Department of Surgery, Trinity Centre for Health Sciences, Trinity College Dublin/St James' Hospital, Dublin 8, Republic of Ireland.
Proc Nutr Soc. 2012 Feb;71(1):181-9. doi: 10.1017/S002966511100320X. Epub 2011 Nov 3.
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.
这篇论文提出了新的证据，将内脏脂肪过多和代谢综合征（MetSyn）与致癌作用联系起来。肥胖与癌症之间的联系在大量强有力的流行病学研究中已经得到明确证实。目前的研究重点是内脏脂肪组织在致癌作用中的作用；因为它被认为是一种重要的代谢组织，会分泌系统性改变免疫、代谢和内分泌环境的因子。过多的内脏脂肪会导致慢性全身炎症，伴有胰岛素抵抗和代谢紊乱，统称为 MetSyn。前瞻性队列研究表明，内脏脂肪过多、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，内脏脂肪过多和 MetSyn 与肿瘤进展增加和生存率降低有关。内脏脂肪过多和 MetSyn 被认为可促进肿瘤发生的机制有多种。这些包括脂联素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 轴的刺激都与内脏脂肪过多有关，并促进肿瘤进展。此外，内脏脂肪组织中炎症细胞的大量存在，包括巨噬细胞和 T 细胞，会导致全身炎症和促进肿瘤发生的环境。从目前的研究中可以清楚地看出，过多的内脏脂肪和相关的代谢紊乱在某些癌症类型的发病机制中起着核心作用。需要进一步研究阐明具体的作用机制，并确定潜在的干预靶点。
