Obesity, white adipose tissue and cancer.

Estel Solsona-Vilarrasa, Karen H Vousden
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Abstract

White adipose tissue (WAT) is crucial for whole-body energy homeostasis and plays an important role in metabolic and hormonal regulation. While healthy WAT undergoes controlled expansion and contraction to meet the body's requirements, dysfunctional WAT in conditions like obesity is characterized by excessive tissue expansion, alterations in lipid homeostasis, inflammation, hypoxia, and fibrosis. Obesity is strongly associated with an increased risk of numerous cancers, with obesity-induced WAT dysfunction influencing cancer development through various mechanisms involving both systemic and local interactions between adipose tissue and tumors. Unhealthy obese WAT affects circulating levels of free fatty acids and factors like leptin, adiponectin, and insulin, altering systemic lipid metabolism and inducing inflammation that supports tumor growth. Similar mechanisms are observed locally in an adipose-rich tumor microenvironment (TME), where WAT cells can also trigger extracellular matrix remodeling, thereby enhancing the TME's ability to promote tumor growth. Moreover, tumors reciprocally interact with WAT, creating a bidirectional communication that further enhances tumorigenesis. This review focuses on the complex interplay between obesity, WAT dysfunction, and primary tumor growth, highlighting potential targets for therapeutic intervention.

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肥胖、白色脂肪组织与癌症
白色脂肪组织(WAT)对全身能量平衡至关重要,并在新陈代谢和激素调节方面发挥着重要作用。健康的白脂肪组织会进行有控制的扩张和收缩,以满足身体的需要,而肥胖等情况下功能失调的白脂肪组织则表现为组织过度扩张、脂质平衡改变、炎症、缺氧和纤维化。肥胖与罹患多种癌症的风险增加密切相关,肥胖引起的脂肪组织功能失调会通过各种机制影响癌症的发展,这些机制涉及脂肪组织与肿瘤之间的全身和局部相互作用。不健康的肥胖脂肪组织会影响游离脂肪酸以及瘦素、脂肪连通素和胰岛素等因子的循环水平,从而改变全身脂质代谢并诱发支持肿瘤生长的炎症。在富含脂肪的肿瘤微环境(TME)中也能观察到类似的局部机制,肥胖症细胞还能引发细胞外基质重塑,从而增强 TME 促进肿瘤生长的能力。此外,肿瘤与 WAT 相互影响,形成双向交流,从而进一步促进肿瘤发生。本综述重点探讨了肥胖、WAT 功能障碍和原发性肿瘤生长之间复杂的相互作用,并强调了治疗干预的潜在靶点。
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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