Middle Age Belly Fat: New Cells & Receptor Linked to Weight Gain
A newly identified type of stem cell that becomes more active with age is a key driver of increasing abdominal fat, according to research published this week in the journal Science. The findings, stemming from work at City of Hope and the University of California, Los Angeles, pinpoint a cellular mechanism behind the midlife expansion of waistlines, moving beyond explanations centered solely on lifestyle or slowing metabolism.
Researchers discovered that aging stimulates the emergence of a novel type of adult stem cell within white adipose tissue – the type of fat that stores energy. These cells exhibit an increased capacity to generate new fat cells, particularly around the abdomen. Unlike other stem cells in the body, the proliferation of these adipose progenitor cells (APCs) accelerates with age, according to the study.
A specific variant of these APCs, termed age-specific committed preadipocytes (CP-As), were identified as central to this process. These CP-As proliferate during middle age and directly contribute to the accumulation of abdominal fat. The research team found that the leukemia inhibitory factor receptor (LIFR) plays a critical role in activating these cells, triggering their multiplication and differentiation into fat tissue.
“This is not simply about gaining weight,” explained Qiong (Annabel) Wang, a co-author of the study. “Even individuals who maintain a stable body weight can experience a loss of muscle mass and an increase in abdominal fat due to these cellular changes.”
The concentration of fat accumulation in the abdominal region is linked to the unique characteristics of white adipose tissue. The LIFR activation mechanism appears to be specific to abdominal white adipose tissue, explaining why this area is particularly susceptible to fat gain during midlife. This localized increase in abdominal fat carries significant health risks, accelerating the aging process and increasing the likelihood of developing type 2 diabetes, cardiovascular diseases, and other metabolic disorders.
The discovery of CP-As provides a biological explanation for the increase in abdominal fat that often occurs with age, challenging the notion that We see solely a result of lifestyle factors. Understanding the mechanisms driving this process, researchers say, could lead to more targeted and effective strategies for preventing age-related metabolic diseases.
Researchers emphasize that inhibiting or modulating the activity of the LIFR could potentially block the formation of new fat cells, offering a therapeutic avenue for preventing abdominal obesity associated with aging. Further investigation into the signaling pathways that regulate CP-A proliferation is expected to reinforce possibilities for future pharmacological interventions.
The team is continuing to investigate the interplay between aging, hormonal changes, and the behavior of these progenitor cells, with the goal of developing interventions to improve metabolic health and extend healthy lifespan.