Obesity is a major and rapidly escalating global public health challenge [1]. According to the World Health Organization, approximately one in eight people worldwide was living with obesity in 2022, with prevalence more than doubling in adults and nearly quadrupling in adolescents since 1990 [2]. An estimated 2.5 billion adults were overweight, including 890 million with obesity, while over 390 million children and adolescents aged 5–19 years were affected [2]. Although obesity has traditionally been attributed to excess caloric intake and sedentary lifestyles, these factors alone do not fully explain the sharp global increase observed in recent decades. This has prompted growing interest in environmental contributors that may influence metabolic regulation and energy homeostasis.

Plastic pollution has emerged as a pervasive environmental and public-health concern. Since 1950, more than 8,300 million metric tons of plastic have been produced, with widespread use driven by low cost, durability, and versatility [3]. Environmental degradation of plastics generates microplastics and nano-plastics (MNPs), which are now detected in food, water, air, and human biological samples. Microplastics (MPs) are generally defined as plastic particles ranging in size from 1 micrometer (µm) up to 5 millimeters (mm) in length [4]. Nano-plastics (NPs) refer to even smaller plastic particles with sizes typically below 1 µm (1,000 nm), with some definitions specifying particles approximately between 1 nm and 100 nm, or from 1 nm up to 1,000 nm [4]. Although MPs and NPs share overlapping environmental and metabolic effects, NPs may exhibit different biological behavior because of their smaller size, including greater cellular uptake, tissue penetration, and potential systemic distribution. MPs may also be classified as primary or secondary particles. Primary MPs are intentionally manufactured at microscopic sizes for industrial or commercial use, whereas secondary MPs result from the environmental degradation and fragmentation of larger plastic materials.

Human exposure to MNPs occurs primarily through ingestion, followed by inhalation and, to a much lesser extent, dermal contact. Dietary sources such as seafood, salt, and bottled water contribute substantially to intake, while indoor air and synthetic materials represent additional inhalation pathways (Figure 1) [5].

Emerging evidence suggests that MNP exposure may begin before birth. MNPs have been detected in placental tissue, raising concern that these particles, or their associated chemicals, may cross the maternal-fetal interface and influence fetal development [6]. This pathway is important because prenatal and neonatal periods represent critical windows for metabolic programming. While human evidence directly linking placental MNP exposure to later obesity is still emerging, early-life exposure may plausibly contribute to long-term metabolic vulnerability and therefore warrants further investigation [6].

Several biological mechanisms have been proposed through which MNPs may influence metabolic health. Plastics contain or adsorb chemical additives, including bisphenols and phthalates, that act as endocrine-disrupting chemicals capable of interfering with hormonal pathways regulating adipogenesis, glucose metabolism, and appetite [7]. In addition, experimental studies show that MNP exposure can induce oxidative stress and low-grade inflammation, processes central to obesity and insulin resistance [8]. Emerging evidence also indicates that MNPs may alter gut microbiota composition and function, potentially affecting metabolic signaling, intestinal permeability, and inflammatory responses [9].

Despite these mechanistic insights, evidence directly linking MNP exposure to obesity prevalence or development in humans remains limited. The current data are largely derived from experimental and observational studies [10]. Methodological limitations, including variability in exposure assessment, particle characterization, and outcome measures, further complicate interpretation of the available evidence. This review aims to synthesize the current evidence on the potential relationship between MNP exposure and obesity. The aim of this manuscript is to provide an evidence-based review of the proposed mechanistic and potentially pathogenic adverse effects of MNPs with obesity, while highlighting key uncertainties and research gaps. For consistency, MNPs are used as an umbrella term where appropriate, although individual studies are described using MPs or NPs when that terminology more accurately reflects the original article. The literature included in this narrative review was identified through searches of PubMed, Scopus, and Web of Science databases up to April 2026 using combinations of terms including “microplastics,” “nanoplastics,” “obesity,” “metabolism,” “gut microbiome,” and “metabolic dysfunction.” Both experimental and human studies were reviewed where relevant to the topic. No formal meta-analysis was performed.

Although MNPs are inert, they are ubiquitous environmental contaminants [3]. Notably, emerging evidence suggests that they may interfere with biological systems and have clinical implications. The particles carry chemical additives and adsorbed pollutants that act as endocrine-disrupting chemicals capable of interacting with hormone receptors and altering metabolic pathways linked to glucose and lipid homeostasis [11]. Experimental studies indicate that microplastic exposure can induce oxidative stress and inflammatory responses [12]. These are fundamental processes implicated in the development of metabolic dysregulation and obesity. Systematic reviews indicate that exposure to MNPs can disrupt gut microbial composition, impair short-chain fatty acid production, and modulate immune pathways [13]. These effects are increasingly recognized as contributors to metabolic syndrome and chronic inflammation [13].

A study by Okamura et al. [14] examined how oral exposure to polystyrene MPs affects metabolic and intestinal health in mice, which were fed either a normal diet or a 4-week high‑fat diet. The study used carboxyl-modified fluorescent polystyrene particles measuring approximately 0.45–0.53 µm in diameter. In mice fed a high-fat diet, co-exposure to these MPs was associated with higher blood glucose levels, increased serum lipid concentrations, and higher non-alcoholic fatty liver disease (NAFLD) activity scores compared with a high-fat diet alone. The high‑fat plus MPs group also had increased intestinal permeability, reduced goblet cell numbers, greater inflammatory cell infiltration in the small intestine, and higher expression of genes related to inflammation and fatty acid transport. In addition, gut microbial composition was altered, with a greater relative abundance of the genus Desulfovibrio in the high-fat diet plus MPs group. In murine intestinal epithelial MODE-K cells, combined exposure to MPs and palmitic acid also reduced Muc2 gene expression. Overall, these findings suggest that oral exposure to polystyrene MPs may exacerbate diet-induced intestinal and metabolic disturbances, including glucose dysregulation and metabolic dysfunction-associated steatotic liver disease (MASLD), particularly under high-fat diet conditions.

In animal and cell studies, MNPs have been observed to promote inflammatory signaling, increase hepatic fat accumulation, and disturb glucose regulation [14]. This suggests potential mechanisms by which these particles may influence adiposity and insulin sensitivity [15] (Table 1).

Moreover, human-focused evidence has detected MPs and their metabolites in blood, placental tissue, and gastrointestinal samples, suggesting systemic exposure and possible impacts on endocrine and immune biomarkers in humans, although causal relationships with clinical metabolic outcomes remain under investigation [10].

Recent human studies have begun to explore associations between MNP exposure and metabolic indicators. Tu et al. [32] evaluated microplastic levels in human blood and fecal samples and used machine-learning approaches to identify potential factors associated with exposure. The study evaluated demographic, lifestyle, socioeconomic, dietary, environmental, and anthropometric factors as potential predictors of microplastic levels in blood and feces. However, these findings remain observational and should be interpreted cautiously, as they cannot establish causality or determine whether MNP exposure contributes directly to obesity or reflects differences in diet, environment, lifestyle, or other confounding factors.

Emerging research suggests that exposure to MNPs may contribute to metabolic disturbances, including insulin resistance, gut dysbiosis, inflammation, and altered lipid metabolism. However, direct evidence linking MNP exposure to clinically measurable obesity outcomes remains limited [10, 13]. MNPs are pervasive environmental contaminants. This presence raises concerns about chronic, low-dose exposure and downstream metabolic effects (Figure 2).

The current evidence is derived from experimental, animal, and mechanistic studies [3, 33]. However, many experimental studies use controlled exposure conditions and MNP concentrations that may exceed estimated real-world human exposure levels, which may limit direct translation of these findings to chronic human metabolic disease. Collectively, the evidence suggests biologically possible pathways through which MNP particles and associated chemicals may influence fat accumulation, obesity development, and related metabolic dysfunction.

One line of evidence linking MNPs with obesity comes from the impact on the gut microbiome, which is a key regulator of host metabolism, energy balance, and nutrient absorption [15]. A systematic review found that exposure to MNPs can disrupt the composition and diversity of the human gut microbiome, leading to alterations in microbial metabolic functions, changes in short-chain fatty acid production, and modulation of immune pathways [15]. This dysbiosis is characterized by a reduction in beneficial microbial species and an increase in those associated with inflammation, and it has been independently linked to obesity and metabolic syndrome in numerous human studies [15].

Although direct human studies of plastic-induced dysbiosis are limited, these mechanistic changes suggest a pathway through which MNPs exposure could contribute to metabolic dysfunction and increased fat deposition. Experimental animal research further supports this possibility. A study using mouse models, when compared to controls, demonstrated that chronic low-dose exposure to polystyrene MPs altered the gut microbiota and impaired metabolic homeostasis, including effects on energy extraction and glucose metabolism [24].

However, findings across studies remain inconsistent. For example, Xu et al. [24] reported no significant differences in body weight between control and polystyrene microplastic-exposed mice under either normal- or high-fat diet conditions, despite observed effects on glucose metabolism and gut microbiota. Therefore, current evidence more strongly supports MNP-associated metabolic perturbation than direct obesity causation.

These results mirror broader patterns seen in obesity research, where disruptions in the relative abundance of microbial species can promote increased energy harvest from the diet, which was associated with mechanistic adverse effects of low-grade chronic inflammation and perturbations in insulin signaling [15, 34]. Recognizably, these are all risk factors for obesity [18, 19]. Although these findings derive from controlled studies in animals, they provide important mechanistic evidence that MPs can, in fact, influence gut-microbiome-related metabolic processes, which are closely tied to body weight regulation.

Notably, MNPs are also potential carriers for a wide range of chemicals, including plastic additives and breakdown products [3]. These agents often act as metabolism-disrupting agents. Plastic-associated chemicals, such as bisphenol substitutes [e.g., bisphenol S (BPS)], phthalate analogs, and perfluorinated compounds, interact with multiple metabolic pathways [34, 35]. These metabolic pathways include those regulating adipocyte differentiation, insulin sensitivity, lipid metabolism, and energy homeostasis [34, 35]. Importantly, many experimental studies are unable to fully distinguish the biological effects of the plastic particles themselves from those of associated chemical additives or adsorbed contaminants, including phthalates and bisphenols, which may independently contribute to metabolic dysfunction.

Inflammation and oxidative stress, which are key contributors to obesity and metabolic syndrome, have also been connected to microplastic exposure. A review of the related health effects reports that MNPs’ component polymers may induce oxidative stress, weaken antioxidant defenses, and activate pro-inflammatory pathways by increasing reactive oxygen species and lipid peroxidation in exposed tissues [36]. Chronic inflammation, in turn, can impair insulin signaling pathways and lead to adipocyte hypertrophy and macrophage infiltration into adipose tissue [36, 37].

Some experimental studies have begun to link MNPs exposure more directly to markers of metabolic dysfunction. Rodent models have shown that exposure to low doses of polystyrene MPs increases susceptibility to diet-induced metabolic dysfunction and liver disease [38]. These comorbid conditions are often correlated with obesity and insulin resistance [18, 19, 38]. Although the primary outcome in these reports was not obesity, the findings highlight how MNPs exposure can potentially worsen metabolic outcomes.

Mechanistic reviews of the impact of MNPs suggest a potential causal association with endocrine disruption. MNPs and related polymer/chemicals can interact with the endocrine systems, altering hormone production, signaling pathways, and metabolic regulation [36, 39]. These processes are fundamental to nutrient partitioning, appetite control, and energy balance [36, 39]. Endocrine disruption has been recognized as a contributing factor to obesity through its effects on adipogenesis and metabolic hormone regulation [39–41]. Although studies focused specifically on microplastic-induced endocrine disruption in humans are limited, the broader literature on plastic-associated endocrine disruptors (e.g., bisphenols and phthalates) consistently links these chemicals to obesity biomarkers and adiposity measures, particularly with early-life exposure [36, 39–42].

A study by Moon et al. [23] investigated the MNP effect on adipose tissue and adipocyte differentiation using a murine model. Following two weeks of daily oral exposure to fluorescent polystyrene MPs approximately 1.7–2.2 µm in size, these particles accumulated in the white fat tissues. This accumulation triggered signs of cellular aging, evidenced by increased activity of senescence markers (such as SA-β-galactosidase) and elevated expression of proteins associated with aging and DNA damage. At the same time, inflammatory markers including nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), and cluster of differentiation 68 (CD68) were higher in exposed tissues [23]. These findings suggest that MPs exposure may further promote inflammatory responses within adipose tissue. Similar effects were observed in human adipose-derived stem cells, where MPs were taken up by cells and increased both aging and inflammation signals. Importantly, these particles disrupted the ability of stem cells to differentiate into mature fat cells, as shown by reduced lipid droplet formation and lower levels of key adipogenic markers: peroxisome proliferator-activated receptor gamma (PPARγ), CCAAT/enhancer-binding protein alpha (C/EBPα), and Adiponectin during differentiation. Overall, the findings suggest that environmental MNPs can accelerate aging processes in fat cells, promote inflammation, and impair normal fat cell development. These outcomes raise concerns about long-term metabolic and health effects from widespread plastic exposure.

The evidence at present, however, is not sufficient to definitively link MNPs to obesity. This may be related to challenges in quantifying individual exposure and isolating MNP effects from other confounding lifestyle and genetic factors [10, 13]. Human toxicological and epidemiological studies are still in early stages, with available evidence often limited to surrogate endpoints or mechanistic biomarkers rather than clinical outcome data [10, 13]. These limitations reflect both the novelty of the research field and the technical challenges inherent in microplastic detection and exposure assessment. Although direct, large-scale human evidence linking MNPs exposure to obesity is not yet available, the convergence of mechanistic, animal, and microbiome evidence forms a compelling, biologically plausible framework.

Disruptions in the gut microbiota, propagation of inflammation and oxidative stress, interaction with metabolism-disrupting chemicals, and synergistic effects with dietary factors all point towards an association with pathways by which MNPs could increase obesity risk [3, 15, 36]. Further well-designed human studies are critically needed to clarify these relationships and quantify the true public health impact of MNPs exposure on obesity.

MNPs have become widespread environmental contaminants with potential impacts across biological systems. Emerging research suggests that MNPs may also be an underrecognized pathogenic contributor to obesity and metabolic dysfunction. These tiny particles can reach the gastrointestinal tract, where they interact with gut microbiota, disrupt microbial balance, and induce low-grade inflammation [9, 15]. These adverse effects may contribute to weight gain, insulin resistance, and altered lipid metabolism. Chronic exposure to MNPs may therefore subtly influence energy homeostasis, creating a hidden metabolic burden that compounds traditional risk factors such as diet, physical inactivity, and genetic predisposition.

Given the potential impact of MNPs on metabolic health, minimizing exposure has become a critical component of obesity prevention strategies (Figure 3). Although several exposure-reduction strategies appear biologically and environmentally reasonable, direct evidence demonstrating that these interventions reduce obesity risk or metabolic disease outcomes in humans remains limited. This challenge cannot be addressed through a single measure. It requires a coordinated, multi-pronged approach to protect populations from a largely invisible but increasingly significant contributor to obesity.

Future research examining MNPs as potential contributors to obesity must urgently shift from isolated laboratory findings toward integrated, real‑world human studies. To date, investigations in cell cultures and animals suggest that MNPs and the chemicals they carry can influence energy balance, fat cell growth, immune responses, and metabolic disturbance, potentially linking plastic exposure with obesity risk, but these early results are far from definitive and require further evaluation.

For example, plastic particles under 10 µm can infiltrate cells and may trigger oxidative stress and disruption in fatty acid metabolism, hinting at mechanisms that could encourage fat accumulation and weight gain in exposed organisms [3]. However, the doses, exposure routes, and biological relevance of such findings require grounding in real‑world human exposure data. It is a gap that has left regulators and scientists without clear exposure-response relationships or safe limits. In addition, publication bias toward positive findings may influence the current literature, while studies reporting negative or null results may be underrepresented. Additionally, reverse causality should be considered in human observational studies, as obesity itself may influence MNP absorption, distribution, retention, or gastrointestinal handling.

Therefore, one crucial direction is establishing rigorous and detailed metabolic profiling to determine the threshold amounts and identifying other patient-specific factors as well as associated demographics to better identify causality links to increases in body mass index, insulin resistance, or dyslipidemia. Additionally, research must prioritize the development of highly sensitive and contamination‑controlled analytical methods capable of identifying and quantifying MNPs within human tissues and biological fluids.

Current challenges in detection have led to debates about whether certain reported findings, such as the presence of MNPs in organs like the brain, might be artifacts of poor controls and methodological limitations, highlighting the need for robust methodologies before biological effects can be reliably interpreted. Another important limitation is that many studies do not fully characterize MNP properties such as particle shape, surface characteristics, or chemical composition, which may influence biological effects and toxicity.

Importantly, current methods for detecting and quantifying MNPs in human tissues remain technically challenging and may be vulnerable to contamination and false-positive results. Thermal methods such as pyrolysis-gas chromatography-mass spectrometry (Py-GC-MS) require caution, as tissue-derived compounds may produce signals overlapping with certain polymers. Therefore, studies reporting systemic MNP distribution should be interpreted cautiously, particularly when contamination controls and validation methods are not clearly described [63].

Moreover, coupled with exposure assessment, mechanistic work in both in vitro and in vivo models should be designed to mimic real human exposure more closely, including the effects of chronic low‑dose ingestion typical of daily life, rather than relying solely on high, artificial doses. These studies should dissect whether effects stem from the physical particles themselves, the chemical additives and adsorbed pollutants they carry, or a combination of both, since many plastic additives such as phthalates and bisphenols are known metabolism disruptors independent of the plastic matrix [33].

Another area of investigation is the evaluation of MNPs’ interaction with the gut microbiome, a critical regulator of metabolism and obesity. Systematic reviews indicate that MNP exposure can lead to microbial dysbiosis, impaired short‑chain fatty acid production, and immune pathway modulation, all of which are proven to cause metabolic syndrome and chronic inflammation. Future research must integrate approaches to determine whether specific microbial shifts precede metabolic disruption and obesity phenotypes, and if interventions that restore microbiome balance might mitigate these effects. This work could also explore whether certain dietary patterns or microbiota compositions confer resilience against MNP-induced metabolic dysregulation. Additionally, specific interventions directed towards MNP-associated dysbiosis, which may be more specifically associated with obesity, are a mitigation strategy that needs to be evaluated.

Furthermore, understanding NPs specifically is essential because their smaller size may allow different biodistribution, cellular uptake, and potentially novel biological effects compared with MPs. There are extremely limited, almost none, studies that examine how these particles interact with intestinal barriers and systemic tissues under realistic exposure scenarios, and whether they alter insulin signaling, adipogenesis, or energy homeostasis in ways relevant to human obesity. These studies would benefit from using advanced imaging and tracing techniques to observe particle translocation and localization in tissues without contamination.

Interdisciplinary collaborations should aim to translate scientific insights into public health policy and prevention strategies. This includes modelling population‑level impacts of MNPs exposure on obesity trends, identifying effective exposure reduction measures, and evaluating whether modifying plastic use, waste management, and food packaging can yield measurable health benefits. Additionally, a shift toward standardized methodologies, human‑relevant exposure assessments, microbiome integration, and mechanistic clarity will be crucial for turning suggestive early findings into clear answers about whether MNPs contribute to the global obesity burden.

Obesity is a multifactorial condition that is fundamentally associated with causal associations with diet, genetics, and physical inactivity. Clearly, however, there is increasing identification of environmental influences which may have a pathogenic role. Among these, MNPs have emerged as contaminants of growing concern. Their pervasive presence in the human food cycle ensures continuous, low-level human exposure. Although research in this field and correlating it with obesity remains relatively new, accumulating experimental and mechanistic evidence suggests that MNPs may interact with biological systems in ways that are relevant to metabolic health. Although MNPs cannot yet be identified as a definitive cause of obesity, the evidence supports their consideration as potential metabolic stressors. Addressing this emerging risk factor may prove essential in understanding and directing the best mitigation strategies for the global obesity epidemic.

Clinicians may also consider discussing practical strategies to reduce unnecessary plastic exposure, such as limiting the use of single-use plastic food containers and minimizing heating of food in plastic materials. In parallel, broader regulatory and public health efforts aimed at reducing environmental plastic contamination may help limit long-term population exposure to MNPs. Future research may also explore whether MNP detection in biological samples such as stool or adipose tissue could serve as a potential marker of exposure or metabolic risk.