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Adipokine dysregulation and adipose tissue inflammation in human obesity

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      Obesity induces a phenotypic switch in adipose tissue macrophage polarization.

      Adipose tissue macrophages (ATMs) infiltrate adipose tissue during obesity and contribute to insulin resistance. We hypothesized that macrophages migrating to adipose tissue upon high-fat feeding may differ from those that reside there under normal diet conditions. To this end, we found a novel F4/80(+)CD11c(+) population of ATMs in adipose tissue of obese mice that was not seen in lean mice. ATMs from lean mice expressed many genes characteristic of M2 or "alternatively activated" macrophages, including Ym1, arginase 1, and Il10. Diet-induced obesity decreased expression of these genes in ATMs while increasing expression of genes such as those encoding TNF-alpha and iNOS that are characteristic of M1 or "classically activated" macrophages. Interestingly, ATMs from obese C-C motif chemokine receptor 2-KO (Ccr2-KO) mice express M2 markers at levels similar to those from lean mice. The antiinflammatory cytokine IL-10, which was overexpressed in ATMs from lean mice, protected adipocytes from TNF-alpha-induced insulin resistance. Thus, diet-induced obesity leads to a shift in the activation state of ATMs from an M2-polarized state in lean animals that may protect adipocytes from inflammation to an M1 proinflammatory state that contributes to insulin resistance.
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        Obesity is associated with macrophage accumulation in adipose tissue

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          Adipokines in inflammation and metabolic disease.

          The worldwide epidemic of obesity has brought considerable attention to research aimed at understanding the biology of adipocytes (fat cells) and the events occurring in adipose tissue (fat) and in the bodies of obese individuals. Accumulating evidence indicates that obesity causes chronic low-grade inflammation and that this contributes to systemic metabolic dysfunction that is associated with obesity-linked disorders. Adipose tissue functions as a key endocrine organ by releasing multiple bioactive substances, known as adipose-derived secreted factors or adipokines, that have pro-inflammatory or anti-inflammatory activities. Dysregulated production or secretion of these adipokines owing to adipose tissue dysfunction can contribute to the pathogenesis of obesity-linked complications. In this Review, we focus on the role of adipokines in inflammatory responses and discuss their potential as regulators of metabolic function.
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            Author and article information

            Affiliations
            [1 ]Metabolic Research Laboratory; Clínica Universidad de Navarra; Pamplona Spain
            [2 ]CIBER Fisiopatología de la Obesidad y Nutrición (CIBEROBN); Instituto de Salud Carlos III; Pamplona Spain
            [3 ]Obesity and Adipobiology Group; Instituto de Investigación Sanitaria de Navarra (IdiSNA); Pamplona Spain
            [4 ]Department of Endocrinology & Nutrition; Clínica Universidad de Navarra; Pamplona Spain
            Journal
            European Journal of Clinical Investigation
            Eur J Clin Invest
            Wiley
            00142972
            September 2018
            September 2018
            August 03 2018
            : 48
            : 9
            : e12997
            10.1111/eci.12997
            © 2018

            http://doi.wiley.com/10.1002/tdm_license_1.1

            http://onlinelibrary.wiley.com/termsAndConditions#vor

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