Research
Hormonal
Adipose tissue immune cell composition shifts in obesity from anti-inflammatory (M2 macrophages, Th2 T cells, Tregs) to pro-inflammatory (M1 macrophages, Th1 T cells, CD8+ T cells), driving local and systemic inflammation that contributes to insulin resistance.
Obesity changes the immune environment of fat tissue. Instead of anti-inflammatory cells that protect insulin sensitivity, pro-inflammatory immune cells (like M1 macrophages and Th1 T cells) take over, releasing chemicals that block insulin action.
GoodSupportsHIGH confidence
In obese mice, the composition of immune cells is dynamically shifted to enhance inflammatory responses in adipose tissue. Classically activated M1 macrophages, Th1 CD4+ T cells, effector CD8+ T cells... are increased and produce inflammatory mediators such as TNF-α, IFN-γ... resulting in insulin resistance.
Why this rating
Supported by multiple citations of immune cell studies in rodents and humans.
Source
Adipokines Mediate Inflammation and Insulin Resistance
Hyokjoon Kwon et al. · Frontiers in Endocrinology · 2013
DOI 10.3389/fendo.2013.00071
narrative_reviewCited 662×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Pro-inflammatory adipokines such as TNF-α and IL-6 induce insulin resistance by activating kinases (JNK, IKKβ) that phosphorylate IRS1/2 on serine residues, thereby inhibiting tyrosine phosphorylation and downstream insulin signaling.Strong
- Obesity-induced insulin resistance is mediated by an imbalance in pro- and anti-inflammatory adipokines, where increased pro-inflammatory adipokines (e.g., TNF-α, IL-6, leptin) and decreased anti-inflammatory adipokines (e.g., adiponectin) trigger inflammatory signaling cascades that suppress insulin receptor substrate (IRS) phosphorylation.Good
- Adiponectin, an anti-inflammatory adipokine, improves insulin sensitivity by activating AMPK to enhance fatty acid oxidation and glucose uptake, but its levels are decreased in obesity due to suppression by inflammatory signals.Good
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