TY  - JOUR
A1  - Püschel, Gerhard
A1  - Klauder, Julia
A1  - Henkel-Oberländer, Janin
T1  - Macrophages, low-grade inflammation, insulin resistance and hyperinsulinemia
BT  - A mutual ambiguous relationship in the development of metabolic diseases
JF  - Journal of Clinical Medicine : open access journal
N2  - 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.
KW  - NAFLD/MAFLD
KW  - type 2 diabetes
KW  - obesity
KW  - vicious cycle
KW  - TLR signaling
KW  - M1/M2 differentiation
KW  - Akt pathway
Y1  - 2022
U6  - https://doi.org/10.3390/jcm11154358
SN  - 2077-0383
VL  - 11
IS  - 15
SP  - 1
EP  - 30
PB  - MDPI
CY  - Basel, Schweiz
ER  -