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营养、胰岛素、胰岛素样生长因子与癌症。

Nutrition, insulin, insulin-like growth factors and cancer.

作者信息

Giovannucci E

机构信息

Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA.

出版信息

Horm Metab Res. 2003 Nov-Dec;35(11-12):694-704. doi: 10.1055/s-2004-814147.

Abstract

The incidence of colon, pancreatic, and kidney cancers, as well as aggressive prostate cancer in men, and breast and endometrial cancer in women is invariably high in Western countries. Nutritional and related factors have been typically implicated. This review presents a model integrating nutrition, insulin and IGF-1 physiology ("bioactive" IGF-1), and carcinogenesis based on the following: (1) insulin and the IGF-1 axis function in an integrated fashion to promote cell growth and survival; (2) chronic exposure to these growth properties enhances carcinogenesis; (3) factors that influence bioactive IGF-1 will affect cancer risk. The model presented here summarizes the data that chronic exposure to high levels of insulin and IGF-1 may mediate many of the risk factors for some cancers that are high in Western populations. This hypothesis may help explain some of the epidemiologic patterns observed for these cancers, both from a cross-national perspective and within populations. Of particular importance is that some of relevant factors are modifiable through nutritional and lifestyle interventions. Out of a variety of perspectives presented, nutritional manipulation through the insulin pathway may be more feasible than attempting to influence total IGF-1 concentrations, which are determined largely by growth hormone. Further study is required to test these conclusions.

摘要

在西方国家,结肠癌、胰腺癌、肾癌的发病率始终居高不下,男性侵袭性前列腺癌以及女性乳腺癌和子宫内膜癌的发病率也同样如此。营养及相关因素通常被认为与此有关。本综述基于以下内容提出了一个整合营养、胰岛素和IGF-1生理学(“生物活性”IGF-1)以及致癌作用的模型:(1)胰岛素和IGF-1轴以整合的方式发挥作用,促进细胞生长和存活;(2)长期暴露于这些生长特性会增强致癌作用;(3)影响生物活性IGF-1的因素将影响癌症风险。此处提出的模型总结了相关数据,即长期暴露于高水平的胰岛素和IGF-1可能介导了西方人群中一些高发癌症的许多风险因素。这一假设可能有助于从跨国角度以及在人群内部解释这些癌症所观察到的一些流行病学模式。特别重要的是,一些相关因素可通过营养和生活方式干预加以改变。在提出的各种观点中,通过胰岛素途径进行营养调控可能比试图影响主要由生长激素决定的总IGF-1浓度更为可行。需要进一步研究来验证这些结论。

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