Study 38 of 47NAD+ (Nicotinamide Adenine Dinucleotide) literatureCell metabolism · ObservationalTop journal2026

Adipose ILC2s depend on acetyl-CoA carboxylase 1 to maintain metabolic health.

ACC1 is critical for the maintenance and function of adipose ILC2s, and its deficiency can lead to metabolic issues in obesity. Supplementation with nicotinamide riboside may help restore ILC2 function.

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this study against the rest of the nad+ (nicotinamide adenine dinucleotide) corpus

Preclinical

Observational · this one

Open-label

Randomised

Reviews

Summary and findings

The study investigates the role of acetyl-CoA carboxylase 1 (ACC1) in adipose group 2 innate lymphoid cells (ILC2s) in the context of high-fat diet-induced obesity in mice. It was found that ACC1 deletion impairs ILC2 function, leading to adipose tissue hypertrophy and inflammation. Supplementation with nicotinamide riboside was shown to restore ILC2 function.

How much of this paper we could read: full text read (0.70). We had a clear abstract, so the summary below closely tracks the paper. What this means →

Not reported in abstract.2026

Abstract

The authors’ words, as Cell metabolism supplied them

Adipose group 2 innate lymphoid cells (ILC2s) are essential to maintain metabolic homeostasis. Obesity severely impairs the number and function of ILC2s, resulting in the progression of metabolic inflammation. How ILC2s are perturbed in obesity remains unknown. Here, we find that high-fat diet (HFD)-induced obesity in mice increases fatty acid oxidation, leading to suppression of acetyl-coenzyme A (CoA) carboxylase 1 (ACC1) in adipose ILC2s. ACC1 is essential for maintaining the citrate shuttle, NAD+/NADH balance, and cellular metabolism. Mimicking the effects of HFD, ACC1 deletion impairs differentiation, maintenance, and function of ILC2s. This results in adipose tissue hypertrophy and inflammation at steady state, predisposing mice to the development of diabetes. Supplementing with the NAD+ precursor nicotinamide riboside rescues ACC1 deficiency, restoring ILC2 function and adipose tissue homeostasis. These findings establish ACC1 as a critical regulator of adipose ILC2 maintenance and function and provide a rationale for the adverse effects of ACC inhibition in obesity.

Background

Not reported in abstract.

Methods

Not reported in abstract.

Results

Not reported in abstract.

Interpretation

Not reported in abstract.

Limitations

Not reported in abstract.

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