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Che cos’è DIETAGENE®?

È un test nutrigenetico che analizza in 8 geni la presenza di specifiche variazioni genetiche associate alla risposta del tuo organismo nei confronti di tre elementi:

  1. grassi saturi della dieta,
  2. carboidrati e zuccheri raffinati della dieta,
  3. esercizio fisico.

Sulla base delle tua sensibilità genetica a questi tre elementi viene elaborata la dieta con una composizione dietetica unica che ti permetterà di raggiungere il tuo peso desiderato e di mantenerlo. Specifico per pazienti obesi o in sovrappeso.

Perché dovrei fare il test DIETAGENE®?

Il controllo del peso corporeo dipende da numerosi fattori di natura ambientale, genetica, psicologica e dallo stile di vita. È noto tuttavia che la genetica gioca un ruolo chiave nel controllo del peso, influenzandone l’aumento e la perdita ed il successo delle diete nel breve e lungo termine. Tutti noi conosciamo esempi di persone che mangiano quello che gli piace senza ingrassare, mentre molti di noi sono meno fortunati; sappiamo anche di persone che riprendono tutto il peso dopo la dieta ed altri che hanno bisogno di esercizio fisico ad intensità più elevata per perdere peso. Conoscendo la tua sensibilità ai grassi saturi, ai carboidrati raffinati e all’esercizio fisico potrai seguire la giusta dieta sia per raggiungere il tuo peso ideale sia per mantenerlo.

Objectives: identifying genetic variations in 8 genes associated with the response to saturated fat, carbohydrates and refined sugars from diet and to physical exercise intensity. On the basis of the number of genetic variation present, a sensitivity score to fat, sugar and exercise is worked out with the aim of adjusting the macronutrient intake and designing an optimal weight loss and maintenance diet. In addition, recommendations are given on the physical exercise level requirement for loosing weight.

SNPs & Genes Function in Personalized Nutrition (Dietagene®)


Gene: ACE; Angiotensin I converting enzyme (peptidyl-dipeptidase A) 1
Variation tested: Ins/Del
Chromosome location: 17q23.3
Total publications on the gene: 1664
Meta-Analysis: 211

This gene encodes an enzyme involved in catalyzing the conversion of angiotensin I into a physiologically active peptide angiotensin II by release of the terminal His-Leu, this results in an increase of the vasoconstrictor activity of angiotensin. Angiotensin II is a potent vasopressor and aldosterone-stimulating peptide that controls blood pressure and fluid-electrolyte balance. This enzyme plays a key role in the renin-angiotensin system. Also able to inactivate bradykinin, a potent vasodilator. Has also a glycosidase activity which releases GPI-anchored proteins from the membrane by cleaving the mannose linkage in the GPI moiety.
Many studies have associated the presence or absence of a 287 bp Alu repeat element in this gene with the levels of circulating enzyme or cardiovascular pathophysiologies. Multiple alternatively spliced transcript variants encoding different isoforms have been identified, and two most abundant spliced variants encode the somatic form and the testicular form, respectively, that are equally active.
The Allele I tested in the DNA-Wellness-Diet and in DIETAGENE is linked to an increased blood pressure with increased NaCl consumption. In addition to this, the allele D can negatively impact glycemic response to sugars, leading to a reduced sensitivity to insulin; this effect is marked in overweight individuals and can be compensated by a regular exercise.

Gene: PPARG; Peroxisome Proliferator-Activated Receptor Gamma
SNP tested: Pro12Ala
Chromosome location: 3p25
Total publications on the gene: 599
Meta-Analysis: 95

This gene encodes a member of the peroxisome proliferator-activated receptor (PPAR) subfamily of nuclear receptors. Three subtypes of PPARs are known: PPAR-alpha, PPAR-delta, and PPAR-gamma. It forms a heterodimer with the retinoic acid receptor RXRA called adipocyte-specific transcription factor ARF6 That regulate transcription of various genes.
This Receptor binds peroxisome proliferators such as hypolipidemic drugs and fatty acids. Once activated by a ligand, the receptor binds to a promoter element in the gene for acyl-CoA oxidase and activates its transcription. It therefore controls the peroxisomal beta-oxidation pathway of fatty acids. It is a key regulator of adipocyte differentiation and glucose homeostasis. Genetic variation in PPARG may in fluence body mass index (BMI). Additionally, PPAR-gamma has been implicated in the pathology of numerous diseases including susceptibility to obesity, to type 2 insulin-resistant diabetes, hypertension, atherosclerosis (with increase of carotid intimal medial thickness-CIMT) and colon cancer. Alternatively spliced transcript variants that encode different isoforms have been described. The SNP tested influences the level of expression of the protein and the Ala version has been associated with a beneficial effect on the glycemic and insulin response to refined sugar. In addition, this SNP may influence the sensitivity to Fats, especially to saturated fats.

Gene: ADRB2; Adrenergic, Beta-2-, Receptor, Surface
Variation tested: Gln27Glu, Arg16Gly
Chromosome location: 5q31-q32
Total publications on the gene: 505
Meta-Analysis: 52

This gene encodes beta-2-adrenergic receptor which is a member of the G protein-coupled receptor superfamily. Beta-adrenergic receptors mediate the catecholamine-induced activation of adenylate cyclase through the action of G proteins. The beta-2-adrenergic receptor binds epinephrine with an approximately 30-fold greater affinity than it does norepinephrine. This receptor is directly associated with one of its ultimate effectors, the class C L-type calcium channel Ca(V)1.2. This receptor-channel complex also contains a G protein, an adenylyl cyclase, cAMP-dependent kinase, and the counterbalancing phosphatase, PP2A. The assembly of the signaling complex provides a mechanism that ensures specific and rapid signaling by this G protein-coupled receptor. This gene is intronless. Different polymorphic forms, point mutations, and/or downregulation of this gene are associated with nocturnal asthma, obesity and type 2 diabetes.
The Gly-16 allele is overrepresented in individuals affected by nocturnal asthma as compared to controls, and appears to be an important genetic factor in the expression of this asthmatic phenotype.
Some individuals have resistance to the lipolytic effects of catecholamines and that this is the result of decreased ADRB2 expression in fat cells. The beta-2 adreno-receptor is a major lipolytic receptor in human fat cells. The variation gln27 to glu was indeed markedly associated with obesity with a relative risk for obesity of approximately 7 and an odds ratio of approximately 10. Homozygotes for glu27 had an average fat mass excess of 20 kg and approximately 50% larger fat cells than controls.
Evidences suggested that genetic variation in the ADRB2 gene may be of major importance for obesity, energy expenditure, and lipolytic ADRB2 function in adipose tissue, at least in women.
The Gly16Arg (P less than 0.005) and Gln27Glu (P less than 0.04) polymorphisms were associated with metabolic syndrome in men, but not in women. A significant association between the gln27-to-glu (Q27E) polymorphism of the ADRB2 gene and obesity (601665) had been demonstrated. The gln27 allele was present in 52% of obese subjects and in 70% of non-obese subjects.
Women carriers of the Arg/Arg genotype had lower fasting plasma NEFAs and greater suppression of NEFAs after an oral glucose load than women bearing the G16 allele.
Exercise produces an increase in sympathetic nervous system activity, a response that may be impaired by ADRB2 dysfunction. A group of 252 female Spanish subjects were studied to examine the association between obesity risk and the glu27 polymorphism of the ADRB2 gene, depending on physical activity. It was found that obese women who are carriers of the glu27 allele do not benefit equally from physical activity compared to non-carriers of the glu27 allele. It was concluded that the glu27 allele of the ADRB2 gene is a physical activity-dependent factor for obesity risk.
In the Dietagene test, the analysed SNPs are correlated to Fat burn resistance to exercise (Glu27 and Gly16) and to a tendency to regain weight after diet(Gly16) and to an increase of visceral fat(Glu27). It is also considered the impact of Glu27 on the increased response and sensitivity to carbohydrates.

Gene: TCF7L2; Transcription factor 7-like 2 (T-cell specific, HMG-box)
Variation tested: C/T
Chromosome location: 10q25.3
Total publications on the gene: 247
Meta-Analysis: 45
GWAS: 15

The TCL7L2 gene product is a high mobility group (HMG) box-containing transcription factor implicated in blood glucose homeostasis. Evidences suggested that TCL7L2 acts through regulation of proglucagon (138030) through repression of the proglucagon gene in enteroendocrine cells via the Wnt signaling pathway.
The protein has been implicated in blood glucose homeostasis. Several transcript variants encoding multiple different isoforms have been found for this gene.
Genetic variations in TCF7L2 are associated with susceptibility to non-insulin-dependent diabetes mellitus (NIDDM) [MIM:125853]. NIDDM is characterized by an autosomal dominant mode of inheritance, onset during adulthood and insulin resistance.
The C to T variation (rs7903146)] tested in the DIETAGENE, is linked to an increased sensitivity to refined carbohydrates and saturated fats from diet. In addition, the SNP indicates the need for a regular or increased Physical activity.


Gene: APOA2; Apolipoprotein A-II
Variation tested: -265T>C
Chromosome location: 1q21-q23
Total publications on the gene: 38
Meta-Analysis: 7

This gene encodes apolipoprotein (apo-) A-II, which is the second most abundant protein of the high density lipoprotein particles (HDL). May stabilize HDL structure by its association with lipids, and affect the HDL metabolism. The protein is found in plasma as a monomer, homodimer, or heterodimer with apolipoprotein D. Defects in this gene may result in apolipoprotein A-II deficiency or hypercholesterolemia.
The APOA2 gene is linked to a gene that controls plasma levels of apoA-II and the APOA2 gene or its product influences, by an unknown mechanism, plasma levels of free fatty acids (FFA). ApoA-II is biochemically and genetically associated with familial combined hyperlipidemia (FCHL) and may serve as a useful marker for understanding the mechanism by which FCHL develops.
A SNP in the promoter region of the gene APOA2 (-265T>C) influences the level of gene expression: in vitro transfection assays showed the transcriptional activity of the APOA2 promoter was reduced by 30% in the -265C allele as compared with the -265T allele.
This SNP -265T-C has been demonstrated to influence the level of total cholesterol and low density lipoprotein (LDL) cholesterol causing hypercholesterolemia in those members who are simultaneously carrier of a mutation in the LDLR gene.
In the Dietagene test, the SNP -265 T>C with the allele C in homozygosis is associated with increased sensitivity to saturated fats.

Gene: ADRB3;Adrenergic, Beta-3-, Receptor, Surface
Variation tested: Arg64Trp
Chromosome location: 8p12
Total publications on the gene: 220
Meta-Analysis: 36

The protein encoded by this gene belongs to the family of beta adrenergic receptors, which mediate catecholamine-induced activation of adenylate cyclase through the action of G proteins. This receptor is located mainly in the adipose tissue and is involved in the regulation of lipolysis and thermogenesis.
The trp64-to-arg (W64R) variant of the ADRB3 gene increases the capacity to gain weight and is also associated with susceptibility to an early onset of non-insulin-dependent diabetes mellitus (NIDDM) and lower metabolic resting rate.
In the Dietagene test, the variant Arg64 is associated to a higher BMI and a reduced lipolysis; furthermore is linked to a reduced sensitivity to exercise, more intense exercise is needed to have the same effect as typical intensity for carriers of the Trp64 variant.

Gene: FABP2; Fatty Acid Binding Protein 2, Intestinal
Variation tested: Ala54Thr
Chromosome location: 4q28-q31
Total publications on the gene: 105
Meta-Analysis: 6

The intracellular fatty acid-binding proteins (FABPs) belong to a multigene family with nearly twenty identified members. FABPs are divided into at least three distinct types, namely the hepatic-, intestinal- and cardiac-type. They form 14-15 kDa proteins and are thought to participate in the uptake, intracellular metabolism and/or transport of long-chain fatty acids and their acyl-CoA esters. They may also be responsible in the modulation of cell growth and proliferation. FABP2 is probably involved in triglyceride-rich lipoprotein synthesis. Binds saturated long-chain fatty acids with a high affinity, but binds with a lower affinity to unsaturated long-chain fatty acids. FABP2 may also help maintain energy homeostasis by functioning as a lipid sensor. Intestinal fatty acid-binding protein 2 gene contains four exons and is an abundant cytosolic protein in small intestine epithelial cells. This gene has a polymorphism at codon 54 that identified an alanine-encoding allele and a threonine-encoding allele. Thr-54 protein is associated with increased fat oxidation and insulin resistance. Scientific findings confirmed the association of the FABP2 thr54 allele with increased concentrations of cholesterol and triglycerides in genotype-discordant sib pairs and that genetic variation in the FABP2 gene may increase susceptibility to stroke.
The ala54-to-thr (A54T) polymorphism of FABP2 is associated with increased intestinal input of triglyceride that can lead to elevated fasting and postprandial plasma triglycerides in type II diabetes.
The variation tested in the Dietagene (Ala54Thr) is associated to increased sensitivity to saturated fat from diet.

Gene: FTO; Fat Mass And Obesity Associated Protein
SNP tested: A/T
Chromosome location: 16q12.2
Total publications on the gene: 258
Meta-Analysis: 47
GWAS: 18

The exact function of this gene is not known. Studies in mice suggest that it may be involved in nucleic acid demethylation, and that its mRNA level is regulated by feeding and fasting. FTO is a dioxygenase that repairs alkylated DNA and RNA by oxidative demethylation; has highest activity towards single-stranded RNA containing 3-methyluracil, followed by single-stranded DNA containing 3-methylthymine. Has low demethylase activity towards single-stranded DNA containing 1-methyladenine or 3-methylcytosine. Has no activity towards 1-methylguanine. Has no detectable activity towards double-stranded DNA; requires molecular oxygen, alpha-ketoglutarate and iron. Contributes to the regulation of the global metabolic rate, energy expenditure and energy homeostasis. Contributes to the regulation of body size and body fat accumulation.
Defects in FTO are the cause of growth retardation developmental delay coarse facies and early death (GRDDCFED) [MIM:612938]. The disease consists of a severe children multiple congenital anomaly syndrome with death by the age of 3 years. All affected individuals had postnatal growth retardation, microcephaly, severe psychomotor delay, functional brain deficits, and characteristic facial dysmorphism. In some patients, structural brain malformations, cardiac defects, genital anomalies, and cleft palate were also observed.
Genomewide association studies of type 2 diabetes indicate this gene as a diabetes susceptibility locus.
At least one intronic variation within the gene predisposes to childhood and adult obesity. A common variant in the FTO gene (610966) on 16q12.2 has been identified as a risk factor for obesity. The authors performed a genomewide association study of type II diabetes by screening 1,924 patients and 2,938 controls from the UK for more than 490,000 autosomal SNPs. Variation in the FTO region showed strong association (as high as p of 5 x 10(-8) for rs9939609) in this screen and in a replication study with an additional 3,757 type II diabetics and 5,346 controls (p of 9 x 10(-6) for rs9939609). The A allele of rs9939609 is associated with increased BMI. The risk attributed to rs9939609 was approximately 20% for obesity (BMI more than 30 kg/m2) and approximately 13% for being overweight (BMI more than 25 kg/m2). About 16% of white Europeans are homozygous for the A allele of rs9939609 and are 1.67 times as likely to be obese compared with those homozygous for the T allele. Study of at-risk children showed that rs9939609 was associated with increased BMI and obesity by the age of 7 years.
A meta-analysis of data from 4 European population-based studies and 3 disease-case series, involving a total of 16,876 individuals of European descent, confirmed the previously reported association between the FTO gene and BMI (p = 3.6 x 10(-8) at rs1121980). The genotype of the intronic FTO SNP rs9939609 (A to T) in a cohort of 3,337 United Kingdom children has revealed, an association between the A allele and increased adiposity; AA homozygotes had significantly reduced Satiety Responsiveness scores (p = 0.008). Mediation analysis indicated that the association of the AA genotype with increased adiposity was explained in part through effects on Satiety Responsiveness.
A meta-analysis of 15 genomewide association studies for BMI comprising 32,387 participants and a follow up in 14 additional cohorts comprising 59,082 participants, strongly confirmed association with FTO, represented by rs9939609, as associated with obesity with a per-allele change in BMI of 0.33 and an overall P value of 4.9 x 10(-74).
In a study of 15,931 Swedish adults without diabetes it was found that the minor A allele of rs9939609 was associated with increased BMI (p less than 0.001 for AA vs TT or TA genotypes) and, after adjustment for age, sex, and BMI, also with self-reported increased physical activity levels (p = 0.02).
The FTO SNP (A to T) tested in the Dietagene is associated with an increased sensitivity (with A allele) to fats, refined carbohydrate and exercise level requirement.

Come avere la Nutrizione Personalizzata?

1. Ordina la consulenza genetica e ricevi il materiale per il prelievo orale 2. Spedisci il campione di saliva e cellule della bocca
4. Ordini i tuoi integratori personalizzati 3. Ricevi il Report Nutri-Genetico sulla tua pagina web personale (15 - 20 giorni)


L’offerta DIETAGENE®

  • Test DIETAGENE® con dieta dimagrante: 190€

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