Aug 2026· Immunology Letters· pp.
107237
· 0 citations· 83 references
Medicine
TL;DR
This review critically summarizes mainly experimental and preclinical evidence linking dietary components, gut microbiota-derived metabolites, and ILC subsets to obesity, insulin resistance, type 2 diabetes mellitus (T2DM), and related metabolic complications.
Abstract
Innate lymphoid cells (ILCs) are innate-like lymphocytes that contribute to tissue homeostasis, barrier immunity, inflammation, and host defense. In metabolic syndrome (MetS), a condition estimated to affect more than 1.5 billion adults worldwide, dietary patterns and gut microbial metabolites are increasingly recognized as regulators of immune and metabolic dysfunction [1-8]. This review critically summarizes mainly experimental and preclinical evidence, with selected human observations where available, linking dietary components, gut microbiota-derived metabolites, and ILC subsets to obesity, insulin resistance, type 2 diabetes mellitus (T2DM), and related metabolic complications. Current evidence suggests that dietary fibers, short-chain fatty acids, lipids, vitamins, and fermented foods can modulate ILC1, ILC2, and ILC3 responses in a context-dependent manner. However, most mechanistic data derive from mouse models, and direct translation to human MetS remains limited. Through integrating diet-microbiota interactions, ILC subset biology, and metabolic inflammation, this review highlights candidate pathways and biomarkers that may guide future therapeutic studies rather than established clinical interventions.
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