Intermittent fasting promotes type 3 innate lymphoid cells secreting IL-22 contributing to the beigeing of white adipose tissue.
Hong ChenLijun SunLu FengXue HanYunhua ZhangWenbo ZhaiZehe ZhangMichael MulhollandWeizhen ZhangYue YinPublished in: eLife (2024)
Mechanism underlying the metabolic benefit of intermittent fasting remains largely unknown. Here, we reported that intermittent fasting promoted interleukin-22 (IL-22) production by type 3 innate lymphoid cells (ILC3s) and subsequent beigeing of subcutaneous white adipose tissue. Adoptive transfer of intestinal ILC3s increased beigeing of white adipose tissue in diet-induced-obese mice. Exogenous IL-22 significantly increased the beigeing of subcutaneous white adipose tissue. Deficiency of IL-22 receptor (IL-22R) attenuated the beigeing induced by intermittent fasting. Single-cell sequencing of sorted intestinal immune cells revealed that intermittent fasting increased aryl hydrocarbon receptor signaling in ILC3s. Analysis of cell-cell ligand receptor interactions indicated that intermittent fasting may stimulate the interaction of ILC3s with dendritic cells and macrophages. These results establish the role of intestinal ILC3s in beigeing of white adipose tissue, suggesting that ILC3/IL-22/IL-22R axis contributes to the metabolic benefit of intermittent fasting.
Keyphrases
- adipose tissue
- insulin resistance
- single cell
- blood glucose
- high intensity
- high fat diet
- dendritic cells
- induced apoptosis
- skeletal muscle
- rna seq
- cell therapy
- nk cells
- metabolic syndrome
- immune response
- cell cycle arrest
- stem cells
- cell death
- blood pressure
- bone marrow
- mesenchymal stem cells
- cell proliferation
- glycemic control
- pi k akt