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      The Link between the Metabolic Syndrome and Cancer

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          Abstract

          Since the incidence of the metabolic syndrome is on the rise in the western world, its coherence to cancer is becoming more apparent. In this review we discuss the different potential factors involved in the increase of cancer in the metabolic syndrome including obesity, dyslipidemia and Type 2 Diabetes Mellitus (T2DM) as well as inflammation and hypoxia. We especially focus on the insulin and IGF systems with their intracellular signaling cascades mediated by different receptor subtypes, and suggest that they may play major roles in this process. Understanding the mechanisms involved will be helpful in developing potential therapeutics.

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          Global prevalence of diabetes: estimates for the year 2000 and projections for 2030.

          Sarah E Wild, Gojka Roglic, Anders Green … (2004)
          The goal of this study was to estimate the prevalence of diabetes and the number of people of all ages with diabetes for years 2000 and 2030. Data on diabetes prevalence by age and sex from a limited number of countries were extrapolated to all 191 World Health Organization member states and applied to United Nations' population estimates for 2000 and 2030. Urban and rural populations were considered separately for developing countries. The prevalence of diabetes for all age-groups worldwide was estimated to be 2.8% in 2000 and 4.4% in 2030. The total number of people with diabetes is projected to rise from 171 million in 2000 to 366 million in 2030. The prevalence of diabetes is higher in men than women, but there are more women with diabetes than men. The urban population in developing countries is projected to double between 2000 and 2030. The most important demographic change to diabetes prevalence across the world appears to be the increase in the proportion of people >65 years of age. These findings indicate that the "diabetes epidemic" will continue even if levels of obesity remain constant. Given the increasing prevalence of obesity, it is likely that these figures provide an underestimate of future diabetes prevalence.
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            Regulation of mTOR function in response to hypoxia by REDD1 and the TSC1/TSC2 tumor suppressor complex.

            James Brugarolas, Kui Lei, Rebecca Hurley … (2004)
            Mammalian target of rapamycin (mTOR) is a central regulator of protein synthesis whose activity is modulated by a variety of signals. Energy depletion and hypoxia result in mTOR inhibition. While energy depletion inhibits mTOR through a process involving the activation of AMP-activated protein kinase (AMPK) by LKB1 and subsequent phosphorylation of TSC2, the mechanism of mTOR inhibition by hypoxia is not known. Here we show that mTOR inhibition by hypoxia requires the TSC1/TSC2 tumor suppressor complex and the hypoxia-inducible gene REDD1/RTP801. Disruption of the TSC1/TSC2 complex through loss of TSC1 or TSC2 blocks the effects of hypoxia on mTOR, as measured by changes in the mTOR targets S6K and 4E-BP1, and results in abnormal accumulation of Hypoxia-inducible factor (HIF). In contrast to energy depletion, mTOR inhibition by hypoxia does not require AMPK or LKB1. Down-regulation of mTOR activity by hypoxia requires de novo mRNA synthesis and correlates with increased expression of the hypoxia-inducible REDD1 gene. Disruption of REDD1 abrogates the hypoxia-induced inhibition of mTOR, and REDD1 overexpression is sufficient to down-regulate S6K phosphorylation in a TSC1/TSC2-dependent manner. Inhibition of mTOR function by hypoxia is likely to be important for tumor suppression as TSC2-deficient cells maintain abnormally high levels of cell proliferation under hypoxia.
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              Mice carrying null mutations of the genes encoding insulin-like growth factor I (Igf-1) and type 1 IGF receptor (Igf1r).

              Jeh-Ping Liu, Julie Baker, Archlbald Perkins … (1993)
              Newborn mice homozygous for a targeted disruption of insulin-like growth factor gene (Igf-1) exhibit a growth deficiency similar in severity to that previously observed in viable Igf-2 null mutants (60% of normal birthweight). Depending on genetic background, some of the Igf-1(-/-) dwarfs die shortly after birth, while others survive and reach adulthood. In contrast, null mutants for the Igf1r gene die invariably at birth of respiratory failure and exhibit a more severe growth deficiency (45% normal size). In addition to generalized organ hypoplasia in Igf1r(-/-) embryos, including the muscles, and developmental delays in ossification, deviations from normalcy were observed in the central nervous system and epidermis. Igf-1(-/-)/Igf1r(-/-) double mutants did not differ in phenotype from Igf1r(-/-) single mutants, while in Igf-2(-)/Igf1r(-/-) and Igf-1(-/-)/Igf-2(-) double mutants, which are phenotypically identical, the dwarfism was further exacerbated (30% normal size). The roles of the IGFs in mouse embryonic development, as revealed from the phenotypic differences between these mutants, are discussed.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Biol Sci
                Journal ID (publisher-id): ijbs
                Title: International Journal of Biological Sciences
                Publisher: Ivyspring International Publisher (Sydney )
                ISSN (Electronic): 1449-2288
                Publication date Collection: 2011
                Publication date (Electronic): 16 August 2011
                Volume: 7
                Issue: 7
                Pages: 1003-1015
                Affiliations
                Diabetes and Metabolism Clinical Research Center of Excellence, Legacy Heritage Clinical Research Institute at Rambam (LHCRIR), Haifa, Israel.
                Author notes
                ✉ Corresponding author: Derek LeRoith, M.D., Ph.D., Director, Diabetes and Metabolism Clinical Research Center of Excellence, Legacy Heritage Clinical Research Institute at Rambam (LHCRIR). Tel: 972-4-854-1260. d_leroith@ 123456rambam.health.gov.il

                Conflict of Interests: The authors have declared that no conflict of interest exists.

                Article
                Publisher ID: ijbsv07p1003
                DOI: 10.7150/ijbs.7.1003
                PMC ID: 3164150
                PubMed ID: 21912508
                SO-VID: 13e36962-bc91-4123-9e39-3d617a001ab8
                Copyright © © Ivyspring International Publisher. This is an open-access article distributed under the terms of the Creative Commons License (http://creativecommons.org/licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited.
                History
                Date received : 16 June 2011
                Date accepted : 24 July 2011
                Categories
                Subject: Review

                ScienceOpen disciplines: Life sciences
                Keywords: metabolic syndrome,cancer
                Data availability:
                ScienceOpen disciplines: Life sciences
                Keywords: metabolic syndrome, cancer

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