Editorial: Metaflammation in obesity and diabetes

Abstract

Lifestyle diseases are indeed becoming life-threatening. Obesity and diabetes are now considered as two major inflammatory diseases that were in disguised over the years as only metabolic diseases. Now there are growing interests in dissecting the role of metaflammation as well as inflammation as a cause and/or consequence for its direct contribution in the pathogenesis and/or pathophysiology of these life-threatening diseases. Since the last decade, cutting-edge research demonstrated obesity as one of the key mediators and predisposing factors in the context of inflammatory pathogenesis of diabetes and beyond, including cancer. Intriguingly, obesity has been presented as the promoter of diabetes as well as cancer through the experimental and clinical research conducted throughout the last 10 years [1][2].Keeping this in mind, the present research topic was conceived with an aim to present the current updates on the topics ranging from the mechanistic insights of inflammatory consequences induced in obesity, signaling defects/dysregulation in cell death pathways and endocrine network, response to infectious agents etc. relevant to clinical progression of diabetes. A total of 7 contributions from 8 countries were received that include 4 original research and 3 review articles. All the 3 reviews and a research article described the mechanistic insights of metaflammation in diabetes and possible therapeutic options while rest of the articles were emphasized on obesity.Low-grade persistent inflammation in obesity is linked to a number of serious health setbacks including diabetes. In compliance to the aim of the present issues, the study by Uroić et al. (https://doi.org/10.3389/fendo.2024.1335371) have revealed a significantly close association between the expression of chemokine ligand/receptor and pathological abnormalities of obesity as well as obesity-induced diabetes viz. abundance of CCR4 + T lymphocytes vs vascular inflammation, CXCR4 + subsets vs albuminuria as well as CXCR3 + T lymphocytes vs dyslipidemia and these chemokine axes have been proposed as potential therapeutic targets. In addition, obese conditions due to overfeeding during early post-natal period has been demonstrated to signal polycystic ovary syndrome (PCOS) and insulin resistance through evoking proinflammatory responses by activating NLRP3 followed by an elevation in IL-1β expression and deactivating AMPK as experimentally documented by Veličković et al. (https://doi.org/10.3389/fendo.2024.1402905). In healthy individuals, antiinflammatory mediators reverse the proinflammatory episodes. Adiponectin (ADP) synthesized in adipocytes is known to act as an anti-inflammatory adipokine that links lipid metabolism and glucose homeostasis to regulate energy balance as well insulin-secretion to prevent obesity [3]. However, a cross-sectional study by Nielsen et al. Prevalence of obesity due to changes in life-style, feed habits and environmental changes is indeed increasing and reports new fatal outcomes are also emerging from both developed and developing countries. In particular, obesity-induced cancer is also threating the world with increasing prevalence with its different subtypes [8], especially colorectal cancer.Interestingly, obesity-induced inflammation and further complications described in this editorial are majorly linked to Toll-like receptor 4 (TLR4) as summarized by Figure 1. Whilst proinflammatory cytokines drives tumorigenesis through inflammation-dysplasianeoplasia sequel. Created in https://BioRender.com.Although

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