Symposium 3: Obesity-related cancers Visceral obesity, metabolic syndrome, insulin resistance and cancer
Symposium 3: Obesity-related cancers Visceral obesity, metabolic syndrome, insulin resistance and cancer
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DOI：
10.1017/s002966511100320x
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发表时间：
2012-02-01
影响因子：
7
通讯作者：
Reynolds, John V.
中科院分区：
文献类型：
--
作者：
Doyle, Suzanne L.;Donohoe, Claire L.;Reynolds, John V.
本文提出了内脏肥胖症和代谢综合征(MetSyn)与致癌相关的新证据。大量强有力的流行病学研究已经清楚地确定了肥胖和癌症之间的联系。现在的研究重点是内脏脂肪组织在癌症发生中的作用；因为它被认为是一种重要的代谢组织，它分泌的因子会系统性地改变免疫、代谢和内分泌环境。过多的内脏脂肪组织会引起一种慢性全身炎症状态，伴随着相关的胰岛素抵抗和代谢障碍，统称为MetSyn。前瞻性队列研究表明，内脏肥胖、MetSyn与乳腺癌、结直肠癌和食管腺癌风险增加之间存在关联。此外，内脏肥胖症和MetSyn与肿瘤进展加快和生存率降低有关。内脏肥胖和MetSyn被认为促进肿瘤发生的机制是多方面的。这些变化包括脂肪因子分泌和细胞信号通路的改变。此外，高胰岛素血症、随后的胰岛素抵抗和胰岛素样生长因子-1轴的刺激都与内脏肥胖和促进肿瘤进展有关。此外，内脏脂肪组织中丰富的炎症细胞，包括巨噬细胞和T细胞，会造成全身炎症和促肿瘤环境。目前的研究清楚地表明，内脏过度肥胖及其相关的代谢异常在某些癌症类型的发病机制中起着核心作用。需要进一步的研究来阐明确切的作用机制，并确定潜在的干预目标。
This paper presents emerging evidence linking visceral adiposity and the metabolic syndrome (MetSyn) with carcinogenesis. The link between obesity and cancer has been clearly identified in a multitude of robust epidemiological studies. Research is now focusing on the role of visceral adipose tissue in carcinogenesis; as it is recognised as an important metabolic tissue that secretes factors that systemically alter the immunological, metabolic and endocrine milieu. Excess visceral adipose tissue gives rise to a state of chronic systemic inflammation with associated insulin resistance and dysmetabolism, collectively known as the MetSyn. Prospective cohort studies have shown associations between visceral adiposity, the MetSyn and increased risk of breast cancer, colorectal cancer and oesophageal adenocarcinoma. Furthermore, visceral adiposity and the MetSyn have been associated with increased tumour progression and reduced survival. The mechanisms by which visceral adiposity and the MetSyn are thought to promote tumorigenesis are manifold. These include alterations in adipokine secretion and cell signalling pathways. In addition, hyperinsulinaemia, subsequent insulin resistance and stimulation of the insulin-like growth factor-1 axis have all been linked with visceral adiposity and promote tumour progression. Furthermore, the abundance of inflammatory cells in visceral adipose tissue, including macrophages and T-cells, create systemic inflammation and a pro-tumorigenic environment. It is clear from current research that excess visceral adiposity and associated dysmetabolism play a central role in the pathogenesis of certain cancer types. Further research is required to elucidate the exact mechanisms at play and identify potential targets for intervention.