Macrophages, Low-Grade Inflammation, Insulin Resistance and Hyperinsulinemia : A Mutual Ambiguous Relationship in the Development of Metabolic Diseases

Title data

Püschel, Gerhard Paul ; Klauder, Julia ; Henkel, Janin:
Macrophages, Low-Grade Inflammation, Insulin Resistance and Hyperinsulinemia : A Mutual Ambiguous Relationship in the Development of Metabolic Diseases.
In: Journal of Clinical Medicine. Vol. 11 (2022) Issue 15 . - 4358.
ISSN 2077-0383
DOI: https://doi.org/10.3390/jcm11154358

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Abstract in another language

Metabolic derangement with poor glycemic control accompanying overweight and obesity is associated with chronic low-grade inflammation and hyperinsulinemia. Macrophages, which present a very heterogeneous population of cells, play a key role in the maintenance of normal tissue homeostasis, but functional alterations in the resident macrophage pool as well as newly recruited monocyte-derived macrophages are important drivers in the development of low-grade inflammation. While metabolic dysfunction, insulin resistance and tissue damage may trigger or advance pro-inflammatory responses in macrophages, the inflammation itself contributes to the development of insulin resistance and the resulting hyperinsulinemia. Macrophages express insulin receptors whose downstream signaling networks share a number of knots with the signaling pathways of pattern recognition and cytokine receptors, which shape macrophage polarity. The shared knots allow insulin to enhance or attenuate both pro-inflammatory and anti-inflammatory macrophage responses. This supposedly physiological function may be impaired by hyperinsulinemia or insulin resistance in macrophages. This review discusses the mutual ambiguous relationship of low-grade inflammation, insulin resistance, hyperinsulinemia and the insulin-dependent modulation of macrophage activity
with a focus on adipose tissue and liver.