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      Recent Insights into Insulin-Like Growth Factor Binding Protein 2 Transcriptional Regulation

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          Abstract

          Insulin-like growth factor binding proteins (IGFBPs) are major regulators of insulin-like growth factor bioavailability and activity in metabolic signaling. Seven IGFBP family isoforms have been identified. Recent studies have shown that IGFBPs play a pivotal role in metabolic signaling and disease, including the pathogenesis of obesity, diabetes, and cancer. Although many studies have documented the various roles played by IGFBPs, transcriptional regulation of IGFBPs is not well understood. In this review, we focus on the regulatory mechanisms of IGFBP gene expression, and we summarize the findings of transcription factor activity in the IGFBP promoter region.

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          Obesity and cancer risk: the role of the insulin-IGF axis.

          Allan Flyvbjerg, Jan Frystyk, Andrew G. Renehan (2006)
          Accumulating epidemiological evidence shows that being either overweight or obese, in other words having excess body weight (EBW), is associated with an increased risk of several, common, adult cancers. The molecular mechanisms that underlie these associations are not understood fully, but insulin resistance is likely to be important. The insulin-cancer hypothesis postulates that chronic hyperinsulinemia is associated with decreased concentrations of insulin-like growth factor binding protein1 (IGFBP-1) and IGFBP-2, leading to increased availability of IGF-I and concomitant changes in the cellular environment that favor tumor formation. However, the situation is likely to be more complex because hyperinsulinemia is also associated with alterations in related molecular systems (e.g. sex steroids and adipocytokines). As the prevalence of EBW increases to epidemic proportions, untangling the links between EBW and the insulin-IGF axis and its wider molecular interactions will become increasingly important in the development of preventive strategies.
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            Insulin-like growth factor-1 deficiency and metabolic syndrome

            G. A. Aguirre, J. Rodríguez De Ita, R. de la Garza … (2016)
            Consistent evidence associates IGF-1 deficiency and metabolic syndrome. In this review, we will focus on the metabolic effects of IGF-1, the concept of metabolic syndrome and its clinical manifestations (impaired lipid profile, insulin resistance, increased glucose levels, obesity, and cardiovascular disease), discussing whether IGF-1 replacement therapy could be a beneficial strategy for these patients. The search plan was made in Medline for Pubmed with the following mesh terms: IGF-1 and “metabolism, carbohydrate, lipids, proteins, amino acids, metabolic syndrome, cardiovascular disease, diabetes” between the years 1963–2015. The search includes animal and human protocols. In this review we discuss the relevant actions of IGF-1 on metabolism and the implication of IGF-1 deficiency in the establishment of metabolic syndrome. Multiple studies (in vitro and in vivo) demonstrate the association between IGF-1 deficit and deregulated lipid metabolism, cardiovascular disease, diabetes, and an altered metabolic profile of diabetic patients. Based on the available data we propose IGF-1 as a key hormone in the pathophysiology of metabolic syndrome; due to its implications in the metabolism of carbohydrates and lipids. Previous data demonstrates how IGF-1 can be an effective option in the treatment of this worldwide increasing condition. It has to distinguished that the replacement therapy should be only undertaken to restore the physiological levels, never to exceed physiological ranges.
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              Reciprocal positive regulation of hypoxia-inducible factor 1alpha and insulin-like growth factor 2.

              Janet B Pak, N Gopalakrishna Iyer, D Feldser … (1999)
              Hypoxia-inducible factor 1 (HIF-1) activates transcription of genes encoding glucose transporters, glycolytic enzymes, vascular endothelial growth factor, and other proteins involved in O2 homeostasis and tumor progression. The expression and transcriptional activity of the HIF-1alpha subunit is regulated by the cellular O2 concentration. We demonstrate that insulin, insulin-like growth factor (IGF)-1, and IGF-2 induce expression of HIF-1alpha, which is required for expression of genes encoding IGF-2, IGF-binding protein (IGFBP)-2 and IGFBP-3. These data provide a novel mechanism by which HIF-1alpha overexpression may occur in tumor cells and contribute to an autocrine growth factor loop.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Endocrinol Metab (Seoul)
                Journal ID (iso-abbrev): Endocrinol Metab (Seoul)
                Journal ID (publisher-id): ENM
                Title: Endocrinology and Metabolism
                Publisher: Korean Endocrine Society
                ISSN (Print): 2093-596X
                ISSN (Electronic): 2093-5978
                Publication date (Print): March 2017
                Publication date (Electronic): 19 January 2017
                Volume: 32
                Issue: 1
                Pages: 11-17
                Affiliations
                [1 ]Department of Microbiology, Kyungpook National University School of Medicine, Daegu, Korea.
                [2 ]Department of Physiology, Keimyung University School of Medicine, Daegu, Korea.
                Author notes
                Corresponding author: Seung-Soon Im. Department of Physiology, Keimyung University School of Medicine, 1095 Dalgubeol-daero, Dalseo-gu, Daegu 42601, Korea. Tel: +82-53-580-3863, Fax: +82-53-580-3795, ssim73@ 123456kmu.ac.kr
                Author information
                http://orcid.org/0000-0001-8679-446X
                http://orcid.org/0000-0001-7568-3211
                http://orcid.org/0000-0002-2743-2108
                Article
                DOI: 10.3803/EnM.2017.32.1.11
                PMC ID: 5368109
                PubMed ID: 28116872
                SO-VID: 19fc6aa4-dbfd-4f5b-81b4-b0a0d3ae1d51
                Copyright © Copyright © 2017 Korean Endocrine Society
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 18 November 2016
                Date revision received : 13 December 2016
                Date accepted : 20 December 2016
                Funding
                Funded by: National Research Foundation of Korea, CrossRef http://dx.doi.org/10.13039/501100003725;
                Award ID: NRF-2013R1A1A1006606
                Award ID: 2015R1D1A1A01057610
                Categories
                Subject: Review Article

                Keywords: insulin-like growth factor binding protein 2,transcriptional regulation,metabolic diseases,liver
                Data availability:
                Keywords: insulin-like growth factor binding protein 2, transcriptional regulation, metabolic diseases, liver

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