrial oxidative phosphorylation. Macrophages are involved in lipid and energy metabolism and mitochondrial function in adipocytes. Adipose tissue macrophages (ATMs) are central players in obesity-associated inflammation and metabolic diseases. Obesity exhibits a correlation with metabolic inflammation and endoplasmic reticulum stress, promoting the progression of metabolic disease such as diabetes, hyperlipidemia, hyperuricemia and so on.