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      Cardiovascular Risk Factors after Childhood Cancer Treatment Are Independent of the FTO Gene Polymorphism?

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          Abstract

          The study objective was to assess the prevalence of cardiovascular disease risk factors in patients treated for childhood cancer ( N = 101) and to determine the involvement of clinical (cancer type and therapy) and/or genetic ( FTO gene rs9939609 polymorphism) factors. Anthropometric features, laboratory findings, and standardized osteodensitometric indices (fat and lean mass) were considered. Overweight/obesity was found in 17.82% of the patients; however, central adiposity was found in as many as 42.5%. At least one abnormality in lipid metabolism was observed in 35.6%. Densitometry revealed elevated levels of fat mass in 44.55% of the patients. None of the parameters studied were associated with the FTO gene polymorphism. Standardized waist circumference was significantly higher in patients treated for leukemia than those treated for solid tumors ( p = 0.04). Our findings indicate a high rate of central adiposity among childhood cancer survivors, especially leukemia patients. The prevalence of risk factors of cardiovascular disease after anticancer therapy is not FTO gene polymorphism-dependent.

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          The obesity-associated FTO gene encodes a 2-oxoglutarate-dependent nucleic acid demethylase.

          Thomas Gerken, Christophe A J Girard, Yi-Chun Tung … (2007)
          Variants in the FTO (fat mass and obesity associated) gene are associated with increased body mass index in humans. Here, we show by bioinformatics analysis that FTO shares sequence motifs with Fe(II)- and 2-oxoglutarate-dependent oxygenases. We find that recombinant murine Fto catalyzes the Fe(II)- and 2OG-dependent demethylation of 3-methylthymine in single-stranded DNA, with concomitant production of succinate, formaldehyde, and carbon dioxide. Consistent with a potential role in nucleic acid demethylation, Fto localizes to the nucleus in transfected cells. Studies of wild-type mice indicate that Fto messenger RNA (mRNA) is most abundant in the brain, particularly in hypothalamic nuclei governing energy balance, and that Fto mRNA levels in the arcuate nucleus are regulated by feeding and fasting. Studies can now be directed toward determining the physiologically relevant FTO substrate and how nucleic acid methylation status is linked to increased fat mass.
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            Obesity in adult survivors of childhood acute lymphoblastic leukemia: a report from the Childhood Cancer Survivor Study.

            Annelien Mertens, Terry Vik, P D Inskip … (2003)
            To determine whether adult survivors (>or= 18 years of age) of childhood acute lymphoblastic leukemia (ALL) are at increased risk for obesity and to assess patient and treatment variables that influence risk. A retrospective cohort of participants of the Childhood Cancer Survivor Study was used to compare 1,765 adult survivors of childhood ALL to 2,565 adult siblings of childhood cancer survivors. Body-mass index (BMI; kilograms per square meter), calculated from self-reported heights and weights, was used to determine the prevalence of being overweight (BMI, 25-29.9) or obese (BMI >or= 30.0). Polytomous logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for being overweight or obese among ALL survivors relative to the sibling control group. The age- and race-adjusted OR for being obese in survivors treated with cranial radiation doses >or= 20 Gy in comparison with siblings was 2.59 for females (95% CI, 1.88 to 3.55; P or= 20 Gy (OR, 3.81; 95% CI, 2.34 to 5.99; P or= 20 Gy is associated with an increased prevalence of obesity, especially in females treated at a young age. It is imperative that healthcare professionals recognize this risk and develop strategies to enhance weight control and encourage longitudinal follow-up.
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              The FTO gene and measured food intake in children.

              C Llewellyn, Jane Wardle, Dan Sanderson … (2008)
              Polymorphisms in the obesity-associated gene, FTO, have been linked with sensitivity to satiety in children, indicating FTO may be influencing one of the regulatory drivers underlying food intake. In this study, we tested the hypothesis that food intake in a standard eating behaviour paradigm in which palatable food is offered under conditions of satiety would be associated with FTO genotype status, after controlling for differences in body mass index (BMI). Participants were 131 children aged 4-5 years, taking part in a behavioural study of food intake for whom DNA was available for genotyping. The phenotypic indicator of intake was the child's consumption of palatable food presented after having eaten a meal. We also assessed physical activity using parental reports of the child's enjoyment of active games, their level of activity relative to other children and a standard measure of fidgetiness. Associations between polymorphisms of the intronic FTO single nucleotide polymorphism (rs9939609) and behaviour (food intake and activity) were assessed by analysis of variance controlling for sex, age and BMI s.d. scores. The distribution of AA (homogenous for A allele), AT (heterogeneous T and A alleles) and TT (homogenous for T allele) genotypes was 18, 50 and 32%, respectively. As predicted, TT homozygotes ate significantly less than heterozygotes (P=0.03) or AA homozygotes (P=0.02). The effect was not diminished by controlling for BMI s.d. scores. There were no significant associations between FTO genotype and any marker of physical activity. We showed that children with two copies of the lower-risk FTO alleles ate less than those with one or two higher-risk alleles. We conclude that the T allele is protective against overeating by promoting responsiveness to internal signals of satiety.
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                Author and article information

                Contributors
                Małgorzata Sawicka-Żukowska:
                ORCID: http://orcid.org/0000-0002-5463-5656
                Journal
                Journal ID (nlm-ta): Int J Endocrinol
                Journal ID (iso-abbrev): Int J Endocrinol
                Journal ID (publisher-id): IJE
                Title: International Journal of Endocrinology
                Publisher: Hindawi
                ISSN (Print): 1687-8337
                ISSN (Electronic): 1687-8345
                Publication date Collection: 2018
                Publication date (Electronic): 20 February 2018
                Volume: 2018
                Electronic Location Identifier: 7495234
                Affiliations
                Department of Pediatric Oncology and Hematology, Medical University of Bialystok, Ul. Waszyngtona 17, 15-274 Bialystok, Poland
                Author notes

                Academic Editor: Andrea Tura

                Author information
                http://orcid.org/0000-0002-5463-5656
                http://orcid.org/0000-0003-0899-5930
                http://orcid.org/0000-0001-5437-7119
                Article
                DOI: 10.1155/2018/7495234
                PMC ID: 5838494
                SO-VID: cda44bf9-992f-4a5e-830c-a30752dbde68
                Copyright © Copyright © 2018 Małgorzata Sawicka-Żukowska et al.
                License:

                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.

                History
                Date received : 17 July 2017
                Date revision received : 5 December 2017
                Date accepted : 17 December 2017
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Endocrinology & Diabetes
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes

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