Immunometabolism in obesity: Understanding the beneficial and detrimental roles of inflammation

TL;DR

The paper explores how inflammation in obesity can both help and harm metabolic health, depending on its stage.

Contribution

It highlights the dual, context-dependent role of metaflammation in obesity, emphasizing its initially adaptive function.

Findings

Metaflammation can support metabolic homeostasis in early obesity.

Chronic metaflammation leads to insulin resistance and metabolic dysfunction.

The transition from beneficial to harmful inflammation is a key focus.

Abstract

In obesity, nutrient excess and altered adipocyte secretory profiles reprogram cell-intrinsic metabolism, leading to the activation of immune cells within metabolically active tissues such as adipose tissue. This obesity-associated chronic low-grade metabolic inflammation (often referred to as metaflammation) is a well-established driver of insulin resistance and metabolic dysfunction. However, several lines of emerging evidence suggest that metaflammation is not merely a pathologic process, but may also serve as an adaptive response that supports metabolic homeostasis, particularly at the early stages of obesity. This Essay discusses immunometabolic mechanisms underlying the dual nature of metaflammation in obesity, highlighting how its initially beneficial effects can transition into detrimental outcomes.

Chronic low-grade metabolic inflammation (known as metaflammation) drives insulin resistance and metabolic dysfunction in obesity. This Essay discusses the immunometabolic mechanisms underlying metaflammation with a focus on its lesser known beneficial effects and how they can transition into detrimental outcomes.

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