Research
Hormonal
High-fat diet-induced obesity reduces intestinal IgA+ immune cells and secretory IgA, which exacerbates insulin resistance by increasing intestinal permeability, microbial encroachment, and systemic inflammation.
Maintaining gut immune health, specifically IgA levels, may be crucial for managing insulin resistance during high-fat diets. While this study is in mice, it suggests that interventions supporting gut immunity (like certain diets or therapies) might help metabolic health.
GoodSupportsHIGH confidence
Here, we show that high fat diet (HFD) feeding alters intestinal IgA+ immune cells and that IgA is a critical immune regulator of glucose homeostasis. Obese mice have fewer IgA+ immune cells and less secretory IgA and IgA-promoting immune mediators. HFD-fed IgA-deficient mice have dysfunctional glucose metabolism... Mechanistically, [IgA] is a link that controls intestinal and adipose tissue inflammation, intestinal permeability, microbial encroachment and the composition of the intestinal microbiome during HFD.
Why this rating
Strong mechanistic evidence in mice with translational relevance to human therapies (metformin, surgery).
Source
Gut-associated IgA+ immune cells regulate obesity-related insulin resistance
Helen Luck et al. · Nature Communications · 2019
DOI 10.1038/s41467-019-11370-y
mechanism_onlyCited 200×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
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