Nutrigenetic Profile

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• What are the genes studied and what does it mean?>

  GEN	OMIM or reference	FONCTION	RELATED DISEASE AND GENE TYPE
  MC4R	155541 601665	It is related to eating behavior because it reduces satiety and increases appetite, which promotes overweight and obesity	OBESITY AND DIABETES :ECONOMIC GENES
  FTO	610966	It reduces satiety and increases appetite for high-calorie foods such as fats and sugars. It also lowers the production of heat of the body, thus promoting the storage of energy in the form of fat
  BDNF	113505 607499	It promotes the storage of fat in stressful situations, it is found more frequently in women.
  UCP1	113730	It regulates the action thyroid hormone responsible for burning calories in the form of heat, although at rest this pendant unites physical activity. If this function is slowed down, the body accumulates fat.
  UCP3	602044	It is involved in the production of heat through the thyroid hormone and also plays a role in the burning of calories on physical activity. These are malfunctions that promote overweight and obesity
  ADRB2	109690 601665	It regulates the response of the body to stress by translating it into a feeling of hunger and responds by storing energy in the form of fat.
  ADRB3	109691	It responds to stress by interpreting it as hunger, which promotes overweight and obesity. It is also associated with insulin resistance and metabolic syndrome. This gene has its effects multiplied in the presence of the gene UCP1.
  PPARG	601487	The ancestral gene is not suitable for contemporary foods such as refined foods (flours and sugars) or processed and saturated fats that promote fat formation and insulin resistance. This gene also complicates the burning of calories. In addition, this gene is the main target of one of the antidiabetic drugs, a good knowledge of this gene allows a personalized treatment
  ACE	106180	This gene regulates blood pressure through the level of sodium in the kidneys and also promotes fat formation, so salt intake not only promotes hypertension, it also causes overweight and obesity.
  IL1B	147720	It promotes chronic inflammation and, associated with the action of the next gene, is directly related to the control of body fat especially in young people. It acts on the regulation of fat formation, the control of intake and energy expenditure and therefore on the impact of obesity.
  IL1RN	147679	It modifies the function of the immune system, promoting inflammation of fat, this being closely related to the development of obesity. Its action is reinforced by that of the previous gene, increasing the amount of total fat.
  IL6	147620	It causes a chronic low-grade inflammation of adipose tissue, induces insulin resistance because it alters its receptor and promotes the development of type 2 diabetes (adult).
  TNFa	191160	It promotes inflammation of the fatty tissue and modifies the insulin receptor and leptitis, causing resistance to these hormones due to the dysfunction of its receptor.
  FABP2	134640	It allows a better absorption of dietary fat in the intestine and alters its oxidation, promoting insulin resistance and increasing the risk of atherosclerosis
  ADIPOQ	605441	It induces insulin resistance that hinders carbohydrate metabolism and promotes the development of obesity and type 2 diabetes.
  IRS1	147545	It causes insulin resistance and therefore a high risk of diabetes because it directly affects the insulin receptor.
  FABP2	134640	It facilitates the absorption of dietary fat in the intestine and alters its oxidation, promoting insulin resistance and increasing the risk of atherosclerosis.	CARDIOVASCULARY RISKS: ECONOMIC GENES
  APOE	107741	It slows the elimination of fats from food ingested in the blood, causing atherosclerosis and secondary vascular disease.
  NOS3	163729	It slows the elimination of fats from food ingested in the blood, causing atherosclerosis and secondary vascular disease.
  MTHFR	607093 188050	It regulates the levels of folic acid (one of the B vitamins), since the deficiency of this nutrient causes thrombosis, vascular embolism and cardiovascular diseases.
  ACE	106180	This gene regulates blood pressure through the level of sodium in the kidneys and also promotes fat formation, so salt intake not only promotes hypertension, it also causes overweight and obesity.
  SERPINE1	173360	This gene regulates blood pressure through the level of sodium in the kidneys and also promotes fat formation, so salt intake not only promotes hypertension, it also causes overweight and obesity.

• How to interpret the results?>

  Twenty-four genes associated with cardiometabolic syndrome and involved in nutritional response are analyzed. The polymorphisms analyzed are variants of normality, so the result of this study should not be considered as a diagnosis, but rather as an indicator of genetic risk. The results obtained can be interpreted as follows:

  

  The genes analyzed are distributed in the report according to their pathophysiological processes:

  • GROUP I: Genes involved in the central control of the input
  • GROUP II: Genes associated with the regulation of thermogenesis
  • GROUP III: Genes related to pro-inflammatory processes in adipose tissue
  • GROUP IV: Genes involved in the development of insulin resistance
  • GROUP V: Genes Associated with Cardiovascular and Cardiometabolic Risk
  • GROUP VI: Complementary analyzes: genetic study of Celiac disease, lactose intolerance and fructose intolerance
• Sensitivity and Specificity>

  The analysis of this gene is carried out using the PCR (Polymerase Chain Reaction) technique and reaction products are studied by reverse hybridization with specific sequence probes (SSOP). Moreover, the results are studied by direct sequencing and subsequent capillary electrophoresis. These molecular biology techniques are commonly used in the field of molecular genetics and exhibit high sensitivity and specificity when using specific primers for each analyzed polymorphism. The reliability of our genetic studies is close to 100%, we apply quality processes certified by competent national and international organizations.

• Guidelines>
  • Aranceta-Bartrina, J., et al. Prevalencia de obesidad general y obesidad abdominal en la población adulta española (25–64 años) 2014–2015: estudio ENPE. Rev Esp Cardiol. 2016;69:579-87 - Vol. 69 Núm.06 DOI: 10.1016/j.recesp.2016.02.010
  • Strandberg,L., et al.; Interleukin-1 System Gene Polymorphisms Are Associated with Fat Mass in Young Men, The Journal of Clinical Endocrinology & Metabolism, Volume 91, Issue 7, 1 July 2006, Pages 2749–2754, https://doi.org/10.1210/jc.2005-2786
  • Corica, F., et al.; Relationship between plasma leptin levels and the tumor necrosis factor-alpha system in obese subjects. Int J Obes Relat Metab Disord. 1999 Apr;23(4):355-60
  • German JB. et al.: Nutrigenomics and Personalized Diets: What Will They Mean for Food? Annu Rev Food Sci Technol. 2011 ; 2: 97–123. doi:10.1146/annurev.food.102308.124147
  • Grimaldi KA. et al.; Proposed guidelines to evaluate scientific validity and evidence for genotype-based dietary advice. Genes & Nutrition (2017) 12:35 DOI 10.1186/s12263-017-0584-0
  • Rescigno T. et al.; Bioactive Nutrients and Nutrigenomics in Age-Related Diseases. Molecules 2017, 22, 105; doi:10.3390/molecules22010105
  • Hetherington y Cecil, 2010. Gene-environment interactions in obesity. Forum Nutr 63: 195-203.
  • Loos et al, 2008. Common variants near MC4R are associated with fat mass, weight and risk of obesity. Nat Genet 40(6): 768-775.
  • Buzzetti et al, 2004. The common PPAR-gamma2 Pro12Ala variant is associated with greater insulin sensitivity. Eur J Hum Genet 12(12):1050-4.
  • de Oliveira et al, 2015. ADIPOQ and IL6 variants are associated with a pro-inflammatory status in obeses with cardiometabolic dysfunction. Diabetology & Metabolic Syndrome 7:34-43.
  • Stephens et al, 2007. Association between plasma IL-6, the IL6 -174G>C gene variant and the metabolic syndrome in type 2 diabetes mellitus. Mol Genet Metab 90(4):422-8.
  • Online Mendelian Inheritance in Man, OMIM®. McKusick- Nathans Institute of Genetic Medicine, Johns Hopkins University (Baltimore, MD), {24/04/2018}. World Wide Web URL: https://omim.org/