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Microplastics induce insulin resistance by causing mitochondrial dysfunction associated with mROS in skeletal muscle in vitro
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Researchers exposed human muscle cells to polystyrene micro and nanoplastics and found that the particles caused insulin resistance, meaning the cells could not properly absorb sugar from the blood. The plastics damaged the cells' mitochondria (the energy-producing structures) and triggered harmful oxidative stress, but a mitochondria-protecting antioxidant reversed the damage. This study suggests that microplastic exposure could contribute to metabolic problems like type 2 diabetes by impairing how muscles process sugar.
Microplastics pose an emerging threat to both ecological and human health. It is worth noting that muscle has proved to be the target organ of microplastic particles. Skeletal muscle is the major site of insulin-stimulated glucose disposal and subsequent glucose homeostasis and plays a key role in the regulation of glucose metabolism in the body. However, studies on the effects of microplastics on glucose metabolism and insulin sensitivity in human skeletal muscle are limited. Herein, human rhabdomyosarcoma (RD) cells were exposed to two sizes (3 μm and 100 nm) of polystyrene microplastics/nanoplastics (PS-MPs/NPs) at three concentrations (75, 150, and 300 μg/mL) to investigate the possible molecular mechanisms. Our results showed that PS-MPs/NPs could be internalized into RD cells and lead to a reduction in cellular uptake of glucose. These results suggest that PS-MPs/NPs may cause skeletal muscle insulin resistance (IR) at the cellular level. Additionally, we observed that PS-MPs/NPs not only resulted in mitochondrial damage but also induced intracellular oxidative stress. However, treatment with the mitochondria-targeted antioxidant MitoQ improved mitochondrial dysfunction and IR at the cellular level. These findings indicate that PS-MPs/NPs induce IR by causing mitochondrial dysfunction associated with mROS in skeletal muscle in vitro. The identification of these molecular mechanisms is helpful for deeply understanding of the health hazards posed by microplastics.
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This review examines how micro- and nanoplastics may worsen diet-related diseases like obesity and type 2 diabetes by damaging mitochondria, the energy-producing structures inside cells. Studies suggest that microplastic exposure combined with unhealthy diets can amplify metabolic problems like insulin resistance and high blood sugar. The findings point to mitochondrial damage as a key link between microplastic exposure and the growing epidemic of metabolic diseases.
Polystyrene microplastics-induced ROS overproduction disrupts the skeletal muscle regeneration by converting myoblasts into adipocytes
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Researchers found that polystyrene microplastics impaired skeletal muscle repair in mice by triggering excess production of reactive oxygen species (ROS) inside muscle stem cells. This oxidative stress redirected muscle stem cells to become fat cells instead of new muscle fibers, resulting in increased fat deposits and reduced muscle fiber size. The study suggests that microplastic exposure could interfere with the body's natural ability to regenerate and maintain muscle tissue.
Exposure to polystyrene nanoplastics promotes premature cellular senescence through mitochondrial ROS production and dysfunction in pre-differentiated skeletal myoblasts
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This lab study found that polystyrene nanoplastics caused premature aging in muscle precursor cells by damaging their mitochondria and triggering excessive production of harmful molecules called reactive oxygen species. The nanoplastics were absorbed into cells, accumulated there, and caused the cells to stop dividing and show signs of aging. This suggests that nanoplastic exposure could contribute to muscle deterioration and aging-related conditions by damaging the cells responsible for muscle repair.
In vitro exposure to polystyrene microplastic induces oxidative stress mediated β-cell dysfunction
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Scientists exposed lab-grown insulin-producing cells to tiny polystyrene microplastic particles (like those found in plastic packaging) and found the plastic got absorbed into the cells, triggered damaging stress, and impaired the cells' ability to function and survive. Since these are the same cells that make insulin in your pancreas, this lab study suggests microplastics could potentially contribute to diabetes risk—though more research is needed to confirm this happens in real human bodies, not just cells in a dish.
Impact of Micro- and Nanoplastics on Mitochondria
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This review examines how micro- and nanoplastics can damage mitochondria, the energy-producing structures inside cells that are critical for metabolism and cell survival. Researchers found that plastic particle exposure can trigger oxidative stress, disrupt mitochondrial membrane function, and interfere with energy production pathways. Since mitochondrial dysfunction is linked to numerous health conditions, the study suggests this may be a key mechanism through which plastic pollution affects human health.
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