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

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 funct...

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Published inJournal of clinical medicine Vol. 11; no. 15; p. 4358
Main Authors Püschel, Gerhard Paul, Klauder, Julia, Henkel, Janin
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 27.07.2022
MDPI
Subjects
Body fat
Clinical medicine
Cytokines
Enzymes
Fatty acids
Glucose
Homeostasis
Inflammation
Insulin resistance
Kinases
Lipids
Liver
M1/M2 differentiation
Metabolic disorders
Musculoskeletal system
NAFLD/MAFLD
Obesity
Overweight
Phosphatase
Phosphorylation
Physiology
Proteins
Review
TLR signaling
type 2 diabetes
vicious cycle
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Summary: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.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
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ISSN:2077-0383
2077-0383
DOI:10.3390/jcm11154358