Preprint Review Version 1 This version is not peer-reviewed

Metabolic and Molecular Mechanisms of Macrophage Polarisation and Adipose Tissue Insulin Resistance

Version 1 : Received: 13 July 2020 / Approved: 14 July 2020 / Online: 14 July 2020 (11:25:48 CEST)

A peer-reviewed article of this Preprint also exists.

Orliaguet, L.; Ejlalmanesh, T.; Alzaid, F. Metabolic and Molecular Mechanisms of Macrophage Polarisation and Adipose Tissue Insulin Resistance. Int. J. Mol. Sci. 2020, 21, 5731. Orliaguet, L.; Ejlalmanesh, T.; Alzaid, F. Metabolic and Molecular Mechanisms of Macrophage Polarisation and Adipose Tissue Insulin Resistance. Int. J. Mol. Sci. 2020, 21, 5731.

Journal reference: Int. J. Mol. Sci. 2020, 21, 5731
DOI: 10.3390/ijms21165731

Abstract

Inflammation plays a key role in the development and progression of type-2 diabetes (T2D), a disease characterised by peripheral insulin resistance and systemic glucolipotoxicity. Visceral adipose tissue (AT) is the main source of inflammation early in disease course. Macrophages are innate immune cells that populate all peripheral tissues, including AT. Dysregulated AT macrophage (ATM) responses to microenvironmental changes are at the root of aberrant inflammation and development of insulin resistance, locally and systemically. The inflammatory activation of macrophages is regulated at multiple levels: cell surface receptor stimulation, intracellular signalling, transcriptionally and metabolically. This review will cover the main mechanisms involved in AT inflammation and insulin resistance in T2D. First, we will describe the physiological and pathological changes in AT that lead to inflammation and insu- lin resistance. We will next focus on the transcriptional and metabolic mechanisms described that lead to the activation of ATMs. We will discuss more novel metabolic mechanisms that influence macrophage polarisation in other disease or tissues contexts that may be relevant to future work in insulin resistance and T2D.

Subject Areas

Adipose tissue; inflammation; insulin resistance; immunometabolism; macrophages; type-2 diabetes; T2D

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