1 Adelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, Australia.
2 South Australian Health and Medical Research Institute (SAHMRI), Adelaide, Australia.
3 Department of Health, Kinesiology, and Applied Physiology, Concordia University, Montréal, Québec, Canada.
4 Metabolism, Obesity, and Nutrition Lab, School of Health, Concordia University, Montréal, Québec, Canada.
5 Centre de Recherche, Centre Intégré Universitaire de Santé et de Services Sociaux du Nord-de-I'Île-de-Montréal, Hôpital du Sacré-Cœur de Montréal (CIUSSS-NIM, HSCM), Montréal, Québec, Canada.

In individuals with obesity, the onset of chronic comorbidities coincides with the excessive accumulation of adipose tissue in various tissue beds. As obesity progresses, adipose tissue becomes increasingly dysfunctional causing chronic low-grade inflammation. Indeed, adipose tissue inflammation, which partially stems from macrophage infiltration and expression of macrophage-derived cytokines, has local and systemic consequences on health and increases the likelihood of developing obesity-associated comorbidities. In addition, cellular changes driven by macrophages may also further aggravate both adipose tissue dysfunction and inflammation, thus contributing to the onset and progression of several comorbidities including type 2 diabetes, cardiovascular diseases, nonalcoholic fatty liver disease, osteoarthritis, some cancers, and dementia. The purpose of this review is to discuss how adipose tissue inflammation relates and contributes to the pathogenesis of obesity-associated comorbidities.