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

Obesity reduces adipose ILC2s by decreasing ACC1, impairing their function and promoting metabolic inflammation in mice.

• Why it matters: Understanding how obesity disrupts ILC2s is crucial because these cells maintain metabolic health, and their impairment accelerates inflammation and diabetes risk.
• What they did: Researchers used high-fat diet-induced obesity models and genetic deletion of ACC1 to study ILC2 function, examining cellular metabolism and immune responses.
• The result: Loss of ACC1 impairs ILC2 differentiation and activity, leading to adipose inflammation and hypertrophy, but NAD+ precursor supplementation can restore ILC2 function and tissue homeostasis.