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      Body Adiposity Changes After Lifestyle Interventions in Children/Adolescents and the NYD-SP18 and TMEM18 Variants

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          Abstract

          Background

          This study was carried out to determine the relationship between the common TMEM-18 (rs4854344, G>T) and NYD-SP18 (rs6971091, G>A) gene variants and weight loss after lifestyle interventions (increased physical activity in conjunction with optimal dietary intake) in overweight/obese children/adolescents.

          Material/Methods

          We genotyped 684 unrelated, white, non-diabetic children (age 12.7±2.1 years, average BMI at baseline 30.66±4.80 kg/m 2). Anthropometric and biochemical examinations were performed before and after 4 weeks of an intensive lifestyle intervention.

          Results

          The mean weight loss achieved was 5.20±2.02 kg (P<0.001). NYDSP-18 AA homozygotes had significantly higher abdominal skinfold value before and after the intervention (both, P=0.001). No significant associations between BMI decrease and the NYD-SP18 and TMEM18 variants were found. Associations between all anthropometrical and biochemical changes and genes remained non-significant after data were adjusted for sex, age, and baseline values.

          Conclusions

          Decreased body weight in overweight/obese children is not significantly influenced by the NYD-SP18 rs6971091 or TMEM18 rs4854344 polymorphisms.

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          Most cited references23

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          Six new loci associated with body mass index highlight a neuronal influence on body weight regulation.

          Lachlan Coin, Joshua Randall, George Davey Smith (2009)
          Common variants at only two loci, FTO and MC4R, have been reproducibly associated with body mass index (BMI) in humans. To identify additional loci, we conducted meta-analysis of 15 genome-wide association studies for BMI (n > 32,000) and followed up top signals in 14 additional cohorts (n > 59,000). We strongly confirm FTO and MC4R and identify six additional loci (P < 5 x 10(-8)): TMEM18, KCTD15, GNPDA2, SH2B1, MTCH2 and NEGR1 (where a 45-kb deletion polymorphism is a candidate causal variant). Several of the likely causal genes are highly expressed or known to act in the central nervous system (CNS), emphasizing, as in rare monogenic forms of obesity, the role of the CNS in predisposition to obesity.
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            The role of obesity-associated loci identified in genome-wide association studies in the determination of pediatric BMI.

            Kai Wang, Edward Frackelton, Donald F Otieno … (2009)
            The prevalence of obesity in children and adults in the United States has increased dramatically over the past decade. Besides environmental factors, genetic factors are known to play an important role in the pathogenesis of obesity. A number of genetic determinants of adult BMI have already been established through genome-wide association (GWA) studies. In this study, we examined 25 single-nucleotide polymorphisms (SNPs) corresponding to 13 previously reported genomic loci in 6,078 children with measures of BMI. Fifteen of these SNPs yielded at least nominally significant association to BMI, representing nine different loci including INSIG2, FTO, MC4R, TMEM18, GNPDA2, NEGR1, BDNF, KCTD15, and 1q25. Other loci revealed no evidence for association, namely at MTCH2, SH2B1, 12q13, and 3q27. For the 15 associated variants, the genotype score explained 1.12% of the total variation for BMI z-score. We conclude that among 13 loci that have been reported to associate with adult BMI, at least nine also contribute to the determination of BMI in childhood as demonstrated by their associations in our pediatric cohort.
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              Obesity-associated geneTMEM18has a role in the central control of appetite and body weight regulation.

              Rachel Larder, M. F. Michelle Sim, Pawan Gulati … (2017)
              An intergenic region of human chromosome 2 (2p25.3) harbors genetic variants which are among those most strongly and reproducibly associated with obesity. The gene closest to these variants isTMEM18, although the molecular mechanisms mediating these effects remain entirely unknown.Tmem18expression in the murine hypothalamic paraventricular nucleus (PVN) was altered by changes in nutritional state. Germline loss ofTmem18in mice resulted in increased body weight, which was exacerbated by high fat diet and driven by increased food intake. Selective overexpression ofTmem18in the PVN of wild-type mice reduced food intake and also increased energy expenditure. We provide evidence that TMEM18 has four, not three, transmembrane domains and that it physically interacts with key components of the nuclear pore complex. Our data support the hypothesis thatTMEM18itself, acting within the central nervous system, is a plausible mediator of the impact of adjacent genetic variation on human adiposity.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Med Sci Monit
                Journal ID (iso-abbrev): Med. Sci. Monit
                Journal ID (publisher-id): Medical Science Monitor
                Title: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research
                Publisher: International Scientific Literature, Inc.
                ISSN (Print): 1234-1010
                ISSN (Electronic): 1643-3750
                Publication date Collection: 2018
                Publication date (Electronic): 20 October 2018
                Volume: 24
                Pages: 7493-7498
                Affiliations
                [1 ]3 rd Department of Medicine, 1 st Faculty of Medicine of Charles University and General University Hospital in Prague, Prague, Czech Republic
                [2 ]Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic
                [3 ]Dr. Filip’s Institute for Children, Poděbrady, Czech Republic
                Author notes
                Corresponding Author: Lukas Zlatohlavek, e-mail: lukas.zlatohlavek@ 123456lf1.cuni.cz
                [A]

                Study Design

                [B]

                Data Collection

                [C]

                Statistical Analysis

                [D]

                Data Interpretation

                [E]

                Manuscript Preparation

                [F]

                Literature Search

                [G]

                Funds Collection

                Article
                Publisher ID: 907180
                DOI: 10.12659/MSM.907180
                PMC ID: 6204654
                PubMed ID: 30341978
                SO-VID: fb1bdea5-b9e4-4f31-a8f4-78065a38023d
                Copyright © © Med Sci Monit, 2018
                License:

                This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International ( CC BY-NC-ND 4.0)

                History
                Date received : 18 September 2017
                Date accepted : 24 April 2018
                Categories
                Subject: Clinical Research

                Keywords: child,intervention studies,obesity,polymorphism, single nucleotide
                Data availability:
                Keywords: child, intervention studies, obesity, polymorphism, single nucleotide

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