Key result
Weight cycling drives distinct dynamic shifts in adipose tissue inflammation compared to stable obesity.
Why the study?
How do weight loss and subsequent weight regain influence adipose tissue inflammation and cardiovascular risk in individuals with obesity?
How do weight loss and subsequent weight regain influence adipose tissue inflammation and cardiovascular risk in individuals with obesity?
Weight regain after weight loss triggers distinct inflammatory changes in adipose tissue that may increase the risk of cardiovascular disease and mortality.
The global rise in obesity underscores the urgent need for effective long-term weight-management strategies. Weight loss (WL) is extremely beneficial in combating obesity complications, justifying the great success of recent WL medications. However, most individuals trying to lose weight will fail to maintain a lower body weight. Weight regain following WL increases the risk of cardiovascular disease and mortality. Adipose tissue inflammation is a critical mediator of metabolic dysfunction in obesity, contributing to cardiovascular complications. In obesity, chronic low-grade inflammation, marked by immune infiltration and dysregulated adipocyte function, contributes to systemic insulin resistance and metabolic comorbidities. However, the adipose tissue response to WL and subsequent weight regain is distinct from that in non–weight-fluctuating obesity and far less studied. This review synthesizes current literature to elucidate the dynamic shifts in adipose tissue across the continuum of obesity, WL, and weight regain.
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Cáceres et al. (2025) conducted a review in Obesity. Weight loss and weight regain vs. Non-weight-fluctuating obesity was evaluated on Adipose tissue inflammation. Weight loss and subsequent weight regain induce distinct dynamic shifts in adipose tissue inflammation compared to non-weight-fluctuating obesity.
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