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Cellular mechanisms of microplastic and nanoparticle exposure and its relationship with metabolic diseases: Literature review
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This literature review examined how microplastic and nanoparticle exposure affects cellular mechanisms related to metabolic disease, finding evidence that these contaminants disrupt insulin signaling, alter lipid metabolism, and may contribute to the development of metabolic syndrome.
Microplastics (MP) and nanoparticles (PS-NPs) are emerging environmental contaminants of significant concern due to their adverse effects on human health. This study systematically reviews the impact of these pollutants on cellular mechanisms, with a specific focus on their association with metabolic diseases. Data were collected from various scientific publications relevant to the research topic. Research findings indicate that exposure to microplastics (MP) can result in a reduction in triglyceride and total cholesterol levels, while also disrupting insulin signaling pathways, thereby contributing to insulin resistance. Additional studies have demonstrated that exposure to nanoparticles (PS-NPs) in pregnant mice may increase the risk of metabolic disorders in their offspring. Moreover, PS-NP exposure has been shown to exacerbate type 2 diabetes by inhibiting the AKT/GSK3β pathway. Collectively, exposure to microplastics and nanoparticles has the potential to aggravate metabolic disorders and increase the risk of metabolic diseases, including diabetes, obesity, and cardiovascular conditions. These findings offer valuable insights into the potential health risks associated with environmental exposure to microplastics and nanoparticles and underscore the critical importance of addressing microplastic pollution to human health.
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Metabolic footprint of microplastics and nanoplastics: From environmental exposure to metabolic diseases
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Tiny plastic particles that get into our bodies through food, water, and air may be quietly messing with how our cells produce energy, process fat, and respond to insulin—potentially raising the risk of obesity, type 2 diabetes, and fatty liver disease. This review pulls together existing research to explain how these particles disrupt gut bacteria and cell function, with smaller plastic pieces generally causing more harm. While more research is needed to confirm long-term effects in humans, the findings suggest reducing plastic exposure where possible may be a smart precaution for metabolic health.
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This review examines growing evidence that micro- and nanoplastics may contribute to diabetes by disrupting blood sugar regulation, insulin signaling, and fat metabolism through oxidative stress and inflammation. Animal studies show that plastic particles can damage the pancreas, liver, and gut in ways that mirror the development of diabetes, though human studies are still limited. The review calls for more research into whether everyday microplastic exposure could be a hidden factor in the global rise of metabolic diseases.
Biological exposure to microplastics and nanoplastics and plastic additives: impairment of glycolipid metabolism and adverse effects on metabolic diseases
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This review examines how exposure to micro- and nanoplastics disrupts the body's ability to process sugars and fats, potentially contributing to diabetes, obesity, and atherosclerosis. The plastics cause inflammation and oxidative stress, damage gut bacteria, trigger insulin resistance, and increase fat buildup in the liver. For people who already have metabolic conditions, plastic exposure may make their disease worse.
Microplastic pollution: A potent threat for metabolic disruption in mammals
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This review examines the evidence linking microplastic exposure to metabolic disruption, covering mechanisms by which microplastics and their associated chemical additives may interfere with hormonal regulation, glucose metabolism, and lipid homeostasis. The authors identify microplastics as a potent emerging threat to metabolic health.
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Researchers reviewed how microplastics and nanoplastics disrupt lipid metabolism across multiple animal species, finding they inhibit digestive enzymes, alter gut microbiota, dysregulate fat storage and breakdown, and activate inflammatory signaling pathways — causing both acute and chronic metabolic damage.
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