New research reveals that microplastics infiltrate fat tissue, driving premature aging and inflammation, heightening the risk of chronic conditions such as diabetes and cardiovascular disease.
Study: Microplastic exposure linked to accelerated aging and impaired adipogenesis in fat cells. Image Credit: Shutterstock AI / Shutterstock.com
In a recent study published in the journal Scientific Reports, researchers investigate the effects of microplastic (MP) exposure on the normal aging and function of adipose tissue.
What are MPs?
MPs are plastic particles less than five millimeters (mm) in length that are either industrially produced or arise from the environmental degradation of larger plastic objects. Due to their small particle sizes, MPs can readily enter biological systems, where they have the potential to cause extensive psychological damage.
MPs have been widely studied in marine ecosystems, and several studies using these models have reported the biomagnification of these pollutants. However, the impact of MPs on terrestrial organisms, including humans, remains poorly understood.
MPs are ubiquitous in the air, food supply, as well as various materials encountered by humans on a daily basis. Alarmingly, the global increase in MP concentrations temporally coincides with rising public health issues, including impaired aging.
How does aging impact adipose tissue?
Adipose tissue, also known as body fat, is crucial for energy and metabolic homeostasis. Aging can have various adverse effects on adipose tissue, including altered immune responses and the infiltration of lipids into other organs.
These age-associated effects on adipose tissue can increase the risk of systemic inflammation, metabolic dysfunction, and accelerated aging. Dyslipidemia, chronic general inflammation, insulin resistance, obesity, type 2 diabetes (T2D), and cardiovascular disease (CVD) are additional consequences that can arise due to aging-related alterations in adipose tissue.
Delaying the aging process of adipose tissue may be a way to prevent age-related diseases."
About the study
The present study utilizes both in vitro human adipose-derived stem cells (hASCs) and in vivo murine models to investigate the physiological impacts and potential mechanisms involved in MPs' effects on adipose tissue.
Senescence-associated β-Galactosidase (SA-β-gal) staining of the inguinal white adipose tissue (iWAT) and epididymal white adipose tissue (eWAT) was performed to elucidate the effects of MP exposure. Immunofluorescence staining was also conducted for MP uptake visualization, whereas western blotting was used for protein extraction and characterization, and quantitative polymerase chain reaction (qPCR) for gene expression assays.
Oil red O (ORO) staining was also performed to assess the rate and characteristics of adipocyte differentiation. Statistical differences between case and control samples were measured using one-way analysis of variance (ANOVA).
Study findings
After 14 days of MP oral administration to mice, immunofluorescence staining provided visualization of MP accumulation in both eWAT and iWAT tissues. Adipose tissue weights were comparable between cases and controls; however, controls exhibited smaller adipocyte sizes than mice exposed to MPs. These size changes corresponded to increased SA-β-gal activity, thus suggesting that MP exposure induces an aging response in adipocytes.
Upregulation of matrix metalloproteinase 3 (MMP3), p21and p16, p-histone H2A.X, laminB1, and high mobility group box 1 (HMGB1) was observed, thus demonstrating the negative impacts of MP exposure on extracellular remodeling, cell cycle arrest, DNA repair, nuclear structure, and inflammatory processes, respectively.
Western blotting and qPCR assays confirmed these findings and further revealed upregulation of nuclear factor-kB (NF-kB), interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), and CD68 pathways. These observations suggest the role of MPs in initiating macrophage infiltration into adipocytes and subsequent inflammation. Likewise, hASCs exposed to MPs exhibited dysfunctional differentiation, early senescence, and enhanced inflammation.
Conclusions
MP exposure led to their accumulation in adipose tissues, wherein these particles accelerate aging by triggering aging-associated senescence markers, particularly β-galactosidase activity, upregulating inflammatory markers, and reduced adipogenic differentiation. Thus, MPs appear to trigger cellular senescence, exacerbate inflammation, and alter normal adipocyte differentiation, thereby accelerating aging and potentially contributing to age-associated chronic disease manifestation.
The study findings provide evidence for the long-term adverse public health impacts of MP exposure and emphasize the importance of improving public health interventions that can mitigate the effects of these environmental contaminants.
These findings contribute to a deeper understanding of the potential adverse effects of environmental contaminants on biological aging and tissue function, offering a foundation for future research and public health initiatives aimed at mitigating these effects."
Journal reference:
- Moon, H., Jeong, D., Choi, J. W., et al. (2024). Microplastic exposure linked to accelerated aging and impaired adipogenesis in fat cells. Scientific Reports 14. doi:10.1038/s41598-024-74892-6