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Insulin Resistance and Cancer Risk: An Overview of the Pathogenetic Mechanisms

Insulin resistance is common in individuals with obesity or type 2 diabetes (T2D), in which circulating insulin levels are frequently increased. Recent epidemiological and clinical evidence points to a link between insulin resistance and cancer. The mechanisms for this association are unknown, but h...

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Autores principales: Arcidiacono, Biagio, Iiritano, Stefania, Nocera, Aurora, Possidente, Katiuscia, Nevolo, Maria T., Ventura, Valeria, Foti, Daniela, Chiefari, Eusebio, Brunetti, Antonio
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3372318/
https://www.ncbi.nlm.nih.gov/pubmed/22701472
http://dx.doi.org/10.1155/2012/789174
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author Arcidiacono, Biagio
Iiritano, Stefania
Nocera, Aurora
Possidente, Katiuscia
Nevolo, Maria T.
Ventura, Valeria
Foti, Daniela
Chiefari, Eusebio
Brunetti, Antonio
author_facet Arcidiacono, Biagio
Iiritano, Stefania
Nocera, Aurora
Possidente, Katiuscia
Nevolo, Maria T.
Ventura, Valeria
Foti, Daniela
Chiefari, Eusebio
Brunetti, Antonio
author_sort Arcidiacono, Biagio
collection PubMed
description Insulin resistance is common in individuals with obesity or type 2 diabetes (T2D), in which circulating insulin levels are frequently increased. Recent epidemiological and clinical evidence points to a link between insulin resistance and cancer. The mechanisms for this association are unknown, but hyperinsulinaemia (a hallmark of insulin resistance) and the increase in bioavailable insulin-like growth factor I (IGF-I) appear to have a role in tumor initiation and progression in insulin-resistant patients. Insulin and IGF-I inhibit the hepatic synthesis of sex-hormone binding globulin (SHBG), whereas both hormones stimulate the ovarian synthesis of sex steroids, whose effects, in breast epithelium and endometrium, can promote cellular proliferation and inhibit apoptosis. Furthermore, an increased risk of cancer among insulin-resistant patients can be due to overproduction of reactive oxygen species (ROS) that can damage DNA contributing to mutagenesis and carcinogenesis. On the other hand, it is possible that the abundance of inflammatory cells in adipose tissue of obese and diabetic patients may promote systemic inflammation which can result in a protumorigenic environment. Here, we summarize recent progress on insulin resistance and cancer, focusing on various implicated mechanisms that have been described recently, and discuss how these mechanisms may contribute to cancer initiation and progression.
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spelling pubmed-33723182012-06-14 Insulin Resistance and Cancer Risk: An Overview of the Pathogenetic Mechanisms Arcidiacono, Biagio Iiritano, Stefania Nocera, Aurora Possidente, Katiuscia Nevolo, Maria T. Ventura, Valeria Foti, Daniela Chiefari, Eusebio Brunetti, Antonio Exp Diabetes Res Review Article Insulin resistance is common in individuals with obesity or type 2 diabetes (T2D), in which circulating insulin levels are frequently increased. Recent epidemiological and clinical evidence points to a link between insulin resistance and cancer. The mechanisms for this association are unknown, but hyperinsulinaemia (a hallmark of insulin resistance) and the increase in bioavailable insulin-like growth factor I (IGF-I) appear to have a role in tumor initiation and progression in insulin-resistant patients. Insulin and IGF-I inhibit the hepatic synthesis of sex-hormone binding globulin (SHBG), whereas both hormones stimulate the ovarian synthesis of sex steroids, whose effects, in breast epithelium and endometrium, can promote cellular proliferation and inhibit apoptosis. Furthermore, an increased risk of cancer among insulin-resistant patients can be due to overproduction of reactive oxygen species (ROS) that can damage DNA contributing to mutagenesis and carcinogenesis. On the other hand, it is possible that the abundance of inflammatory cells in adipose tissue of obese and diabetic patients may promote systemic inflammation which can result in a protumorigenic environment. Here, we summarize recent progress on insulin resistance and cancer, focusing on various implicated mechanisms that have been described recently, and discuss how these mechanisms may contribute to cancer initiation and progression. Hindawi Publishing Corporation 2012 2012-06-04 /pmc/articles/PMC3372318/ /pubmed/22701472 http://dx.doi.org/10.1155/2012/789174 Text en Copyright © 2012 Biagio Arcidiacono et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Arcidiacono, Biagio
Iiritano, Stefania
Nocera, Aurora
Possidente, Katiuscia
Nevolo, Maria T.
Ventura, Valeria
Foti, Daniela
Chiefari, Eusebio
Brunetti, Antonio
Insulin Resistance and Cancer Risk: An Overview of the Pathogenetic Mechanisms
title Insulin Resistance and Cancer Risk: An Overview of the Pathogenetic Mechanisms
title_full Insulin Resistance and Cancer Risk: An Overview of the Pathogenetic Mechanisms
title_fullStr Insulin Resistance and Cancer Risk: An Overview of the Pathogenetic Mechanisms
title_full_unstemmed Insulin Resistance and Cancer Risk: An Overview of the Pathogenetic Mechanisms
title_short Insulin Resistance and Cancer Risk: An Overview of the Pathogenetic Mechanisms
title_sort insulin resistance and cancer risk: an overview of the pathogenetic mechanisms
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3372318/
https://www.ncbi.nlm.nih.gov/pubmed/22701472
http://dx.doi.org/10.1155/2012/789174
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