Macrophages, low-grade inflammation, insulin resistance and hyperinsulinemia
- 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. ThisMetabolic 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.…
Verfasserangaben: | Gerhard PüschelORCiDGND, Julia KlauderGND, Janin Henkel-OberländerORCiDGND |
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DOI: | https://doi.org/10.3390/jcm11154358 |
ISSN: | 2077-0383 |
Pubmed ID: | https://pubmed.ncbi.nlm.nih.gov/35955975 |
Titel des übergeordneten Werks (Englisch): | Journal of Clinical Medicine : open access journal |
Untertitel (Englisch): | A mutual ambiguous relationship in the development of metabolic diseases |
Verlag: | MDPI |
Verlagsort: | Basel, Schweiz |
Publikationstyp: | Wissenschaftlicher Artikel |
Sprache: | Englisch |
Datum der Erstveröffentlichung: | 27.07.2022 |
Erscheinungsjahr: | 2022 |
Datum der Freischaltung: | 07.12.2022 |
Freies Schlagwort / Tag: | Akt pathway; M1/M2 differentiation; NAFLD/MAFLD; TLR signaling; obesity; type 2 diabetes; vicious cycle |
Band: | 11 |
Ausgabe: | 15 |
Aufsatznummer: | 4358 |
Seitenanzahl: | 30 |
Erste Seite: | 1 |
Letzte Seite: | 30 |
Fördernde Institution: | German Research Foundation (DFG) |
Fördernummer: | HE 7032/1-3 |
Fördernummer: | 491466077 |
Organisationseinheiten: | Mathematisch-Naturwissenschaftliche Fakultät / Institut für Ernährungswissenschaft |
Extern / Extern | |
DDC-Klassifikation: | 6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit |
Peer Review: | Referiert |
Fördermittelquelle: | Publikationsfonds der Universität Potsdam |
Publikationsweg: | Open Access / Gold Open-Access |
Lizenz (Deutsch): | CC-BY - Namensnennung 4.0 International |
Externe Anmerkung: | Zweitveröffentlichung in der Schriftenreihe Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe ; 1279 |