Die wissenschaftlichen Grundlagen
DNA Analyse deiner Speichelprobe
Wir nutzen das derzeit fortschrittlichste Verfahren zur Genanalyse – das sogenannte Illumina Verfahren.
Welches Verfahren zur DNA-Analyse nutzen wir?
Dein DNA-Profil wird im Labor mithilfe modernster Analysetechnik ausgewertet. Dabei untersuchen wir gezielt Genmarker, die Einfluss auf Stoffwechsel, Nährstoffaufnahme und Regeneration haben.
Wir nutzen das Illumina-Verfahren des weltweit führenden Herstellers Illumina.
Der im Illumina Verfahren genutzte GSA-Chip wertet über 700.000 genetische Marker (SNPs) hocheffizient aus.
Wie funktioniert das Illumina-Verfahren?
Das Illumina-Verfahren, auch bekannt als Sequenzierung durch Synthese, ist eine Methode des Next-Generation-Sequencing (NGS) zur Bestimmung der DNA-Sequenz. Dabei wird die DNA zunächst in Fragmente zerlegt, die an eine Glasoberfläche (Flow Cell) gebunden werden. Anschließend werden durch Einsatz einer Brücken-PCR und von fluoreszierenden Nukleotiden in Echtzeit Millionen von DNA-Clustern parallel sequenziert.
Mit dieser Technologie kann eine große Zahl genetischer Marker (SNPs) akkurat, rasch und kosteneffizient ausgewertet werden.
Die Hauptschritte des Illumina-Verfahrens:
1. Probenvorbereitung (Library Preparation)
- Fragmentierung: Die zu analysierende DNA aus deiner Speichelprobe wird zunächst in viele kleine Stücke zerlegt.
- Adapter-Anbringung: An den Enden dieser DNA-Fragmente werden spezielle Adapter-Sequenzen angebracht. Diese dienen später als Bindestellen für die Festlegung an den Sequenzier-Fließzellen und für die PCR-Amplifikation.
2. Cluster-Generierung
- Bindung an Fließzelle: Die vorbereiteten DNA-Fragmente werden in eine sogenannte Fließzelle gegeben. Die Oberfläche dieser Zelle ist mit Oligonukleotiden (kurzen DNA-Sequenzen) beschichtet, die komplementär zu den Adaptern an den DNA-Fragmenten sind. Die DNA-Fragmente binden sich an diese Oligonukleotide.
- Brückenamplifikation: Enzyme vervielfältigen die DNA-Fragmente an Ort und Stelle, sodass auf der Fließzelle klonale Cluster entstehen. Jeder Cluster besteht aus Millionen identischer Kopien eines einzigen DNA-Fragments.
3. Sequenzierung durch Synthese (SBS)
- zyklische Anlagerung: In Zyklen werden der Fließzelle vier verschiedene Nukleotide (A, T, C, G) zugeführt. Jedes Nukleotid ist mit einem reversiblen Terminator und einem eindeutigen fluoreszierenden Farbstoff markiert.
- Farbmarkierungsdetektion: Wenn ein Nukleotid an den wachsenden DNA-Strang anlagert, wird das Fluoreszenzsignal dieses Nukleotids von einer Kamera erfasst.
- Terminator-Entfernung: Danach wird der Terminator chemisch entfernt, sodass der nächste Zyklus mit dem nächsten Nukleotid beginnen kann.
- Basisbestimmung: Dieser Prozess wiederholt sich, bis die gesamte Sequenz des Fragments erfasst ist. Aus den erfassten Fluoreszenzsignalen wird die Basenabfolge bestimmt.
4. Datenanalyse
- Rohdatenverarbeitung: Die aufgenommenen Bilddaten der Fluoreszenzsignale werden mithilfe spezieller Software in die Rohsequenzdaten umgewandelt.
- Alignment: Die erfassten Sequenzen (sogenannte Reads) werden mit einer Referenzgenom-Sequenz abgeglichen, um ihre ursprüngliche Position zu bestimmen.
- Ergebnisauswertung: Schließlich erfolgt die Interpretation der Daten, um genetische Variationen, wie Mutationen oder Genfusionen, zu identifizieren.
Vorteile des Illumina-Verfahrens
- Massiv parallele Sequenzierung: Ermöglicht die gleichzeitige Analyse von Millionen von DNA-Fragmenten, was einen hohen Datendurchsatz ermöglicht.
- Hohe Genauigkeit: Die Methode liefert sehr präzise Sequenzdaten.
- Breites Anwendungsspektrum: Illumina-Technologie wird für eine Vielzahl von Anwendungen eingesetzt, darunter die Sequenzierung ganzer Genome, Exome-Sequenzierung, Transkriptomik (RNA-Seq) und epigenetische Analysen.
Quellenverzeichnis der wissenschaftlichen Studien
Vitamin D
T. J. Wang ‚Common genetic determinants of vitamin D insufficiency: a genome-wide association study,‘ Lancet, vol. 376, n. 9736, pp. 180-188, 2010.
K. C. Simon, K. L. Munger, P. Kraft, D. J. Hunter, P. L. De Jager, A. Ascherio ‚Genetic predictors of 25-hydroxyvitamin D levels and risk of multiple sclerosis,‘ J. Neurol., vol. 258, n. 9, 1676-1682, 2011.
M. Enlund-Cerullo et al. ‚Genetic Variation of the Vitamin D Binding Protein Affects Vitamin D Status and Response to Supplementation in lnfants,‘ The Journal of Clinical Endocrinology & Metabolism, v. 104, n. 11, pp. 5483-5498, 2019.
Z. M. Lafi et al. ‚Association of rs7041 and rs4588 Polymorphisms of the Vitamin D Binding Protein and the rs10741657 Polymorphism of CYP2R1 with Vitamin D Status Among Jordanian Patients‘, Genet Test Mol Biomarkers, vol. 19, n. 11, pp. 629-636, 2015.
Hereditäre Fruktoseintoleranz
Ali M., Rellos P., Cox T. M. ‚Hereditary fructose intolerance,‘ Med Genet, 35(5):353-65, 1998
Coffee E. M., Tolan D. R. ‚Mutations in the promoter region of the aldolase B gene that cause hereditary fructose intolerance,‘ lnherit Metab Dis, 33(6):715-25, 2010
Santer et. al. ‚The spectrum of aldolase B (ALDOB) mutations and the prevalence of hereditary fructose intolerance in Central Europe,‘ Human Mutat, 25(6):594, 2005
Dazzo C., Tolan D. R. ‚Molecular evidence for compound heterozygosity in hereditary fructose intolerance,‘ Hum Genet, 46(6):1194-9, 1990
Hegde V. S., Sharman T. ‚Hereditary Fructose lntolerance,‘ StatPearls Publishing, 2022
Schrodi et al. ‚Prevalence estimation for monogenic autosomal recessive diseases using population-based genetic data,‘ Hum Genet, 134(6):659-69, 2015
Quintana et al. ‚Secondary disorders of glycosylation in inborn errors of fructose metabolism,‘ lnherit Metab Dis, 32 Suppl 1: S273-8, 2009
Glutenunverträglichkeit
Henderson KN, Tye-Din JA, Reid HH, Chen Z, Borg NA, Beissbarth T, Tatham A, Mannering Sl, Purcell AW, Dudek NL, van Heel DA, McCluskey J, Rossjohn J, Anderson RP. A structural and immunological basis for the role of human leukocyte antigen DQ8 in celiac disease. lmmunity. 2007 Jul;27(1):23-34.
Ahn R, Ding YC, Murray J, Fasano A, Green PH, Neuhausen SL, Garner C. Association analysis of the extended MHC region in celiac disease implicates multiple independent susceptibility loci. PLoS One. 2012;7(5):e36926. doi: 10.1371/journal.pone.0036926. Epub 2012 May 17.
Senapati S, Sood A, Midha V, Sood N, Sharma S, Kumar L, Thelma BK. Shared and unique common genetic determinants between pediatric and adult celiac disease. BMC Med Genomics. 2016 Jul 22;9(1):44. doi: 10.1186/s12920-016-0211-8. PMlD: 27449795; PMClD: PMC4957920
Romanos J. Genetics of celiac disease and its diagnostic value. Groningen: Faculty of Medical Sciences/UMCG; 2011
Sallese M, Lopetuso LR, Efthymakis K, Neri M. Beyond the HLA Genes in Gluten-Related Disorders. Front Nutr. 2020 Nov 12;7:575844.
Koskinen L, Romanos J, Kaukinen K, Mustalahti K, Korponay-Szabo l, Barisani D, Bardella MT, Ziberna F, Vatta S, Szeles G, Pocsai Z, Karell K, Haimila K, Adany R, Not T, Ventura A, Mäki M, Partanen J, Wijmenga C, Saavalainen P. Cost-effective HLA typing with tagging SNPs predicts celiac disease risk haplotypes in the Finnish, Hungarian, and ltalian populations. lmmunogenetics. 2009 Apr;61(4):247-56. doi: 10.1007/s00251-009-0361-3. Epub 2009 Mar 3.
Monsuur AJ, de Bakker Pl, Zhernakova A, Pinto D, Verduijn W, Romanos J, Auricchio R, Lopez A, van Heel DA, Crusius JB, Wijmenga C. Effective detection of human leukocyte antigen risk alleles in celiac disease using tag single nucleotide polymorphisms. PLoS One. 2008 May 28;3(5):e2270. doi: 10.1371/journal.pone.0002270. Erratum in: PLoS One. 2009;4(5)
Dubois PC et al. Multiple common variants for celiac disease influencing immune gene expression. Nat Genet. 2010 Apr;42(4):295-302.
Einfluss der mediterranen Ernährung auf das Lebensalter
S. Garcia-Calz6n et al. ‚Pro12Ala Polymorphism of the PPARy2 Gene lnteracts With a Mediterranean Diet to Prevent Telomere Shortening in the PREDlMED-NAVARRA Randomized Trial,‘ Circulation: Cardiovascular Genetics, vol. 8, pp. 91-99, 2014.
S. Davinelli et al. ‚The potential nutrigeroprotective role of Mediterranean diet and its functional components on telomere length dynamics,‘ Ageing Research Reviews, vol. 49, pp. 1-10, 2019.
M. Fit6 and V. Konstantinidou ‚Nutritional Genomics and the Mediterranean Diet’s Effects on Human Cardiovascular Health,‘ Nutrients, vol. 8, n. 4, pp. 218, 2016.
Kaffee und Koffein
N. Koonrungsesomboon, R. Khatsri, P. Wongchompoo and S. Teekachunhatean ‚The impact of genetic polymorphisms on CYP1A2 activity in humans: a systematic review and meta-analysis,‘ The Pharmacogenomics Journal vol. 18, pp. 760-768, 2018.
G. Nikrandt, J. Mikolajczyk-Stecyna, M. Mlodzik-Czyzewska and A. Chmurzynska ‚Functional
single-nucleotide polymorphism (rs762551) in CYP1A2 gene affects white coffee intake in healthy 20- to 40-year-old adults,‘ Nutr. Res., vol. 105, pp. 77-81, 2022.
E. M. Rodenburg et al. ‚CYP1A2 and coffee intake and the modifying effect of sex, age, and smoking,‘ Am. J. Clin. Nutr., vol. 96, n. 1, pp. 182-187, 2012.
E. Childs et al. ‚Association between ADORA2A and DRD2 Polymorphisms and Caffeine-lnduced Anxiety,‘ Neuropsychopharmacology, vol. 33, n. 12, pp. 2791-2800, 2008.
P. J. Rogers et al. ‚Association of the Anxiogenic and Alerting Effects of Caffeine with ADORA2A and ADORA1 Polymorphisms and Habitual Level of Caffeine Consumption,‘ Neuropsychopharmacology, vol. 35, n. 9, pp. 1973-1983, 2010.
Omega-3-6 Fettsäuren
S. Bokor et al. ‚Single nucleotide polymorphisms in the FADS gene cluster are associated with delta-5 and delta-6 desaturase activities estimated by serum fatty acid ratios,‘ J. Lipid Res., vol. 51, n. 8, pp. 2325-2333, 2010.
J. Dumont et al. ‚FADS1 Genetic Variability lnteracts with Dietary a-Linolenic Acid lntake to Affect Serum Non-HDL-Cholesterol Concentrations in European Adolescents,‘ The Journal of Nutrition, vol. 141, n. 7, pp. 1247-1253, 2011.
J. Juan et al. ‚Joint effects of fatty acid desaturase 1 polymorphisms and dietary polyunsaturated fatty acid intake on circulating fatty acid proportions,‘ Am. J. Clin. Nutr., vol. 107, n. 5, pp. 826-833, 2018.
A. AlSaleh et al. ‚Genetic predisposition scores for dyslipidaemia influence plasma lipid concentrations at baseline, but not the changes after controlled intake of n-3 polyunsaturated fatty acids,‘ Genes Nutr., vol. 9, n. 4, pp. 412, 2014.
R. N. Lemaitre ‚Genetic loci associated with plasma phospholipid n-3 fatty acids: a meta-analysis of genome-wide association studies from the CHARGE Consortium,‘ PLoS Genet., vol. 7, n. 7, pp. e1002193, 2011.
R. Y. Kwong et al. ‚Genetic profiling of fatty acid desaturase polymorphisms identifies patients who may benefit from high-dose omega-3 fatty acids in cardiac remodeling after acute myocardial infarction-Post-hoc analysis from the OMEGA-REMODEL randomized controlled trial,‘ PLos One, vol. 14, n. 9, e0222061, 2019.
X. Chen et al. ‚Effects of the rs3834458 Single Nucleotide Polymorphism in FADS2 on Levels of n-3 Long-chain Polyunsaturated Fatty Acids: A Meta-analysis,‘ Prostaglandins Leukot. Essent. Fatty Acids, vol. 150, pp. 1-6, 2019.
Ernährungstyp
J. Antonio et al. ‚Assessment of the FTO gene polymorphisms (rs1421085, rs17817449 and rs9939609) in exercise-trained men and women: the effects of a 4-week hypocaloric diet,‘ J. lnt. Soc. Sports. Nutr., vol. 16, n. 1, pp. 36, 2019.
M. Pichler et al. ‚Association of the melanocortin-4 receptor V103l polymorphism with dietary intake in severely obese persons,‘ Am. J. Clin. Nutr., vol. 88, n. 3, pp.797-800, 2008.
S. L. Park et al. ‚Association of the FTO Obesity Risk Variant rs8050136 With Percentage of Energy lntake From Fat in Multiple Racial/Ethnic Populations,‘ Am. J. Epidemiol., vol. 178, n. 5, pp. 780-790, 2013.
T. Drabsch, J. Gatzemeier, L. Pfadenhauer, H. Hauner and C. Holzapfel ‚Associations between Single Nucleotide Polymorphisms and Total Energy, Carbohydrate, and Fat lntakes: A Systematic Review,‘ Adv. Nutr., vol. 9, n.4, pp. 425-453, 2018.
S. K. Vasan, F. Karpe, H. F. Gu, K. Brismar, C. H. Fall, E. lngelsson, T. Fall ‚FTO genetic variants and risk of obesity and type 2 diabetes: A meta-analysis of 28,394 lndians,‘ Obesity, vol. 22, n. 3, pp. 964-970, 2014.
Veranlagung zu Übergewicht
J. R. Speakman ‚The ‚Fat Mass and Obesity Related‘ (FTO) gene: Mechanisms of lmpact on Obesity and Energy BalanceBalance,‘ Curr. Obes. Rep., vol 4, n. 1, pp. 73-91, 2015.
N. Genet ‚Six new loci associated with body mass index highlight a neuronal influence on body weight regulation,‘ Europe PMC Author Manuscripts, vol. 4, n. 1, pp. 25-34, 2009.
L. A. Lotta, et al, ‚Farooqi lS. Human Gain-of-Function MC4R Variants Show Signaling Bias and Protect against Obesity,‘ Cell, vol. 17, n. 3, pp. 597-607, 2019.
G. Thorfleifsson et al. ‚Genome-wide association yields new sequence variants at seven loci that associate with measures of obesity,‘ Nat. Genet., vol. 41, n. 1, pp. 8-24, 2008.
F. Renström et al. ‚Replication and extension of genome-wide association study results for obesity in 4923 adults from northern Sweden,‘ Hum. Mol. Genet., vol. 18, n. 8, pp. 1489-1496, 2009.
C. Holzapfel et al. ‚Genes and lifestyle factors in obesity: results from 12,462 subjects from MONlCA/KORA,‘ lnt. J. Obes., vol. 34, n. 10., pp. 1538-1545, 2010.
S. C. Hunt, S. Stone and Y. Xin ‚Association of the FTO gene with BMl,‘ Obesity, vol. 16, n. 4, pp. 902-904, 2008.
Effekt einer Lebensstiländerung auf das Gewicht
C. Thamer et al. ‚Variations in PPARD determine the change in body composition during lifestyle intervention: a whole-body magnetic resonance study,‘ J. Clin. Endocrinol. Metab., vol. 93, n. 4, pp. 1497-1500, 2008.
N. Stefan et al. ‚Genetic variations in PPARD and PPARGC1A determine mitochondrial function and change in aerobic physical fitness and insulin sensitivity during lifestyle intervention,‘ J Clin Endocrinol Metab, vol. 92, n.5, pp. 1827-1833, 2007.
Salzige Ernährung und Blutdruck
X. Gu et al. ‚Resequencing Epithelial Sodium Channel Genes ldentifies Rare Variants Associated With Blood Pressure Salt-Sensitivity: The GenSalt Study,‘ Am. J. Hypertens., vol. 31, n. 2, pp. 205-211, 2018.
S. R. S. Freitas ‚Molecular Genetics of Salt-Sensitivity and Hypertension: Role of Renal Epithelial Sodium Channel Genes,‘ Am. J. Hyperten., vol. 31, n. 2, pp. 172-174, 2018.
Schmecken von Süß
A. A. Fushan et al. ‚Allelic Polymorphism within the TAS1R3 Promoter is Associated with Human Taste Sensitivity to Sucrose,‘ Curr. Biol., vol. 19, n. 15, pp. 1288-1293, 2009.
E. Haznedaroglu et al. ‚Association of Sweet Taste Receptor Gene Polymorphisms with Dental Caries Experience in School Children,‘ Caries Res., vol. 49, n. 3, pp. 275-281, 2015.
Schmecken von Bitterkeit
N. J. Timpson et al. ‚TAS2R38 (phenylthiocarbamide) haplotypes, coronary heart disease traits, and eating behavior in the British Women’s Heart and Health Study,‘ The American Journal of Clinical Nutrition, vol. 81, n. 5, pp. 1005-10011, 2005.
S. Perna et al. ‚Association of the bitter taste receptor gene TAS2R38 (polymorphism RS713598) with sensory responsiveness, food preferences, biochemical parameters and body-composition markers. A cross-sectional study in ltaly,‘ lnt. J. Food Sci. Nutr., vol. 69, n. 2, pp. 245-252, 2018.
A. L. Allen, J. E. McGeary, J. E. Hayes ‚Polymorphisms in TRPV1 and TAS2Rs Associate with Sensations from Sampled Ethanol,‘ Alcohol. Clin. Exp. Res., vol. 38, n. 10, pp. 2550-2560, 2014.
L. Hwang et al. ‚Bivariate genome-wide association analysis strengthens the role of bitter receptor clusters on chromosomes 7 and 12 in human bitter taste,‘ BMC Genomics, vol. 19, n. 1, pp. 678, 2018.
L. Calancie et al. ‚TAS2R38 Predisposition to Bitter Taste Associated with Differential Changes in Vegetable lntake in Response to a Community-Based Dietary lntervention,‘ G3 (Bethesda), vol. 8, n. 6, pp.
2107-2119, 2018.
Völlegefühl nach dem Essen
J. Wardle et al. ‚Obesity associated genetic variation in FTO is associated with diminished satiety,‘ J. Clin. Endocrinol. Metab., vol. 93, no. 9, pp. 3640-3643, 2008.
M. Tanofsky-Kraff ‚The FTO gene rs9939609 obesity-risk allele and loss of control over eating,‘ Am. J. Clin. Nutr., vol. 90, n. 6, pp. 1483-1488, 2009.
Snacking Verhalten
M. de Krom ‚Common Genetic Variations in CCK, Leptin, and Leptin Receptor Genes Are Associated With Specific Human Eating Patterns,‘ Diabetes, vol. 56, n. 1,pp. 276-280
nM. B. M. van den Bree, L.J. Eaves and J. T. Dwyer ‚Genetic and environmental influences on eating patterns of twins aged >= 50 y.,‘ Am. J. Clin. Nutr., vol. 70, pp.456-465,1999.
J. M. de Castro ‚Genetic influences on daily intake and meal patterns of humans,‘ Physiol Behav., vol. 53, pp. 777-782,1993. J. M. de Castro ‚lndependence of heritable influences on the food intake of free-living humans,‘ Nutrition, vol. 18, pp.11-16,2002.
. l. Steinle et. al. ,,Eating behaviour in the Old Order Amish: heritability analysis and a genome-wide linkage analysis,‘ Am. J. Clin. Nutr., vol. 75, pp. 1098-1106,2002.
S. Tholin, F. Rasmussen, P. Tynelius, J. Karlsson ‚Genetic and environmental influences on eating behavior: the Swedish Young Male Twins study,‘ Am. J. Clin Nutr., vol. 81, pp. 564-569,2005.
Jo-Jo Effekt
C. Thonusin, K. Shinlapawittayatorn, S. C. Chattipakorn and N. Chattipakorn ‚The impact of genetic polymorphisms on weight regain after successful weight loss,‘ British Journal of Nutrition, vol. 124, n. 8, pp. 809-823, 2020.
S. M. Byrne, Z. Cooper and C.G. Fairburn ‚Psychological predictors of weight regain in obesity,‘ Behav. Res. Ther., vol. 42, pp. 1341-1356., 2004.
C. E. Elks et al. ‚Variability in the heritability of body mass index: a systematic review and meta-regression,‘ Front. Endocrinol., vol. 3, pp. 29, 2012.
B. M. Herrera and C.M. Lindgren ‚The genetics of obesity,‘ Curr. Diab. Rep., vol. 10, pp. 498-505, 2010.
Primäre Laktoseintoleranz
Bersaglieri T. ‚Genetic signatures of strong recent positive selection at the lactase gene,‘ Am J Hum Genet,74(6): 1111-20. doi: 10.1086/421051, 2004.
Ledochowski M, Bair H, Fuchs D. ‚Laktoseintoleranz,‘ Ernährungsmed, 5(1): 7-14, 2003.
Misselwitz B, Pohl D, Fruhauf H et al. ‚Lactose malabsorption and intolerance: pathogenesis, diagnosis and treatment,’United European Gastroenterol J, 1(3): 151-159, 2013.
Shaukat A, Levitt MD, Taylor BC et al. ‚Systematic review: effective management strategies for lactose intolerance,‘ Ann lntern Med, 152(12): 797-803, 2010.
Sahi T. ‚Genetics and epidemiology of adult-type hypolactasia with emphasis on the situation in Europe,‘ Scand J Nutr Näringsforskning, 45(1): 161-162, 2001.
Rosenkranz W. et al. ‚Distribution of human adult lactase phenotypes in the population of Austria,‘ Hum Genet, 62: 158-61, 1982.
McSweeney PLH. ‚Biochemistry of cheese ripening,‘ lnternational Journal of Dairy Technology, 57(2-3):127-144,2004.
T. He, et al. ‚Effects of yogurt and bifidobacteria supplementation on the colonic microbiota in lactose-intolerant subjects,‘ Journal of Applied Microbiology, vol. 2, no. 104, pp. 595 – 604, 2007.
D. H. Juers, B. W. Matthews and R. E. Huber, ‚LacZ ß-galactosidase: Structure and function of an enzyme of historical and molecular biological importance,‘ Protein Science, vol. 21, no. 12, pp. 1792-1807, 2012.
R. G. Montes, T. M. Bayless, J. M. Saavedra and J. A. Perman, ‚Effect of Milks lnoculated with Lactobacillus acidophilus or a Yogurt Starter,‘ Journal of Dairy Science, vol. 78, no. 8, pp. 1657-1664, 1995.
M. N. Pakdaman, J. K. Udani, P. M. Jhanna and S. Michael, ‚The effects of the DDS-1 strain of lactobacillus on symptomatic relief for lactose intolerance – a randomized, double-blind, placebo-controlled, crossover clinical trial,‘ Nutrition Journal, vol. 15, no. 1, pp. 1-11, 2016.
Histaminintoleranz
Agundez J. A: B. et al. ‚The Diamine Oxidase Gene ls Associated with Hypersensitivity Response to Non-Steroidal Anti-lnflammatory Drugs,‘ PLoS One, 7(11): e47571, 2012
Ercan-Sencicek G. et al. ‚L-histidine decarboxylase and Tourette’s syndrome,‘ N Engl J Med, 20;362(20):1901-8, 2010
L. Maintz et al. ‚Association of single nucleotide polymorphisms in the diamine oxidase gene with diamine oxidase serum activities,‘ Allergy, 66(7):893-902, 2011
Shulpekova Y. O. et al. ‚Food lntolerance: The Role of Histamine,‘ Nutrients, 13(9): 3207, 2021
Ayuso P., Garcfa-Martfn E., Martfnez C., Agundez J. A. G. ‚Genetic variability of human diamine oxidase: occurrence of three nonsynonymous polymorphisms and study of their effect on serum enzyme activity,‘ Pharmacogenet Genomics,17(9):687-93, 2007
Yoshikawa T., Nakamura T. and Yanai K. ‚Histamine N-Methyltransferase in the Brain,‘ lnt J Mol Sci, 20(3): 737, 2019
Meza-Velazquez R. et al. ‚Association of diamine oxidase and histamine N-methyltransferase polymorphisms with presence of migraine in a group of Mexican mothers of children with allergies,‘ Neurologfa (English Edition), 32(8):500-507, 2017
Hon Y. Y. et al. ‚Endogenous histamine and cortisol levels in subjects with different histamine
N-methyltransferase C314T genotypes: a pilot study,‘ Molecular diagnosis and therapy, 10(2):109-114, 2006
Gervasini G. et al. ‚Variability of the L-Histidine decarboxylase gene in allergic rhinitis,‘ Allergy, 65(12):1576-84, 2010
Nahrungsmittelallergien
Osborne N. J. et al. ‚Prevalence of challenge-proven lgE-mediated food allergy using population-based sampling and predetermined challenge criteria in infants,‘ J. Allergy Clin. lmmunol., 127: 668-676, 2011
Marenholz l. et al. ‚Genome-wide association study identifies the SERPlNB gene cluster as a susceptibility locus for food allergy,‘ Nature Communications, 8: 1056, 2017
Sicherer S. H. et al. ‚Genetics of peanut allergy: a twin study,‘ J. Allergy Clin. lmmunol., 106: 53-56, 2000 Howell W. M. and Holgate S. T. ‚HLA genetics and allergic disease,‘ Thorax, 50(8): 815-818, 1995
Ullemar V. et al. ‚Heritability and confirmation of genetic association studies for childhood asthma in twins,‘ Allergy, 71: 230-238, 2016
Diät und Diätverhalten
J. R. Speakman ‚The ‚Fat Mass and Obesity Related‘ (FTO) gene: Mechanisms of lmpact on Obesity and Energy BalanceBalance,‘ Curr. Obes. Rep., vol 4, n. 1, pp. 73-91, 2015.
N. Genet ‚ Six new loci associated with body mass index highlight a neuronal influence on body weight regulation,‘ Europe PMC Author Manuscripts, vol. 4, n. 1, pp. 25-34, 2009.
L. A. Lotta, et al, ‚Farooqi lS. Human Gain-of-Function MC4R Variants Show Signaling Bias and Protect against Obesity, ‚Cell, vol. 17, n. 3, pp. 597-607, 2019.
G. Thorleifsson et al. ‚Genome-wide association yields new sequence variants at seven loci that associate with measures of obesity,‘ Nat. Genet., vol. 41, n. 1, pp. 8-24, 2008.
F. Renström et al. ‚Replication and extension of genome-wide association study results for obesity in 4923 adults from northern Sweden,‘ Hum. Mol. Genet., vol. 18, n. 8, pp. 1489-1496, 2009.
C. Holzapfel et al. ‚Genes and lifestyle factors in obesity: results from 12, 462 subjects from MONlCA/KORA,‘ lnt. J. Obes., vol. 34, n. 10., pp. 1538-1545, 2010.
S. C. Hunt and S. Stone and Y. Xin ‚Association of the FTO gene with BMl,‘ Obesity, vol. 16, n. 4, pp. 902-904, 2008.
R. J. F. Loos et al. ‚Common variants near MC4R are associated with fat mass, weight and risk of obesity,‘ Nat. Genet., vol. 40, n. 6, pp. 768-75, 2008.
. Drabsch et al. ‚Associations between Single Nucleotide Polymorphisms and Total Energy, Carbohydrate, and Fat lntakes: A Systematic Review,‘ Advances in Nutrition, vol. 9, n. 4, pp. 425-453, 2018.
Selbstbeherrschung bei Diäten
D. Kirac et al. ‚Effects of MC4R, FTO, and NMB gene variants to obesity, physical activity, and eating behavior phenotypes,‘ lUBMB Life., vol 68, n. 10, pp. 777-835,2016.
. Bouchard et al. ‚Neuromedin ß: a strong candidate gene linking eating behaviors and susceptibility to obesity,‘ The American Journal of Clinical Nutrition., vol 80, n. 6, pp. 1478-1486, 2004.
Calcium
Cerani et al. ‚Genetic predisposition to increased serum calcium, bone mineral density, and fracture risk in individuals with normal calcium levels: mendelian randomisation study,‘ BMJ, vol. 366, pp. l4410, 2019.
P. Yin ‚Serum calcium and risk of migraine: a Mendelian randomization study,‘ vol. 26, n. 4, pp. 820-828, 2017.
Kreatin
B. Youn, S. Ko, J. Y. Kim ‚Genetic basis of elite combat sports athletes: a systematic review‘, Biol Sport, vol. 38, n. 4, vol. 667-675, 2021.
O. V. Balberova et al. ‚Candidate Genes of Regulation of Skeletal Muscle Energy Metabolism in Athletes‘, Genes (Basel), vol. 12, n. 11, pp. 1682, 2021.
V. Gineviciene et al. ‚CKM Gene rs8111989 Polymorphism and Power Athlete Status‘, Genes (Basel), vol. 12, n. 10, pp. 1499, 2021.
Magnesium
M. Sarac et al. ‚Magnesium-permeable TRPM6 polymorphisms in patients with meningomyelocele,‘ Springerplus, vol. 5, n. 1, pp. 1703, 2016.
M. W. Hess et al. ‚Common single nucleotide polymorphisms in transient receptor potential melastatin type 6 increase the risk for proton pump inhibitor-induced hypomagnesemia: a case-control study,‘ Pharmacogenet Genomics, vol. 27, n. 3, pp. 83-88, 2017.
Y. Song et al. ‚Common genetic variants of the ion channel transient receptor potential membrane melastatin 6 and 7 (TRPM6 and TRPM7), magnesium intake, and risk of type 2 diabetes in women,‘ BMC Med. Genet., vol. 10, pp. 4, 2009.
C. Fu et al. ‚lncreased risk of post-stroke epilepsy in Chinese patients with a TRPM6 polymorphism,‘ Neurol. Res., vol. 41, n. 4, pp. 378-383, 2019.
T. E. Meyer et al. ‚Genome-Wide Association Studies of Serum Magnesium, Potassium, and Sodium Concentrations ldentify Six Loci lnfluencing Serum Magnesium Levels,‘ vol. 6, n. 8, e1001045, 2010.
Y. Chou et al. ‚A Genetic Polymorphism (rs17251221) in the Calcium-Sensing Receptor Gene (CASR) ls Associated with Stone Multiplicity in Calcium Nephrolithiasis,‘ PLoS One, vol. 6, n. 9, 2011.
Vitamin A
P. Borel et al. ‚Genetic variants in BCMO1 and CD36 are associated with plasma lutein concentrations and macular pigment optical density in humans,‘ Ann. Med., vol. 43, n. 1, pp. 47-59, 2011.
W. C. Leung et al. ‚Two common single nucleotide polymorphisms in the gene encoding beta-carotene 15,15′-monoxygenase alter beta-carotene metabolism in female volunteers,‘ The FASEB Journal, vol. 23, n. 4, pp. 1041-1053, 2009.
N. E. Moran et al. ‚Single Nucleotide Polymorphisms in ß-Carotene Oxygenase 1 are Associated with Plasma Lycopene Responses to a Tomato-Soy Juice lntervention in Men with Prostate Cancer,‘ J. Nutr., vol. 149, n. 3, pp. 381-397, 2019.
X. Cai et al. ‚Carotenoid metabolic (BCO1) polymorphisms and personal behaviors modify the risk of coronary atherosclerosis: a nested case-control study in Han Chinese with dyslipidaemia (2013-2016),‘ Asia Pac. J. Clin. Nutr., vol. 28, n. 1, pp. 192-202, 2019.
K. Fransen et al. ‚Polymorphism in the retinoic acid metabolizing enzyme CYP26B1 and the development of Crohn’s Disease,‘ PLoS One, vol. 8, n. 8, e72739, 2013.
O. Krivospitskaya et al. ‚A CYP26B1 Polymorphism Enhances Retinoic Acid Catabolism and May Aggravate Atherosclerosis,‘ Mol. Med., vol. 18, n. 1, pp. 712-718, 2012.
Vitamin E
S. Galmes, F. Serra and A. Palou ‚Vitamin E Metabolic Effects and Genetic Variants: A Challenge for Precision Nutrition in Obesity and Associated Disturbances,‘ Nutrients, vol. 10, n. 12, pp. 1919, 2018.
A. England et al. ‚Variants in the genes encoding TNF-a, lL-10, and GSTP1 influence the effect of a-tocopherol on inflammatory cell responses in healthy men,‘ Am. J. Clin. Nutr., vol. 95, n. 6, pp. 1461-1467, 2012
P. Borel and C. Desmarchelier ‚Genetic Variations lnvolved in Vitamin E Status,‘ lnt. J. Mol. Sci., vol. 17, n. 12, pp. 2094, 2016.
V. Zanon-Moreno et al. ‚Effects of polymorphisms in vitamin E-, vitamin C-, and glutathione peroxidase-related genes on serum biomarkers and associations with glaucoma,‘ Mol. Vis., vol. 19, pp. 231-242, 2013.
K. T. Hall et al. ‚COMT and Alpha-Tocopherol Effects in Cancer Prevention: Gene-Supplement lnteractions in Two Randomized Clinical Trials,‘ J. Nat. Cancer lnst., vol. 111, n. 7, pp. 684-694, 2019.
Vitamin K
P. Borgiani et al. ‚CYP4F2 genetic variant (rs2108622) significantly contributes to warfarin dosing variability in the ltalian population,‘ Pharmacogenomics, vol. 10, n. 2, pp. 261-266, 2009.
O. Singh, E. Sandanaraj, K. Subramanian, L. H. Lee and B. Chowbay ‚lnfluence of CYP4F2 rs2108622 (V433M) on warfarin dose requirement in Asian patients,‘ Drug Metab. Pharmacokinet., vol. 26, n. 2, pp. 130-136, 2011.
D. Liao, X. Yi, B. Zhang, Q. Zhou and J. Lin ‚lnteraction Between CYP4F2 rs2108622 and CPY4A11 rs9333025 Variants ls Significantly Correlated with Susceptibility to lschemic Stroke and
20-Hydroxyeicosatetraenoic Acid Level,‘ Genet. Test. Mol. Biomarkers, vol. 20, n. 5, pp. 223-228, 2016.
C. Meng, J. Wang, W. Ge, S. Tang and G. Xu ‚Correlation between CYP4F2 gene rs2108622 polymorphism and susceptibility to ischemic stroke,‘ lnt. J. Clin. Exp. Med., vol. 8, n. 9, pp. 16122-16126, 2015.
B. Patillon et al. ‚Positive Selection in the Chromosome 16 VKORC1 Genomic Region Has Contributed to the Variability of Anticoagulant Response in Humans,‘ PLoS One, vol. 7, n. 12, e53049, 2012.
Y. l. Dubovyk, V. Y. Harbuzova and A. V. Ataman ‚G-1639A but Not C1173T VKORC1 Gene Polymorphism ls Related to lschemic Stroke and lts Various Risk Factors in Ukrainian Population,‘ Biomed. Res. lnt., vol. 2016, n. 6, pp. 1-10, 2016.
Vitamin B2
C. J. Garcfa-Minguillan et al.’Riboflavin status modifies the effects of methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) polymorphisms on homocysteine,‘ Genes. Nutr., vol. 9, n. 6, pp.435, 2014.
P. A. Abhinand et al.’lnsights on the structural perturbations in human MTHFR Ala222Val mutant by protein modeling and molecular dynamics,‘ J. Biomol. Struct. Dyn., vol. 34, n. 4, pp. 892-905, 2016.
B. Troesch, P. Weber and M. H. Mohajeri’Potential Links between lmpaired One-Carbon Metabolism Due to Polymorphisms, lnadequate B-Vitamin Status, and the Development of Alzheimer’s Disease,‘ Nutrients, vol. 8, n. 12, pp. 803, 2016.
Vitamin B6
T. Tanaka et al. ‚Genome-wide association study of vitamin B6, vitamin B12, folate, and homocysteine blood concentrations,‘ Am. J. Hum. Genet., vol. 84, n. 4, pp. 477-482, 2009.
A. Hazra et al. ‚Genome-wide significant predictors of metabolites in the one-carbon metabolism pathway,‘ Hum. Mol. Genet., vol. 18, n. 23, pp. 4677-4687, 2009.
Vitamin B12
T. Tanaka et al. ‚Genome-wide association study of vitamin B6, vitamin B12, folate, and homocysteine blood concentrations,‘ Am. J. Hum. Genet., vol. 84, n. 4, pp. 477-482, 2009.
Hazra et al. ‚Genome-wide significant predictors of metabolites in the one-carbon metabolism pathway,‘ Hum. Mol. Genet., vol. 18, n. 23, pp. 4677-4687, 2009.
V. S. Tanwar et al. ‚Common variant in FUT2 gene is associated with levels of vitamin B12 in lndian population,‘ Gene, vol. 515, n. 1, pp. 224-228, 2013.
N. Grarup et al. ‚Genetic Architecture of Vitamin B12 and Folate Levels Uncovered Applying Deeply Sequenced Large Datasets,‘ PLoS Genet., vol 9., n. 6, e1003530, 2013.
Biotin
D. M. Raben ‚Vitamins: A Biochemical Perspective‘, Encyclopedia of Cell Biology (Second Edition), vol. 1, n. 1, pp. 390-406, 2023.
A. Dasgupta ‚Biotin and Other lnterferences in lmmunoassays‘, A Concise Guide, vol. 1, pp. 70-216, 2019.
K. L. Swango et al. ‚Partial biotinidase deficiency is usually due to the D444H mutation in the biotinidase gene,‘ Hum. Genet., vol. 102, n. 5, pp. 571-575, 1998.
K. J. Norrgard, R. J. Pomponio, J. Hymes and B. Wolf ‚Mutations Causing Profound Biotinidase Deficiency in Children Ascertained by Newborn Screening in the United States Occur at Different Frequencies than in Symptomatic Children,‘ Pediatric Research, vol. 46, pp. 20-27, 1999.
O. Oz et al. ‚BTD Gene Mutations in Biotinidase Deficiency: Genotype-Phenotype Correlation,‘ J. Coll. Physicians Surg. Pak., vol. 30, n. 7, pp. 780-785, 2021.
Folsäure
M. Hiraoka and Y. Kagawa ‚Genetic polymorphisms and folate status,‘ Wiley Congenit. Anom., vol. 57, n. 5, pp. 142-149, 2017.
D. Zhang, X. Wen ,W. Wu, Y. Guo and W. Cui ‚Elevated Homocysteine Level and Folate Deficiency Associated with lncreased Overall Risk of Carcinogenesis: Meta-Analysis of 83 Case-Control Studies lnvolving 35,758 lndividuals,‘ PLoS One, vol. 10, n. 5, e0123423, 2015.
T. Tanaka et al. ‚Genome-wide Association Study of Vitamin B6, Vitamin B12, Folate, and Homocysteine Blood Concentrations,‘ Am. J. Hum. Genet., vol. 84, n. 4, pp. 477-482, 2009.
K. L. Keene et al. ‚Genetic Associations with Plasma B12, B6, and Folate Levels in an lschemic Stroke Population from the Vitamin lntervention for Stroke Prevention (VlSP) Trial,‘ Front Public Health, vol. 2, pp. 112, 2014.
Q. Peng et al. ‚A molecular-beacon-based asymmetric PCR assay for detecting polymorphisms related to folate metabolism,‘ J. Clin. Lab. Anal., vol. 34, n. 8, e23337, 2020.
D. J. Gaughan et al. ‚The methionine synthase reductase (MTRR) A66G polymorphism is a novel genetic determinant of plasma homocysteine concentrations,‘ Atherosclerosis, vol. 157, n. 2, pp. 451-456, 2001.
Vitamin C
N. J. Timpson et al. ‚Genetic variation at the SLC23A1 locus is associated with circulating levels of
L-ascorbic acid (Vitamin C). Evidence from 5 independent studies with over 15000 participants, ‚Am. J. Clin. Nutr., vol. 92, n. 2, pp. 375-382, 2010.
E. J. Duell et al. ‚Vitamin C transporter gene (SLC23A1 and SLC23A2) polymorphisms, plasma vitamin C levels, and gastric cancer risk in the EPlC cohort,‘ Genes & Nutrition, vol. 8, pp. 549-560, 2013.
P. Eck ‚Nutrigenomics of vitamin C absorption and transport,‘ Current Opinion in Food Science, vol. 20, pp. 100-104, 2018.
Eisen
T. Tanaka et al. ‚A genome-wide association analysis of serum iron concentrations,‘ Blood, vol. 115, n. 1,
pp. 94-96, 2010.
Pichler et al. ‚ldentification of a common variant in the TFR2 gene implicated in the physiological regulation of serum iron levels,‘ Hum. Mol. Genet., vol. 20, n. 6, pp. 1232-1240, 2011.
P. An et al. ‚TMPRSS6, but not TF, TFR2 or BMP2 variants are associated with increased risk of iron-deficiency anemia,‘ Hum. Mol. Genet., vol. 21, n. 9, pp. 2124-2131, 2012.
D. Shinta et al. ‚The Association of TMPRSS6 Gene Polymorphism and lron lntake with lron Status among Under-Two-Year-Old Children in Lombok, lndonesia,‘ Nutrients, vol. 11, n. 4, pp. 878, 2019.
Kupfer
D. M. Evans et al. ‚Genome-wide association study identifies loci affecting blood copper, selenium and zinc‘, Human Molecular Genetics, vol. 22, n. 19, pp. 3998-4006, 2013.
J. Zhou et al. ‚Genetically predicted circulating levels of copper and zinc are associated with osteoarthritis but not with rheumatoid arthritis‘, Osteoarthritis and Cartilage, vol. 29, n. 7, pp. 1029-1035, 2021.
W. Yang et al. ‚Genome-wide association and Mendelian randomization study of blood copper levels and 213 deep phenotypes in humans‘, communications biology, vol. 5, n. 405, pp. 2153, 2022.
S. Shibazaki et al. ‚Copper deficiency caused by excessive alcohol consumption‘, BMJ Case Reports, bcr-2017-220921, 2017.
H. P. Kodali et al. ‚Effects of copper and zinc on ischemic heart disease and myocardial infarction: a Mendelian randomization study‘, The American Journal of Clinical Nutrition, vol. 108, n. 2, pp. 237-242, 2018.
Selen
K. Batai et al. ‚Genome-Wide Association Study of Response to Selenium Supplementation and Circulating Selenium Concentrations in Adults of European Descent‘, The Journal of Nutrition, vol. 151, n. 2, pp. 293-302, 2021.
N. Karunasinghe et al. ‚Serum selenium and single-nucleotide polymorphisms in genes for selenoproteins: relationship to markers of oxidative stress in men from Auckland, New Zealand‘, vol. 7, n. 2, pp. 179-190, 2012.
J. L. S. Donadio et al. ‚The influence of nutrigenetics on biomarkers of selenium nutritional status‘, Nutrition Reviews, vol. 79, n. 11, pp. 1259-1273, 2021.
T. J.Rocha et al. ‚SLC30A3 and SEP15 gene polymorphisms influence the serum concentrations of zinc and selenium in mature adults‘, Nutr Res, vol. 34, n. 9, pp. 742-748, 2014.
S. Gonza’lez et al. ‚Serum Selenium ls Associated with Plasma Homocysteine Concentrations in Elderly Humans‘, The Journal of Nutrition, vol. 134, n. 7, pp. 1736-1740, 2004.
M. L. Cooper et al. ‚lnteraction between SNPs in selenoprotein P and mitochondrial superoxide dismutase determines prostate cancer risk‘, Cancer Res, vol. 68, n. 25, pp. 10171-10177, 2008.
M. C. Cornelis et al. ‚Genome-wide association study of selenium concentrations‘, Hum Mol Genet, vol. 24, n. 5, pp. 1469-1477, 2015.
D. M. Evans et al. ‚Genome-wide association study identifies loci affecting blood copper, selenium and zinc‘, Hum Mol Genet, vol. 22, n. 19, pp. 3998-4006, 2013.
Zink
D. M. Evans et al. ‚Genome-wide association study identifies loci affecting blood copper, selenium and zinc, ‚ Hum. Mol. Genet., vol. 22, n. 19, pp. 3998-4006, 2013.
E. Mocchegiani et al. ‚Zinc: dietary intake and impact of supplementation on immune function in elderly,‘ Age (Dordr), vol. 35, n. 3, pp. 839-860, 2013.
K. J. Day, M. M. Adamski, A. L. Dordevic and C. Murgia ‚Genetic Variations as Modifying Factors to Dietary Zinc Requirements-A Systematic Review,‘ Nutrients, vol. 9, n. 2, pp. 148, 2017.
Cholin
l. Muramatsu et al. ‚A New Aspect of Cholinergic Transmission in the Central Nervous System‘, Nicotinic Acetylcholine Receptor Signaling in Neuroprotection‘, vol. 3, pp. 978-981, 2018.
Velazquez et al. ‚Lifelong choline supplementation ameliorates Alzheimer’s disease pathology and associated cognitive deficits by attenuating microglia activation‘, Aging Cell, vol. 18, n. 6, e13037, 2019.
B. Ganz et al. ‚Genetic Variation in Choline-Metabolizing Enzymes Alters Choline Metabolism in Young Women Consuming Choline lntakes Meeting Current Recommendations‘, lnt J Mol Sci, vol. 18, n. 2, pp. 252, 2017.
Bale et al. ‚Whole-Exome Sequencing ldentifies a Variant in Phosphatidylethanolamine
N-Methyltransferase Gene to be Associated with Lean-Nonalcoholic Fatty Liver Disease‘, J Clin Exp Hepatol, vol. 9, n. 5, pp. 561-568, 2019.
L. Tan et al. ‚Phosphatidylethanolamine N-methyltransferase gene rs7946 polymorphism plays a role in risk of nonalcoholic fatty liver disease: evidence from meta-analysis‘, Pharmacogenet Genomics, vol. 26, n. 2, pp. 88-95, 2016.
A. Costa et al. ‚ldentification of new genetic polymorphisms that alter the dietary requirement for choline and vary in their distribution across ethnic and racial groups‘, FASEB J, vol. 28, n. 7, pp. 2970-2978, 2014.
E. Christensen et al. ‚The MTHFD1 p.Arg653Gln variant alters enzyme function and increases risk for congenital heart defects‘, Hum Mutat, vol. 30, n. 2, pp. 212-220, 2009.
Kohlmeier et al. ‚Genetic variation of folate-mediated one-carbon transfer pathway predicts susceptibility to choline deficiency in humans‘, Proc Natl Acad Sci U S A, vol. 102, n. 44, pp. 16025-16030, 2005.
M. N. llozumba et al. ‚Associations between Plasma Choline Metabolites and Genetic Polymorphisms in One-Carbon Metabolism in Postmenopausal Women: The Women’s Health lnitiative Observational Study‘, The Journal of Nutrition, vol. 150, n. 11, pp. 2874-2881, 2020.
Ren et al. ‚Association between the BHMT gene rs3733890 polymorphism and the efficacy of oral folate therapy in patients with hyperhomocysteinemia‘, Ann Hum Genet, vol. 83, n. 6, pp. 434-444, 2019.
Das FTO Gen und Gewicht
Emond, J.A. et al. (2017) ‚FTO genotype and weight status among preadolescents: Assessing the mediating effects of obesogenic appetitive traits‘, Appetite, 117, S. 321-329. https://doi.org/10.1016/j.appet.2017.07.009.
Castellini, G. et al. (2017) ‚Fat mass and obesity-associated gene (FTO) is associated to eating disorders susceptibility and moderates the expression of psychopathological traits‘, PLoS ONE, 12(3), S. e0173560. https://doi.org/10.1371/journal.pone.0173560.
Frayling, T.M. et al. (2007) ‚A Common Variant in the FTO Gene ls Associated with Body Mass lndex and Predisposes to Childhood and Adult Obesity‘, Science, 316(5826), S. 889-894. https://doi.org/10.1126/science.1141634.
AMPD1 Mangel
Del Coso, J. und Lucia, A. (2021) ‚Genetic influence in exercise performance‘, Genes, 12(5), S. 651. https://doi.org/10.3390/genes12050651.
Leonska-Duniec, A. u. a. (2020) ‚AMPD1 C34T Polymorphism (rs17602729) ls Not Associated with Post-Exercise Changes of Body Weight, Body Composition, and Biochemical Parameters in Caucasian Females‘, Genes, 11(5), S. 558. https://doi.org/10.3390/genes11050558.
Rannou, F. u. a. (2017) ‚Effects of AMPD1 common mutation on the metabolic-chronotropic relationship: lnsights from patients with myoadenylate deaminase deficiency‘, PLoS ONE, 12(11), S. e0187266. https://doi.org/10.1371/journal.pone.0187266.
