Mechanisms of obesogens and their impact on adipose tissue, hormones, and inflammation

Taiwo Ogunjobi, C. Omiyale, Tolulope Gbayisomore, O. Olofin, P. Nneji, Damilola Onikeku, Moses Oluwole, Somtochukwu Ezeano, Dayo Soleye, Dasola Fadipe, Samson Fakojo, Tobi Sulaiman, Rufus Ajayi
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Abstract

The complex interactions of genetic, environmental, and behavioral factors that contribute to obesity, a pervasive global health issue, continue to be a severe concern for people all over the world. This manuscript examines the field of obesogen research, seeking to understand the mechanisms by which certain environmental chemicals contribute to the development of obesity. We explore the obesogenic effects by focusing on pathways such as inflammation, hormone interference, and the activation of peroxisome proliferator-activated receptors (PPARs). The text focuses on the significance of PPAR isoforms, especially PPARγ, and how they play a role in adipose tissue growth. We examine how obesogens such as tributyltin (TBT) and bisphenol A (BPA) influence these receptors. Additionally, we examined the impact of obesogens on hormonal regulation, including disruptions to leptin and adiponectin, and investigated the intricate relationship between chronic inflammation and obesity. In the methodology of our study, we utilized a systematic search to identify peer-reviewed articles of relevance. This search spanned various model systems, including in vitro, in vivo, and epidemiological studies, providing insights into the distinct advantages and limitations associated with each. Epigenetic modifications and the influence of obesogens on the development of adipose tissue, metabolism, and appetite control further enrich our understanding of this complex field. Finally, we assess the role of endocrine disruptors in amplifying the risk of obesity, emphasizing the heightened susceptibility during crucial developmental periods. This comprehensive review aims to contribute to the ongoing discourse surrounding obesogens, paving the way for targeted interventions and a more profound comprehension of the global obesity epidemic.
肥胖原的作用机制及其对脂肪组织、激素和炎症的影响
肥胖症是一个普遍的全球性健康问题,其遗传、环境和行为因素之间复杂的相互作用继续引起全世界人民的严重关切。本手稿探讨了肥胖源研究领域,试图了解某些环境化学物质导致肥胖的机制。我们将重点放在炎症、激素干扰和过氧化物酶体增殖激活受体(PPARs)激活等途径上,探讨肥胖的致病作用。文中重点介绍了 PPAR 异构体(尤其是 PPARγ)的重要性,以及它们如何在脂肪组织生长中发挥作用。我们研究了三丁基锡(TBT)和双酚 A(BPA)等肥胖原如何影响这些受体。此外,我们还研究了肥胖原对激素调节的影响,包括对瘦素和脂肪连通素的干扰,并调查了慢性炎症与肥胖之间错综复杂的关系。在研究方法上,我们采用了系统搜索的方法来确定同行评审的相关文章。这种搜索跨越了各种模型系统,包括体外、体内和流行病学研究,从而深入了解了每种模型系统的独特优势和局限性。表观遗传修饰和肥胖原对脂肪组织发育、新陈代谢和食欲控制的影响进一步丰富了我们对这一复杂领域的理解。最后,我们评估了内分泌干扰物在增加肥胖风险方面的作用,强调了在关键的发育时期易患肥胖症的程度。这篇全面的综述旨在为目前围绕肥胖源的讨论做出贡献,为有针对性的干预措施和更深刻地理解全球肥胖流行病铺平道路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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