Year: 2025
Type: article
Abstract: Adipose tissue maintains energy homeostasis by storing lipids during nutrient surplus and releasing them through lipolysis in times of energy demand. While lipolysis is essential for short term metabolic adaptation, prolonged metabolic stress requires adaptive changes that preserve energy reserves. Here, we report that β-adrenergic activation of adipocytes induces a transient and depot-specific infiltration of neutrophils into white adipose tissue (WAT), particularly in lipid-rich visceral WAT. Neutrophil recruitment requires the stimulation of both lipolysis and p38 MAPK activation in adipocytes. Recruited neutrophils locally secrete IL-1β, which suppresses lipolysis and limits excessive energy expenditure. Neutrophil depletion or blockade of IL-1β production increased lipolysis, leading to reduced WAT mass upon repeated β3-adrenergic stimulation. Together, these findings reveal an unexpected role of neutrophil-derived IL-1β in preserving lipid stores during metabolic stress, highlighting a physiological function of innate immune cells in maintaining energy homeostasis.
Source: Nature
Authors: Seunghwan Son, Cindy Xu, Haipeng Fu, Churaibhon Wisessaowapak, Joseph M. Valentine, Garam An, Janice Jang, Maddox Dinh, Yang Dai, Weiwei Fan, Ruth T. Yu, Michael Downes, Wei Ying, Yuliya Skorobogatko, Ronald M. Evans, Alan R. Saltiel
Language: English
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: green
Awards: G173899888, G2390658127, Adipose tissue plasticity in health and disease, G2923804148, Hormonal Regulation of Mammalian Gene Expression, Hormonal regulation of LDL receptor trafficking, Regulating energy expenditure in adipose tissue, G7577838933, G8198795195, Inflammation and hepatic lipid metabolism, Regulation of glycogen in health and disease, Diabetes Research Center (DRC)
OpenAlex ID: W4417199160