# PET microplastics induce lipotoxicity in the porcine pancreas **Authors:** Karol Mierzejewski, Aleksandra Kurzyńska, Monika Golubska, Robert Stryiński, Ismena Gałęcka, Jarosław Całka, Paula Borrajo, Manuel Pazos, Mónica Carrera, Iwona Bogacka PMC · DOI: 10.1186/s12864-025-12507-8 · BMC Genomics · 2026-01-07 ## TL;DR This study shows that PET microplastics can cause lipotoxic stress and affect pancreatic function in pigs, potentially leading to metabolic issues. ## Contribution The study identifies a novel pathway linking PET microplastics to lipotoxicity and pancreatic dysfunction using proteomic analysis in pigs. ## Key findings - PET microplastics altered protein abundance in a dose-dependent manner, affecting fatty acid biosynthesis and lipid peroxidation. - High doses of PET microplastics increased free fatty acids and impaired pancreatic exocrine function. - The findings suggest a link between microplastics exposure and metabolic disturbances via oxidative stress. ## Abstract Microplastics are a relatively new discovered environmental hazard that can contribute to the disruption of many physiological processes in the organism. There is evidence that they affect the physiology of the pancreas, but research in this area remains limited. Therefore, the aim of the study was to determine the effects of PET microplastics on the global proteomic profile of the pancreas using LC–MS/MS analysis, with the pig as a model organism. The pigs were treated either with a low (0.1 g/day) or a high dose (1 g/day) of PET microplastics for four weeks. The analysis revealed that PET microplastics affected protein abundance in a dose-dependent manner – the low dose altered the abundance of 7 proteins, while the high dose – 17. The differentially regulated proteins were involved in fatty acid biosynthesis (FASN, KAS), lipid peroxidation (CBR1) and digestive enzyme production (trypsinogen). Complementary colorimetric assays confirmed a significant increase in free fatty acids under the influence of a high dose of PET microplastics. Taken together, these results indicate that PET microplastics may affect oxidative status, induce lipotoxic stress and impair pancreatic exocrine function, suggesting a novel pathway through which microplastics may cause metabolic disturbances. The online version contains supplementary material available at 10.1186/s12864-025-12507-8. ## Linked entities - **Genes:** FASN (fatty acid synthase) [NCBI Gene 2194], KAS (hypothetical protein) [NCBI Gene 20228121], CBR1 (carbonyl reductase 1) [NCBI Gene 873] - **Proteins:** prss1 (serine protease 1) - **Species:** Sus scrofa (taxon 9823) ## Full-text entities - **Genes:** OXSM (3-oxoacyl-ACP synthase, mitochondrial) [NCBI Gene 102162360], TXN (thioredoxin) [NCBI Gene 397581] {aka TRX1}, HYOU1 (hypoxia up-regulated 1) [NCBI Gene 100516870] {aka HYOU1_tv1}, GCG (glucagon) [NCBI Gene 397595] {aka GLP-1}, SERBP1 (SERPINE1 mRNA binding protein 1) [NCBI Gene 100518613], RPL5 (ribosomal protein L5) [NCBI Gene 100135671], PRDX5 (peroxiredoxin 5) [NCBI Gene 397273], TXNRD1 (thioredoxin reductase 1) [NCBI Gene 396681] {aka TRXR1}, GP2 (glycoprotein 2) [NCBI Gene 100303610], FASN (fatty acid synthase) [NCBI Gene 397561], GAPDH (glyceraldehyde-3-phosphate dehydrogenase) [NCBI Gene 396823] {aka GAPD}, CBR1 (carbonyl reductase 1) [NCBI Gene 397143] {aka PG-9-KR}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, BSDC1 (BSD domain containing 1) [NCBI Gene 100620186], ANXA11 (annexin A11) [NCBI Gene 100156481], LOC100625049 (isopentenyl-diphosphate Delta-isomerase 1) [NCBI Gene 100625049] {aka IDI1}, OLA1 (Obg like ATPase 1) [NCBI Gene 100155803], RPL23A (ribosomal protein L23a) [NCBI Gene 100514795], LDHB (lactate dehydrogenase B) [NCBI Gene 100621540] {aka LDH-B, LDH-H}, GNB2 (G protein subunit beta 2) [NCBI Gene 100516546], INS (insulin) [NCBI Gene 397415] - **Diseases:** hyperglycemia (MESH:D006943), DRPs (MESH:D012734), beta-cell dysfunction (MESH:D007340), mitochondrial damage (MESH:D028361), cytotoxicity (MESH:D064420), type 2 diabetes (MESH:D003924), cancers (MESH:D009369), exocrine insufficiency (MESH:D010188), fibrosis (MESH:D005355), death (MESH:D003643), diabetes (MESH:D003920), insulin resistance (MESH:D007333), metabolic disturbances (MESH:D024821), HD (MESH:D008228), T1D (MESH:D003922), AP (MESH:D010195), pancreatic carcinogenesis (MESH:D063646), inflammation (MESH:D007249), metabolic disease (MESH:D008659) - **Chemicals:** tocopherolquinone (MESH:C002421), PVC (MESH:D011143), propanoate (MESH:D011422), pyruvate (MESH:D019289), stearate (MESH:D013228), Glucose (MESH:D005947), singlet oxygen (MESH:D026082), nitrogen (MESH:D009584), fatty acid (MESH:D005227), lipid (MESH:D008055), malonyl-CoA (MESH:D008316), carboxylic acid (MESH:D002264), FFA (MESH:D005230), PET (MESH:D011093), 4-HNE (-), atropine (MESH:D001285), carbohydrate (MESH:D002241), MPs (MESH:D000080545), C18:0 (MESH:C031183), polyunsaturated fatty acid (MESH:D005231), polymers (MESH:D011108), polystyrene (MESH:D011137), acetone (MESH:D000096), oxoacid (MESH:D007651), C (MESH:D002244), hydroxyl radicals (MESH:D017665), NADP (MESH:D009249), H2O2 (MESH:D006861), palmitic acid (MESH:D019308), folate (MESH:D005492), sodium pentobarbital (MESH:D010424), palmitate (MESH:D010168), xylazine (MESH:D014991), acetyl-CoA (MESH:D000105), NAD (MESH:D009243), PBS (MESH:D007854), quinones (MESH:D011809) - **Species:** Sus scrofa (pig, species) [taxon 9823], Homo sapiens (human, species) [taxon 9606] - **Cell lines:** ES306031/1 — Homo sapiens (Human), Ewing sarcoma, Cancer cell line (CVCL_1198) ## Full text _Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12870336/full.md ## Figures 3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12870336/full.md ## References 4 references — full list in the complete paper: https://tomesphere.com/paper/PMC12870336/full.md --- Source: https://tomesphere.com/paper/PMC12870336