Whether acetyl-CoA carboxylase 1 (ACC1) is required for adipose ILC2 maintenance and function, and whether NAD+ precursor supplementation (nicotinamide riboside) can rescue ACC1 deficiency in a mouse high-fat diet (HFD) obesity model.
ACC1 deletion in mice impaired ILC2 differentiation, maintenance, and function, causing adipose tissue hypertrophy, inflammation, and predisposition to diabetes; supplementing with the NAD+ precursor nicotinamide riboside restored ILC2 function and adipose tissue homeostasis by rescuing NAD+/NADH balance.
Study is conducted entirely in mice; direct clinical translation to human obesity and ILC2 biology is unproven. The mechanism focuses on the citrate shuttle and NAD+/NADH balance, but other metabolic pathways affected by ACC1 loss are not fully characterized.
ACC inhibitors used clinically (e.g., for metabolic or fibrotic disease) may inadvertently impair adipose ILC2s and worsen metabolic inflammation — clinicians should be aware of this potential adverse effect. Nicotinamide riboside supplementation warrants investigation as a strategy to preserve ILC2 function in obesity.
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