Insulin Resistance and Cancer Risk: An Overview of the Pathogenetic Mechanisms
Autor: | Daniela Foti, Katiuscia Possidente, Aurora Nocera, Antonio Brunetti, Eusebio Chiefari, Maria T. Nevolo, Valeria Ventura, Biagio Arcidiacono, Stefania Iiritano |
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Jazyk: | angličtina |
Rok vydání: | 2012 |
Předmět: |
Risk
medicine.medical_specialty lcsh:Internal medicine lcsh:Specialties of internal medicine Endocrinology Diabetes and Metabolism medicine.medical_treatment Adipose tissue lcsh:Medicine Apoptosis Type 2 diabetes Tumor initiation Review Article Biology medicine.disease_cause Models Biological lcsh:Diseases of the endocrine glands. Clinical endocrinology Insulin resistance lcsh:RC581-951 Diabetes mellitus Internal medicine Neoplasms Sex Hormone-Binding Globulin medicine Animals Humans Obesity Insulin-Like Growth Factor I lcsh:RC31-1245 Cell Proliferation lcsh:RC648-665 Insulin Ovary lcsh:R Cancer General Medicine medicine.disease Gene Expression Regulation Neoplastic Endocrinology Diabetes Mellitus Type 2 Female Steroids Insulin Resistance Carcinogenesis Reactive Oxygen Species DNA Damage |
Zdroj: | Experimental Diabetes Research, Vol 2012 (2012) Experimental Diabetes Research |
ISSN: | 1687-5303 1687-5214 |
Popis: | 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. |
Databáze: | OpenAIRE |
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