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Çevresel Kirleticilerin Metabolik Sendrom Üzerine Etkilerinin Balıklarda Modellenmesi

Year 2025, Volume: 5 Issue: 2, 53 - 63, 13.10.2025
https://doi.org/10.59838/etoxec.1745448

Abstract

Metabolik sendrom; abdominal obezite, insülin direnci, hipertansiyon ve dislipidemi gibi birden fazla metabolik bozukluğun birlikte görüldüğü karmaşık ve çok faktörlü bir hastalık tablosudur. Günümüzde bu sendromun yalnızca genetik ve yaşam tarzına bağlı etmenlerle değil, aynı zamanda kimyasallarla da tetiklenebileceği giderek daha net biçimde anlaşılmaktadır. Kalıcı organik kirleticiler, endokrin bozucular, pestisitler ve ağır metaller metabolik düzenleyici yolaklar üzerinde bozucu etkiler yaratabilmektedir. Metabolik sendrom analizinin sistematik ilişkisini anlamada model organizmalar kritik öneme sahip olmaktadır. Bu çalışma, kimyasalların etkilerini gözlemlemek için sıklıkla seçilen sucul organizmalar olan balıklar üzerinde çevresel kirleticilerin metabolik sendrom faktörlerine etkilerinin modellerini sunacaktır. Balıkların model olarak kullanıldığı uygulamalar sonucunda, çeşitli kimyasallara maruz bırakılan bireylerde diyabet, obezite, dislipidemi ve potansiyel olarak hipertansiyonun biyokimyasal ve fizyopatolojik modelleri sağlanmıştır. Özellikle zebra balığı (Danio rerio), insanla yüksek oranda genetik ve metabolik benzerlik göstermesi, şeffaf embriyo yapısı ve kısa nesil süresi gibi olumlu özellikleri nedeniyle bilimsel incelemelerde tercih edilen bir model organizma görevi almaktadır. Bununla birlikte, balıkların poikilotermik yapısı, farklı metabolik yanıt dağılımı ve insanla tam olarak uyumlu olmayan bazı genetik özellikleri, bu modellemenin translasyonel kullanımında kısıtlamalar oluşturmaktadır. Gelecekte, bu tür uygulamaların olası sonuçlarının daha sağlıklı anlaşılabilmesi için balık modellerinden elde edilen kayıtlı modeller ve insan sayısal sistemleriyle bütüncül biçimde değerlendirilmesini ortaya koyacaktır.

References

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  • K. Benchoula et al., “The promise of zebrafish as a model of metabolic syndrome,” Exp Anim, vol. 68, no. 4, pp. 407–416, 2019.
  • M. D. DeBoer, S. L. Filipp, M. Sims, S. K. Musani, and M. J. Gurka, “Risk of ischemic stroke increases over the spectrum of metabolic syndrome severity,” Stroke, vol. 51, no. 8, pp. 2548–2552, 2020.
  • G. M. Reaven, “Banting lecture 1988. Role of insulin resistance in human disease.,” Diabetes, vol. 37, no. 12, pp. 1595–1607, 1988.
  • R. M. Sargis and R. A. Simmons, “Environmental neglect: endocrine disruptors as underappreciated but potentially modifiable diabetes risk factors,” Diabetologia, vol. 62, pp. 1811–1822, 2019.
  • A. Kortenkamp, M. Faust, M. Scholze, and T. Backhaus, “Low-level exposure to multiple chemicals: reason for human health concerns?,” Environ Health Perspect, vol. 115, no. Suppl 1, pp. 106–114, 2007.
  • H. K. Lee and Y. K. Pak, “Persistent organic pollutants, mitochondrial dysfunction, and metabolic syndrome,” Mitochondrial Dysfunction Caused by Drugs and Environmental Toxicants, pp. 691–707, 2018, doi: 10.1002/9781119329725.ch44.
  • H. E. Esmer Duruel, “Sucul Ekosistemlerdeki Antropojenik Kirliliğin Değerlendirilmesi,” in Biyoloji Bilimlerinde Yeni Güncel Konular I, A. Bilgili, Ed., Ankara: Bidge Yayınları, 2024, ch. 1, pp. 6–28. doi: 10.70269/10.70269/2965252294.
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  • J. J. Heindel, R. Newbold, and T. T. Schug, “Endocrine disruptors and obesity,” Nat Rev Endocrinol, vol. 11, no. 11, pp. 653–661, 2015.
  • E. Haverinen, M. F. Fernandez, V. Mustieles, and H. Tolonen, “Metabolic syndrome and endocrine disrupting chemicals: an overview of exposure and health effects,” Int J Environ Res Public Health, vol. 18, no. 24, p. 13047, 2021.
  • J. Legler et al., “Obesity, diabetes, and associated costs of exposure to endocrine-disrupting chemicals in the European Union,” J Clin Endocrinol Metab, vol. 100, no. 4, pp. 1278–1288, 2015.
  • Y. Tang, G. Qin, N. Qian, X. Zeng, R. Li, and K. P. Lai, “Bisphenol A and its replacement chemicals as endocrine disruptors and obesogens,” Environmental Chemistry and Ecotoxicology, 2025.
  • N. E. De Long and A. C. Holloway, “Early-life chemical exposures and risk of metabolic syndrome,” Diabetes Metab Syndr Obes, pp. 101–109, 2017.
  • M. Dalamaga et al., “The role of endocrine disruptors bisphenols and phthalates in obesity: current evidence, perspectives and controversies,” Int J Mol Sci, vol. 25, no. 1, p. 675, 2024.
  • W. J. Meggs and K. L. Brewer, “Weight gain associated with chronic exposure to chlorpyrifos in rats,” Journal of Medical Toxicology, vol. 3, pp. 89–93, 2007.
  • S. A. Mansour and A.-T. H. Mossa, “Lipid peroxidation and oxidative stress in rat erythrocytes induced by chlorpyrifos and the protective effect of zinc,” Pestic Biochem Physiol, vol. 93, no. 1, pp. 34–39, 2009.
  • F. Kayhan, G. Kaymak, H. E. E. Duruel, and Ş. T. Kızılkaya, “Biyolojik araştırmalarda zebra balığının (Danio rerio Hamilton, 1822) kullanılması ve önemi,” Gaziosmanpaşa Bilimsel Araştırma Dergisi, vol. 7, no. 2, pp. 38–45, 2018.
  • L. Zang, Y. Shimada, Y. Nishimura, T. Tanaka, and N. Nishimura, “Repeated blood collection for blood tests in adult zebrafish,” J Vis Exp, no. 102, p. 53272, 2015.
  • R. V Intine, A. S. Olsen, and M. P. Sarras Jr, “A zebrafish model of diabetes mellitus and metabolic memory,” J Vis Exp, no. 72, p. 50232, 2013.
  • L. Zang, L. A. Maddison, and W. Chen, “Zebrafish as a model for obesity and diabetes,” Front Cell Dev Biol, vol. 6, p. 91, 2018.
  • C. Yashaswini, N. S. Kiran, and A. Chatterjee, “Zebrafish navigating the metabolic maze: insights into human disease–assets, challenges and future implications,” J Diabetes Metab Disord, vol. 24, no. 1, pp. 1–19, 2025.
  • R. L. Beer, M. J. Parsons, and M. Rovira, “Centroacinar cells: At the center of pancreas regeneration,” Dev Biol, vol. 413, no. 1, pp. 8–15, 2016.
  • F. Tonon and G. Grassi, “Zebrafish as an experimental model for human disease,” 2023, MDPI.
  • B. Ghaddar et al., “Impaired brain homeostasis and neurogenesis in diet-induced overweight zebrafish: a preventive role from A. borbonica extract,” Sci Rep, vol. 10, no. 1, p. 14496, 2020.
  • K. R. Rao, N. Lal, and N. V Giridharan, “Genetic & epigenetic approach to human obesity,” Indian Journal of Medical Research, vol. 140, no. 5, pp. 589–603, 2014.
  • K. E. Claflin and J. L. Grobe, “Control of energy balance by the brain renin-angiotensin system,” Curr Hypertens Rep, vol. 17, pp. 1–7, 2015.
  • M. Türkoğlu et al., “The potential effect mechanism of high-fat and high-carbohydrate diet-induced obesity on anxiety and offspring of zebrafish,” Eating and Weight Disorders-Studies on Anorexia, Bulimia and Obesity, pp. 1–15, 2022.
  • S. Tian et al., “New insights into bisphenols induced obesity in zebrafish (Danio rerio): Activation of cannabinoid receptor CB1,” J Hazard Mater, vol. 418, p. 126100, 2021.
  • W. Wang et al., “Bisphenol S induces obesogenic effects through deregulating lipid metabolism in zebrafish (Danio rerio) larvae,” Chemosphere, vol. 199, pp. 286–296, 2018.
  • J.-S. Lim, D.-H. Lee, and D. R. Jacobs Jr, “Association of brominated flame retardants with diabetes and metabolic syndrome in the US population, 2003–2004,” Diabetes Care, vol. 31, no. 9, pp. 1802–1807, 2008.
  • S. Shibata and T. Fujita, “24 Renin Angiotensin Aldosterone System,” Hypertension: A Companion to Braunwald’s Heart Disease E-Book, p. 230, 2017.
  • S. A. Rider, L. J. Mullins, R. F. Verdon, C. A. MacRae, and J. J. Mullins, “Renin expression in developing zebrafish is associated with angiogenesis and requires the Notch pathway and endothelium,” American Journal of Physiology-Renal Physiology, vol. 309, no. 6, pp. F531–F539, 2015.
  • B. Joshi, G. Wagh, H. Kaur, and C. Patra, “Zebrafish model to study angiotensin ii-mediated pathophysiology,” Biology (Basel), vol. 10, no. 11, p. 1177, 2021.
  • A. J. Berberich and R. A. Hegele, “A modern approach to dyslipidemia,” Endocr Rev, vol. 43, no. 4, pp. 611–653, 2022.
  • M. Hölttä-Vuori et al., “Zebrafish: gaining popularity in lipid research,” Biochemical Journal, vol. 429, no. 2, pp. 235–242, 2010.
  • E. J. Flynn, C. M. Trent, and J. F. Rawls, “Ontogeny and nutritional control of adipogenesis in zebrafish (Danio rerio),” J Lipid Res, vol. 50, no. 8, pp. 1641–1652, 2009.
  • A. Seth, D. L. Stemple, and I. Barroso, “The emerging use of zebrafish to model metabolic disease,” Dis Model Mech, vol. 6, no. 5, pp. 1080–1088, 2013.
  • B. Ghaddar and N. Diotel, “Zebrafish: a new promise to study the impact of metabolic disorders on the brain,” Int J Mol Sci, vol. 23, no. 10, p. 5372, 2022.
  • J. P. Meador, F. C. Sommers, K. A. Cooper, and G. Yanagida, “Tributyltin and the obesogen metabolic syndrome in a salmonid,” Environ Res, vol. 111, no. 1, pp. 50–56, 2011.
  • W. Wang et al., “Bisphenol S exposure accelerates the progression of atherosclerosis in zebrafish embryo-larvae,” J Hazard Mater, vol. 426, p. 128042, 2022.
  • R. S. Angom and N. M. R. Nakka, “Zebrafish as a model for cardiovascular and metabolic disease: the future of precision medicine,” Biomedicines, vol. 12, no. 3, p. 693, 2024.
  • M. Michel, P. S. Page-McCaw, W. Chen, and R. D. Cone, “Leptin signaling regulates glucose homeostasis, but not adipostasis, in the zebrafish,” Proceedings of the National Academy of Sciences, vol. 113, no. 11, pp. 3084–3089, 2016.
  • G. Cakan-Akdogan, A. M. Aftab, M. C. Cinar, K. A. Abdelhalim, and O. Konu, “Zebrafish as a model for drug induced liver injury: State of the art and beyond,” Exploration of Digestive Diseases, vol. 2, no. 2, pp. 44–55, 2023.

Modeling the Effects of Environmental Pollutants on Metabolic Syndrome in Fish

Year 2025, Volume: 5 Issue: 2, 53 - 63, 13.10.2025
https://doi.org/10.59838/etoxec.1745448

Abstract

Metabolic syndrome is a complex and multifactorial disease characterized by the coexistence of multiple metabolic disorders such as abdominal obesity, insulin resistance, hypertension, and dyslipidemia. Today, it is becoming increasingly clear that this syndrome can be triggered not only by genetic and lifestyle factors, but also by chemicals. Persistent organic pollutants, endocrine disruptors, pesticides, and heavy metals can have disruptive effects on metabolic regulatory pathways. Model organisms are critical for understanding the systematic relevance of metabolic syndrome analysis. This study will present models of the effects of environmental pollutants on metabolic syndrome factors in fish, which are aquatic organisms commonly selected to observe the effects of chemicals. As a result of applications using fish as models, biochemical and pathophysiological models of diabetes, obesity, dyslipidemia, and potentially hypertension have been provided in individuals exposed to various chemicals. In particular, zebrafish (Danio rerio) are preferred as model organisms in scientific studies due to their high degree of genetic and metabolic similarity to humans, transparent embryo structure, and short generation time. However, the poikilothermic nature of fish, their different metabolic response distribution, and certain genetic characteristics that are not fully compatible with humans impose limitations on the translational use of this model. In the future, it will demonstrate that recorded models obtained from fish models and human numerical systems should be evaluated holistically in order to better understand the possible consequences of such applications.

References

  • M. G. Saklayen, “The global epidemic of the metabolic syndrome,” Curr Hypertens Rep, vol. 20, no. 2, pp. 1–8, 2018.
  • K. Benchoula et al., “The promise of zebrafish as a model of metabolic syndrome,” Exp Anim, vol. 68, no. 4, pp. 407–416, 2019.
  • M. D. DeBoer, S. L. Filipp, M. Sims, S. K. Musani, and M. J. Gurka, “Risk of ischemic stroke increases over the spectrum of metabolic syndrome severity,” Stroke, vol. 51, no. 8, pp. 2548–2552, 2020.
  • G. M. Reaven, “Banting lecture 1988. Role of insulin resistance in human disease.,” Diabetes, vol. 37, no. 12, pp. 1595–1607, 1988.
  • R. M. Sargis and R. A. Simmons, “Environmental neglect: endocrine disruptors as underappreciated but potentially modifiable diabetes risk factors,” Diabetologia, vol. 62, pp. 1811–1822, 2019.
  • A. Kortenkamp, M. Faust, M. Scholze, and T. Backhaus, “Low-level exposure to multiple chemicals: reason for human health concerns?,” Environ Health Perspect, vol. 115, no. Suppl 1, pp. 106–114, 2007.
  • H. K. Lee and Y. K. Pak, “Persistent organic pollutants, mitochondrial dysfunction, and metabolic syndrome,” Mitochondrial Dysfunction Caused by Drugs and Environmental Toxicants, pp. 691–707, 2018, doi: 10.1002/9781119329725.ch44.
  • H. E. Esmer Duruel, “Sucul Ekosistemlerdeki Antropojenik Kirliliğin Değerlendirilmesi,” in Biyoloji Bilimlerinde Yeni Güncel Konular I, A. Bilgili, Ed., Ankara: Bidge Yayınları, 2024, ch. 1, pp. 6–28. doi: 10.70269/10.70269/2965252294.
  • Y. Lee, K. Kim, D. R. Jacobs Jr, and D. Lee, “Persistent organic pollutants in adipose tissue should be considered in obesity research,” Obesity Reviews, vol. 18, no. 2, pp. 129–139, 2017.
  • J. J. Heindel, R. Newbold, and T. T. Schug, “Endocrine disruptors and obesity,” Nat Rev Endocrinol, vol. 11, no. 11, pp. 653–661, 2015.
  • E. Haverinen, M. F. Fernandez, V. Mustieles, and H. Tolonen, “Metabolic syndrome and endocrine disrupting chemicals: an overview of exposure and health effects,” Int J Environ Res Public Health, vol. 18, no. 24, p. 13047, 2021.
  • J. Legler et al., “Obesity, diabetes, and associated costs of exposure to endocrine-disrupting chemicals in the European Union,” J Clin Endocrinol Metab, vol. 100, no. 4, pp. 1278–1288, 2015.
  • Y. Tang, G. Qin, N. Qian, X. Zeng, R. Li, and K. P. Lai, “Bisphenol A and its replacement chemicals as endocrine disruptors and obesogens,” Environmental Chemistry and Ecotoxicology, 2025.
  • N. E. De Long and A. C. Holloway, “Early-life chemical exposures and risk of metabolic syndrome,” Diabetes Metab Syndr Obes, pp. 101–109, 2017.
  • M. Dalamaga et al., “The role of endocrine disruptors bisphenols and phthalates in obesity: current evidence, perspectives and controversies,” Int J Mol Sci, vol. 25, no. 1, p. 675, 2024.
  • W. J. Meggs and K. L. Brewer, “Weight gain associated with chronic exposure to chlorpyrifos in rats,” Journal of Medical Toxicology, vol. 3, pp. 89–93, 2007.
  • S. A. Mansour and A.-T. H. Mossa, “Lipid peroxidation and oxidative stress in rat erythrocytes induced by chlorpyrifos and the protective effect of zinc,” Pestic Biochem Physiol, vol. 93, no. 1, pp. 34–39, 2009.
  • F. Kayhan, G. Kaymak, H. E. E. Duruel, and Ş. T. Kızılkaya, “Biyolojik araştırmalarda zebra balığının (Danio rerio Hamilton, 1822) kullanılması ve önemi,” Gaziosmanpaşa Bilimsel Araştırma Dergisi, vol. 7, no. 2, pp. 38–45, 2018.
  • L. Zang, Y. Shimada, Y. Nishimura, T. Tanaka, and N. Nishimura, “Repeated blood collection for blood tests in adult zebrafish,” J Vis Exp, no. 102, p. 53272, 2015.
  • R. V Intine, A. S. Olsen, and M. P. Sarras Jr, “A zebrafish model of diabetes mellitus and metabolic memory,” J Vis Exp, no. 72, p. 50232, 2013.
  • L. Zang, L. A. Maddison, and W. Chen, “Zebrafish as a model for obesity and diabetes,” Front Cell Dev Biol, vol. 6, p. 91, 2018.
  • C. Yashaswini, N. S. Kiran, and A. Chatterjee, “Zebrafish navigating the metabolic maze: insights into human disease–assets, challenges and future implications,” J Diabetes Metab Disord, vol. 24, no. 1, pp. 1–19, 2025.
  • R. L. Beer, M. J. Parsons, and M. Rovira, “Centroacinar cells: At the center of pancreas regeneration,” Dev Biol, vol. 413, no. 1, pp. 8–15, 2016.
  • F. Tonon and G. Grassi, “Zebrafish as an experimental model for human disease,” 2023, MDPI.
  • B. Ghaddar et al., “Impaired brain homeostasis and neurogenesis in diet-induced overweight zebrafish: a preventive role from A. borbonica extract,” Sci Rep, vol. 10, no. 1, p. 14496, 2020.
  • K. R. Rao, N. Lal, and N. V Giridharan, “Genetic & epigenetic approach to human obesity,” Indian Journal of Medical Research, vol. 140, no. 5, pp. 589–603, 2014.
  • K. E. Claflin and J. L. Grobe, “Control of energy balance by the brain renin-angiotensin system,” Curr Hypertens Rep, vol. 17, pp. 1–7, 2015.
  • M. Türkoğlu et al., “The potential effect mechanism of high-fat and high-carbohydrate diet-induced obesity on anxiety and offspring of zebrafish,” Eating and Weight Disorders-Studies on Anorexia, Bulimia and Obesity, pp. 1–15, 2022.
  • S. Tian et al., “New insights into bisphenols induced obesity in zebrafish (Danio rerio): Activation of cannabinoid receptor CB1,” J Hazard Mater, vol. 418, p. 126100, 2021.
  • W. Wang et al., “Bisphenol S induces obesogenic effects through deregulating lipid metabolism in zebrafish (Danio rerio) larvae,” Chemosphere, vol. 199, pp. 286–296, 2018.
  • J.-S. Lim, D.-H. Lee, and D. R. Jacobs Jr, “Association of brominated flame retardants with diabetes and metabolic syndrome in the US population, 2003–2004,” Diabetes Care, vol. 31, no. 9, pp. 1802–1807, 2008.
  • S. Shibata and T. Fujita, “24 Renin Angiotensin Aldosterone System,” Hypertension: A Companion to Braunwald’s Heart Disease E-Book, p. 230, 2017.
  • S. A. Rider, L. J. Mullins, R. F. Verdon, C. A. MacRae, and J. J. Mullins, “Renin expression in developing zebrafish is associated with angiogenesis and requires the Notch pathway and endothelium,” American Journal of Physiology-Renal Physiology, vol. 309, no. 6, pp. F531–F539, 2015.
  • B. Joshi, G. Wagh, H. Kaur, and C. Patra, “Zebrafish model to study angiotensin ii-mediated pathophysiology,” Biology (Basel), vol. 10, no. 11, p. 1177, 2021.
  • A. J. Berberich and R. A. Hegele, “A modern approach to dyslipidemia,” Endocr Rev, vol. 43, no. 4, pp. 611–653, 2022.
  • M. Hölttä-Vuori et al., “Zebrafish: gaining popularity in lipid research,” Biochemical Journal, vol. 429, no. 2, pp. 235–242, 2010.
  • E. J. Flynn, C. M. Trent, and J. F. Rawls, “Ontogeny and nutritional control of adipogenesis in zebrafish (Danio rerio),” J Lipid Res, vol. 50, no. 8, pp. 1641–1652, 2009.
  • A. Seth, D. L. Stemple, and I. Barroso, “The emerging use of zebrafish to model metabolic disease,” Dis Model Mech, vol. 6, no. 5, pp. 1080–1088, 2013.
  • B. Ghaddar and N. Diotel, “Zebrafish: a new promise to study the impact of metabolic disorders on the brain,” Int J Mol Sci, vol. 23, no. 10, p. 5372, 2022.
  • J. P. Meador, F. C. Sommers, K. A. Cooper, and G. Yanagida, “Tributyltin and the obesogen metabolic syndrome in a salmonid,” Environ Res, vol. 111, no. 1, pp. 50–56, 2011.
  • W. Wang et al., “Bisphenol S exposure accelerates the progression of atherosclerosis in zebrafish embryo-larvae,” J Hazard Mater, vol. 426, p. 128042, 2022.
  • R. S. Angom and N. M. R. Nakka, “Zebrafish as a model for cardiovascular and metabolic disease: the future of precision medicine,” Biomedicines, vol. 12, no. 3, p. 693, 2024.
  • M. Michel, P. S. Page-McCaw, W. Chen, and R. D. Cone, “Leptin signaling regulates glucose homeostasis, but not adipostasis, in the zebrafish,” Proceedings of the National Academy of Sciences, vol. 113, no. 11, pp. 3084–3089, 2016.
  • G. Cakan-Akdogan, A. M. Aftab, M. C. Cinar, K. A. Abdelhalim, and O. Konu, “Zebrafish as a model for drug induced liver injury: State of the art and beyond,” Exploration of Digestive Diseases, vol. 2, no. 2, pp. 44–55, 2023.
There are 44 citations in total.

Details

Primary Language English
Subjects Hydrobiology, Aquatic Toxicology
Journal Section Reviews
Authors

Harika Eylül Esmer Duruel 0000-0002-0792-2062

Publication Date October 13, 2025
Submission Date July 18, 2025
Acceptance Date September 15, 2025
Published in Issue Year 2025 Volume: 5 Issue: 2

Cite

IEEE H. E. Esmer Duruel, “Modeling the Effects of Environmental Pollutants on Metabolic Syndrome in Fish”, Etoxec, vol. 5, no. 2, pp. 53–63, 2025, doi: 10.59838/etoxec.1745448.