From:  Microplastics, nanoplastics, and obesity: current evidence and biological mechanisms

 Summary of recent experimental animal and cell studies linking MNPs to metabolic dysfunction and obesity.

YearStudyModelExposureMain findings
2022Zhao et al. “Polystyrene bead ingestion promotes adiposity and cardiometabolic disease in mice.” [16]MicePolystyrene (PS) beads 0.5 and 5 µm in drinking water for 12 weeksAccelerated weight gain, increased body fat, hyperglycemia, insulin resistance markers, gut microbiome changes consistent with obesity, and adipogenic gene-expression changes in perivascular adipose tissue.
2022Shiu et al. “Dietary exposure to polystyrene nanoplastics impairs fasting-induced lipolysis in adipose tissue from high-fat diet fed mice.” [17]High-fat diet (HFD) mice; adipocytes in vitro/ex vivo60 nm PS nanoplasticsNanoplastics accumulated in white adipose tissue, reduced beta-adrenergic lipolysis, impaired fasting lipid mobilization, enlarged subcutaneous adipocytes, and increased liver lipid accumulation.
2022Huang et al. “Polystyrene microplastic exposure induces insulin resistance in mice via dysbacteriosis and pro-inflammation.” [18]Mice on normal chow and HFDPS microplastics (MPs)Induced insulin resistance and aggravated HFD-induced insulin resistance; associated with gut dysbiosis, inflammation, tissue accumulation, and impaired hepatic insulin signaling.
2023Okamura et al. “Oral Exposure to Polystyrene Microplastics of Mice on a Normal or High-Fat Diet and Intestinal and Metabolic Outcomes.” [14]MiceOral PS MPsMPs with HFD induced metabolic disturbances, such as diabetes and non-alcoholic fatty liver disease (NAFLD).
2023Huang et al. “Polystyrene microplastics trigger adiposity in mice by remodeling gut microbiota and boosting fatty acid synthesis.” [19]MicePS MPsLow/intermediate exposure caused overweight/adiposity, increased appetite, lower activity, altered cecal microbiota, and increased hepatic fatty-acid synthesis; high concentrations caused weight loss, showing non-monotonic effects.
2023Du et al. “Combined effects of high-fat diet and polystyrene microplastic exposure on microplastic bioaccumulation and lipid metabolism in zebrafish.” [20]Zebrafish50 µm PS MPsHFD increased PS accumulation; PS exposure aggravated hepatic lipid accumulation and liver injury and disrupted lipid/energy metabolism genes.
2024Zhang et al. “Polystyrene nanoplastics inhibit beige fat function and exacerbate metabolic disorder in high-fat diet-fed mice.” [21]HFD mice + primary beige adipocytesPS nanoplasticsImpaired beige adipocyte thermogenic function and worsened systemic metabolic performance in HFD mice.
2024Zhai et al. “Long-Term Exposure to Polystyrene Microspheres and High-Fat Diet-Induced Obesity in Mice: Evaluating a Role for Microbiota Dysbiosis.” [22]HFD miceLong-term PS microspheresReported greater body weight, liver weight, adipose tissue, and serum lipids in HFD mice exposed to PS; evaluated microbiota dysbiosis as a mechanism.
2024Zhao et al. “Obesogenic polystyrene microplastic exposures disrupt the gut-liver-adipose axis.” [9]Mice0.5 and 5 µm PS beads in water for 13 weeksConfirmed potentiated weight gain and adipose expansion; found adipose macrophage changes, altered bile acids, hepatic cholesterol, and nuclear receptor signaling.
2024Moon et al. “Microplastic exposure linked to accelerated aging and impaired adipogenesis in fat cells.” [23]Mice + Human adipose-derived stem cells (hASC)Oral PS MPs in mice; in vitro hASC exposureMPs accumulated in mouse white adipose tissue and induced adipose senescence/inflammation; in human adipose-derived cells, MPs impaired adipogenic differentiation.
2024Xu et al. “Impact of Microplastic Exposure on Blood Glucose Levels and Gut Microbiota: Differential Effects under Normal or High-Fat Diet Conditions.” [24]Mice, normal vs. HFDPS MPsMP exposure worsened blood-glucose disruption under HFD conditions and altered gut microbiota; less effect under normal diet.
2025Kim et al. “Mixtures of polystyrene micro and nanoplastics affects fat and glucose metabolism in 3T3-L1 adipocytes and zebrafish larvae.” [25]3T3-L1 adipocytes + HFD zebrafish larvaeMixed PS micro/nanoplasticsIncreased adipogenesis/lipogenesis markers, reduced glucose uptake and insulin signaling in adipocytes; zebrafish showed increased body weight and blood glucose.
2025Jhang et al. “Impact of polyethylene terephthalate and polylactic acid nanoplastics on cellular uptake and lipid metabolism in differentiated 3T3-L1 adipocytes.” [26]3T3-L1 adipocytesPET and PLA nanoplasticsPET nanoplastics entered adipocytes and altered lipid handling via AMPK/HSL-mediated lipolysis; PLA did not show the same effect.
2025Kou et al. “Polystyrene microplastics impair brown and beige adipocyte function via the gut microbiota-adipose tissue crosstalk in high-fat diet mice.” [27]HFD micePS MPsReduced energy expenditure, increased lipid accumulation, impaired BAT/iWAT thermogenesis, worsened gut dysbiosis; microbiota transplantation reproduced lipid/thermogenic effects.
2025Shen et al. “Exposure to Nanoplastics During Pregnancy Induces Brown Adipose Tissue Whitening in Male Offspring.” [28]Pregnant mice and offspringGestational PS nanoplasticsMale offspring developed beige adipose tissue whitening, larger white adipocytes, increased lipogenesis, and inhibited lipophagy.
2025Hsu et al. “Polystyrene nanoplastics disrupt the intestinal microenvironment by altering bacteria-host interactions through extracellular vesicle-delivered microRNAs.” [29]Mice, enterocyte model100 nm PS nanoplastics orally for 12 weeksIncreased body-weight gain without significant liver weight change; showed intestinal barrier and microbiota mechanisms.
2025Han et al. “Chronic Nanoplastic Exposure Promotes the Development and Progression of Metabolic Dysfunction-Associated Steatotic Liver Disease.” [30]Animal liver/metabolic disease modelNanoplasticsChronic NP exposure promoted metabolic dysfunction-associated steatotic liver disease (MASLD) progression.
2026Liebgott et al. “A Western-style diet shapes the gut and liver responses to low-dose, fit-for-purpose polystyrene nanoplastics in mice.” [31]Mice, chow vs. Western dietapproximately 600 nm PS nanoplastics for 90 daysLow-dose PS-NPL exposure increased body-weight gain in a non-monotonic pattern, worsened glucose intolerance in Western-diet mice, and promoted hepatic lipid accumulation.