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Background: Cardiometabolic diseases are principal contributors to mortality, morbidity, and healthcare costs. Additionally, many Single Nucleotide Polymorphisms (SNPs) have been associated with cardiovascular health outcomes. Nutrition professionals' perspectives on genetic-based nutritional services play a pivotal role in treating and preventing non-communicable diseases (NCDs). Objectives: This study aims to explore Indonesian nutritionists' viewpoints on genebased nutrition services. Methods: Employing a qualitative phenomenological approach, six Indonesian nutritionists from key provinces (DKI Jakarta, West Java, Central Java, East Java, and DI Yogyakarta) participated in in-depth interviews. Themes encompassed nutritionists' views on gene-based nutrition's role in NCD prevention, genetics science, and genetic testing understanding. Thematic analysis was performed using Nvivo v.12. Results: Results showed that nutritionists had a substantial understanding of genetics and gene-based nutrition services, despite concerns about test costs. They comprehended gene-based nutrition's role in NCD prevention and acknowledged its significance in preventing NCDs. Conclusions: Within this study, Nutritionists express the importance of gene-based nutrition services in NCD prevention. To enhance engagement, nutritionists are encouraged to communicate genetic testing's value to the community. This dissemination will help advance NCD prevention efforts. [ABSTRACT FROM AUTHOR]

Abstract Objective Gene-diet interaction plays a key role in the inter-individual differences in lipid abnormalities as a major risk factor for cardiovascular diseases (CVDs). Thus, we explored the interaction between CETP TaqB1 polymorphism with dietary acid load (DAL) on lipid profile among type 2 diabetes mellitus (T2DM). Method This cross-sectional study conducted on 220 Iranian patients with T2DM. Dietary acid load (PRAL and NEAP) was calculated via a validated food-frequency questionnaire (FFQ). The polymerase chain reaction (PCR) used for genotyping Taq1B polymorphism. Biochemical markers were measured by standard protocol. The interaction between CETP Taq1B polymorphism and DAL (PRAL and NEAP) on lipid profile was performed by a generalized linear regression model (GLM). Results The overall prevalence of rs708272 genotypes was 8.6%, 72.7% and 18.6% for B1B1, B1B2 and B2B2 genotype respectively. This study showed that people with the B1B1 genotype had greater LDL, TC, LDL/HDL, and TG when they consumed diets that scored higher on the NEAP and PRAL indexes than those with the B1B2 and B2B2 genotypes. Besides, carriers of the B1B1 allele who were in the highest tertile of NEAP, had lower HDL (P Interaction

A high-fiber diet can reduce the triglyceride levels of hyperlipidemic subjects. FiberCreme-IMO is a non-dairy creamer product containing fiber that potentially improves the triglyceride profile. Genetic variants of ChREBP rs3812316 may affect triglyceride response on the consumption of FiberCreme-IMO cookies. This study investigated the effect of FiberCreme-IMO on triglyceride levels and the interaction between FiberCreme-IMO and genotypes of ChREBP rs3812316 on triglyceride levels of hyperlipidemic subjects. Fifty adults with hyperlipidemia were assigned into two groups: one group consumed cookies made from FiberCreme-IMO (n=25), and another consumed control cookies containing coconut milk powder (n=25). Each subject consumed 80 grams of cookies per day for four weeks. Serum triglycerides were measured at baseline and four weeks after treatment. Genotypes of ChREBP rs3812316 were analyzed at the end of the study using PCR-RFLP. FiberCreme-IMO cookies reduced the triglyceride levels compared to control cookies, but the reduction was not statistically significant (p>0.05). There was no significant interaction between FiberCreme-IMO cookies and ChREBP rs3812316 on the triglyceride levels. This study suggests that FiberCreme-IMO ameliorated the triglyceride levels of hyperlipidemic subjects after four weeks of consumption. [ABSTRACT FROM AUTHOR]

Objective: Gene-diet interaction plays a key role in the inter-individual differences in lipid abnormalities as a major risk factor for cardiovascular diseases (CVDs). Thus, we explored the interaction between CETP TaqB1 polymorphism with dietary acid load (DAL) on lipid profile among type 2 diabetes mellitus (T2DM). Method: This cross-sectional study conducted on 220 Iranian patients with T2DM. Dietary acid load (PRAL and NEAP) was calculated via a validated food-frequency questionnaire (FFQ). The polymerase chain reaction (PCR) used for genotyping Taq1B polymorphism. Biochemical markers were measured by standard protocol. The interaction between CETP Taq1B polymorphism and DAL (PRAL and NEAP) on lipid profile was performed by a generalized linear regression model (GLM). Results: The overall prevalence of rs708272 genotypes was 8.6%, 72.7% and 18.6% for B1B1, B1B2 and B2B2 genotype respectively. This study showed that people with the B1B1 genotype had greater LDL, TC, LDL/HDL, and TG when they consumed diets that scored higher on the NEAP and PRAL indexes than those with the B1B2 and B2B2 genotypes. Besides, carriers of the B1B1 allele who were in the highest tertile of NEAP, had lower HDL (P Interaction < 0.05). Conclusions: In summary, the lipid profile might be improved in B1B1 homozygotes by less adherence to DAL indexes, however, the findings should be validated in high-quality interventional studies. [ABSTRACT FROM AUTHOR]

Abstract This investigation with aimed the effect of APOA2–265 T > C polymorphism and dietary acid load (DAL) as either potential renal acid load (PRAL) and net endogenous acid production (NEAP) intake interaction on metabolic markers in type 2 diabetes mellitus (T2DM). In present cross-sectional study, 737 patients with T2DM (290 men and 447 women) were enlisted from diabetes centers in Tehran. The dietary intakes of all participants during the last year was acquired by a validated semi-quantitative food frequency (FFQ) questionnaire. Polymerase chain reaction (PCR) was used for genotyping the APOA2–265 T > C. Biochemical indises containing leptin, ghrelin, total cholesterol (Bailey et al., J Clin Invest 97:1147–1453, 1996), low-density lipoprotein cholestrol (LDL-C), high-density lipoprotein cholestrol (HDL-C), triglyceride (TG), superoxide dismutase (SOD), high sensitivy C-reactive protein (hs-CRP), total antioxidant capacity (TAC), pentraxin-3 (PTX3), prostaglandin F2α (PGF2α) and interleukin 18 (IL18) were measured by standard method. Atherogenic indices (AIP, AC, CR-I, CR-II) were calculated. The gene-diet interactions were evaluated using an GLM. The frequency overall prevalence of rs5082 genotypes was 63.82 and 36.17% for T-allele and C-allele respectively. TG, Ghrelin, and hs-CRP concentrations were significantly higher among carriers with C allele than TT homozygotes. However, TC/CC genotypes have lower PTX3 than TT homozygotes (P

Eloy A Zepeda-Carrillo,1,2,&ast; Omar Ramos-Lopez,3 Erika Martínez-López,4 Elisa Barrón-Cabrera,5 J Antonio Bernal-Pérez,6 Luisa E Velasco-González,6 Ernesto Rangel-Rios,6 J Fausto Bustamante Martínez,2 Rafael Torres-Valadez1,7,&ast; 1Specialized Unit in Research, Development and Innovation in Genomic Medicine, Nayarit Center for Innovation and Technology Transfer, Autonomous University of Nayarit, Tepic, Nayarit, Mexico; 2Civil Hospital “Dr. Antonio González Guevara”, Health Services in Nayarit, Tepic, Nayarit, Mexico; 3Medicine and Psychology School, Autonomous University of Baja California, Tijuana, B.C, Mexico; 4Institute of Translational Nutrigenetics and Nutrigenomics, Department of Molecular and Genomic Biology, University Center of Health Sciences, University of Guadalajara, Guadalajara, Jalisco, Mexico; 5Faculty of Nutrition and Gastronomy Sciences, Autonomous University of Sinaloa, Culiacan, Sinaloa, Mexico; 6Family Medicine Unit No. 24 “Ignacio García Téllez”, Mexican Social Security Institute, Tepic, Nayarit, Mexico; 7Integral Health Academic Unit, Autonomous University of Nayarit, Tepic, Nayarit, Mexico&ast;These authors contributed equally to this workCorrespondence: Rafael Torres-Valadez, Nayarit Center for Innovation and Technology Transfer, Autonomous University of Nayarit, Tepic, Nayarit, Mexico, Tel +52-3312523644, Email rafael.torres@uan.edu.mxPurpose: Differences in metformin effect on glycemic control in type 2 Diabetes (T2D) have been associated with diet, obesity, years since T2D diagnosis and genetic factors, such as the Met408Val (rs628031) SLC22A1/OCT1 gene polymorphism. This study aimed to analyze the effect of metformin and diet on glycemic control and its association with the Met408Val polymorphism in patients with T2D from western Mexico.Patients and Methods: A total of 240 T2D adult patients were enrolled in this cross-sectional study. Anti-hyperglycemic therapy, dietary intake, body composition and glycemic profile were recorded and the determination of genotypes of SLC22A1/OCT1 gene (rs628031) was performed using an allelic discrimination assay.Results: The type of metformin therapy was 47% monotherapy, 45% dual therapy (metformin+glibenclamide or metformin+insulin) and 8% triple therapy (metformin+glibenclamide+insulin). Individuals with metformin monotherapy had a higher glycemic control frequency (%HbA1c < 7.0) compared with the dual and triple treatment schemes (77% vs 35% and 15%, respectively; p< 0.001). Interestingly, a high potassium intake was documented in the three anti-hyperglycemic therapies and a lower intake of micronutrients, including calcium, magnesium, and zinc. An interaction was found between calcium intake and carriers of the risk allele A (408Val) with %HbA1c (P interaction=0.028), and potassium intake with the TyG index (P interaction=0.027). In addition, there was a positive correlation between calcium intake and %HbA1c (r=0.682; p=0.010), and potassium intake vs TyG index (r=0.593; p=0.033) in risk allele A (408Val) carriers with metformin monotherapy. Genotype frequencies were GG homozygotes (76.6%), GA heterozygotes (21.5%) and AA homozygotes (1.9%). The allele frequency was 87.4% for the ancestral allele G and 12.6% for the risk allele A.Conclusion: These findings suggest a differing effect of metformin on glycemic control regarding calcium and potassium intake and the Met408Val SLC22A1/OCT1 gene polymorphism in T2D patients.Keywords: nutrigenetic, pharmacogenetic, SLC22A1/OCT1 gene, gene-nutrient interactions, calcium intake, potassium intake

Background healthy dietary patterns have been associated with lower risk for age-related cognitive decline. However, little is known about the specific role of dietary fibre on cognitive decline in older adults. Objective this study aimed to examine the association between dietary fibre and cognitive decline in older adults and to assess the influence of genetic, lifestyle and clinical characteristics in this association. Design and participants the Invecchiare in Chianti, aging in the Chianti area study is a cohort study of community-dwelling older adults from Italy. Cognitive function, dietary and clinical data were collected at baseline and years 3, 6, 9 and 15. Our study comprised 848 participants aged ≥ 65 years (56% female) with 2,038 observations. Main outcome and measures cognitive decline was defined as a decrease ≥3 units in the Mini-Mental State Examination score during consecutive visits. Hazard ratios for cognitive decline were estimated using time-dependent Cox regression models. Results energy-adjusted fibre intake was not associated with cognitive decline during the 15-years follow-up (P  > 0.05). However, fibre intake showed a significant interaction with Apolipoprotein E (APOE) haplotype for cognitive decline (P  = 0.02). In participants with APOE-ɛ4 haplotype, an increase in 5 g/d of fibre intake was significantly associated with a 30% lower risk for cognitive decline. No association was observed in participants with APOE-ɛ2 and APOE-ɛ3 haplotypes. Conclusions and relevance dietary fibre intake was not associated with cognitive decline amongst older adults for 15 years of follow-up. Nonetheless, older subjects with APOE-ɛ4 haplotype may benefit from higher fibre intakes based on the reduced risk for cognitive decline in this high-risk group. [ABSTRACT FROM AUTHOR]

The progression of cardiometabolic diseases is determined by both genetic and environmental factors. Gene–diet interactions may therefore be important in modulating the risks of developing metabolic diseases. The objectives were to investigate the effect of the interaction between brain-derived neurotrophic factor (BDNF) Val66Met polymorphisms and dietary insulin index (DII) and dietary insulin load (DIL) on cardiometabolic markers among diabetic patients. In this cross-sectional study, blood samples were collected from 667 patients. DIL and DII were defined using a validated FFQ. Genotyping the BDNF Val66Met polymorphism was conducted by the PCR-Restriction fragment length polymorphism (RFLP) method. Interactions between dietary indices and gene variants were evaluated using a generalised linear model. PGF2a concentrations were significantly higher among Val homozygotes than Met-allele carrier. This study revealed that, compared with individuals with the Val/Val genotype, those with the Met/Val or Met/Met genotype had lower BMI (Pinteraction = 0·04), TAG (Pinteraction = 0·04), leptin (Pinteraction = 0·01), LDL (Pinteraction = 0·04) and total cholesterol (Pinteraction = 0·01) when they consumed diets higher on the DIL index. Moreover, the highest quartile of the DIL, compared with the lowest, showed increase in waist circumference (Pinteraction = 0·02) and LDL/HDL (Pinteraction = 0·04) for Val/Val homozygotes compared with Met-allele carriers. BDNF Val66Met variants may interact with DIL and DII, thus be involved in the development of cardiometabolic risk factors. If diabetic patients with Met alleles regulate dietary intakes, they have a protective opportunity to regulate their cardiometabolic markers. [ABSTRACT FROM AUTHOR]

This investigation with aimed the effect of APOA2–265 T > C polymorphism and dietary acid load (DAL) as either potential renal acid load (PRAL) and net endogenous acid production (NEAP) intake interaction on metabolic markers in type 2 diabetes mellitus (T2DM). In present cross-sectional study, 737 patients with T2DM (290 men and 447 women) were enlisted from diabetes centers in Tehran. The dietary intakes of all participants during the last year was acquired by a validated semi-quantitative food frequency (FFQ) questionnaire. Polymerase chain reaction (PCR) was used for genotyping the APOA2–265 T > C. Biochemical indises containing leptin, ghrelin, total cholesterol (Bailey et al., J Clin Invest 97:1147–1453, 1996), low-density lipoprotein cholestrol (LDL-C), high-density lipoprotein cholestrol (HDL-C), triglyceride (TG), superoxide dismutase (SOD), high sensitivy C-reactive protein (hs-CRP), total antioxidant capacity (TAC), pentraxin-3 (PTX3), prostaglandin F2α (PGF2α) and interleukin 18 (IL18) were measured by standard method. Atherogenic indices (AIP, AC, CR-I, CR-II) were calculated. The gene-diet interactions were evaluated using an GLM. The frequency overall prevalence of rs5082 genotypes was 63.82 and 36.17% for T-allele and C-allele respectively. TG, Ghrelin, and hs-CRP concentrations were significantly higher among carriers with C allele than TT homozygotes. However, TC/CC genotypes have lower PTX3 than TT homozygotes (P < 0.05). C-allele carriers had highest mean of BMI (PNEAP=0.04, PPRAL = 0.006), WC (PNEAP=0.04, PPRAL = 0.04), TC (PNEAP=0.03, PPRAL = 0.01), ghrelin (PNEAP=0.01, PPRAL = 0.04), and leptin (PNEAP=0.04, PPRAL = 0.03) when placed in top tertiles of NEAP and PRAL.BMI, WC, TC, ghrelin, and leptin levels may be modified in C carriers by decreasing DAL, though, further investigations are required to confirm these findings. [ABSTRACT FROM AUTHOR]

Objective: Nutrition is one of the most important factors today in prevention and maintaining health, as well as in treatment of diseases. Despite many efforts, the challenges related to nutrition are becoming more and more common every day. Persian medicine is one of the oldest medical approaches in the world, and nutrition has a special and fundamental place in this medical thought. So much so, that a large portion of Persian medicine is related to nutrition. Individualized nutrition in Persian medicine based on temperament (Mizaj) is well in correspondence today with the topic of nutrigenomics or nutrigenetic, or epigenetic, and strongly proposes a unique model of nutrition in a strategic way. This study focuses to describe the importance of nutrition based on individualized temperament from the perspective of Persian medicine and the findings of modern one. Materials and Methods: This study is a narrative literature review using keywords including Persian medicine, Traditional Persian medicine, temperament (Mizaj), nutrition, individualized nutrition, individualized medicine, precision nutrition, functional food, bioactive food, nutrigenomics, nutrigenetic, epigenetic, and TEF, in Persian and English were used to explore related articles in databases such as Pub Med and also using Google Scholar, without any time constraints. Extracted articles were carefully studied. Also, Persian medicine books and conventional medicine ones were studied. The relevant content were collected, reviewed and the results were written in the form of individualized nutrition, based on temperament. Findings: According to the principles of Persian medicine, the temperament of every healthy person is based on a balanced and specific range. Maintaining this range and its balance is cornerstone to a healthy person. On the other hand, and from view point of Persian medicine, all foods and drinks have their own temperament too. A review of modern scientific sources also shows that these topics have been considered by common medical science and in these sources, topics such as individualized nutrition and individualized medicine along with topics such as nutrigenomics, epigenetic, and nutrigenetic have been addressed. Also, the discussion about the quality of the effect of foods on the body of people, which has been presented in the form of functional food, is in accordance with the statements of Persian medical scholars about possession of different temperaments for foods. Conclusion: Findings of this article strongly suggests that, what current medicine emphasizes today on individualized nutrition that is essential to promote human health, which is known in the traditional Persian medicine, as personal temperament. Thus combination of traditional Persian medicine recommendations (in the form of holistic medicine), and modern medical science recommendations (in the form of analytic medicine), is essential to accelerate developments in the medical sciences. [ABSTRACT FROM AUTHOR]

Background: We examined the influence of superoxide dismutase 3 (SOD3) Arg213Gly and Peroxisome Proliferator-Activated α-Receptor (PPARα) 7G/C polymorphisms to a single dose of purple grape juice supplementation on time-to-exhaustion running test, redox balance and muscle damage in recreational runners. Methods: Forty-seven male recreational runners performed a running test until exhaustion after supplementation with grape juice or a control drink. Serum total antioxidant capacity (TAC), malondialdehyde (MDA), plasma nitrite (NO), creatine kinase (CK) and lactate dehydrogenase (LDH) were measured pre and post exercise. Also, polymorphisms were analyzed in DNA extracted from the oral mucosa. Results: Grape juice improved the time-to-exhaustion. When analyzed by genotype, the recreational runners with GG+CG genotypes of the SOD3 gene had greater time-to-exhaustion than the CC genotype, but was no different for the PAPRα gene. A slight difference was noted in TAC, since the CC genotype of the SOD3 gene showed higher TAC values in the post-exercise compared to the baseline and with pre-exercise, but these values did not increase compared to the CG+GG group, respectively. The SOD3 and PPARα genes were similar at all times for the other biochemical variables. Conclusion: The ergogenic effect of grape juice was genotype-dependent for SOD3 Arg213Gly. However, biochemical redox balance markers did not explain this difference. [ABSTRACT FROM AUTHOR]

Increasing evidence on the significance of nutrition in reproduction is emerging from both animal and human studies, suggesting a mutual association between nutrition and female fertility. Different "fertile" dietary patterns have been studied; however, in humans, conflicting results or weak correlations are often reported, probably because of the individual variations in genome, proteome, metabolome, and microbiome and the extent of exposure to different environmental conditions. In this scenario, "precision nutrition", namely personalized dietary patterns based on deep phenotyping and on metabolomics, microbiome, and nutrigenetics of each case, might be more efficient for infertile patients than applying a generic nutritional approach. In this review, we report on new insights into the nutritional management of infertile patients, discussing the main nutrigenetic, nutrigenomic, and microbiomic aspects that should be investigated to achieve effective personalized nutritional interventions. Specifically, we will focus on the management of low-grade chronic inflammation, which is associated with several infertility-related diseases. [ABSTRACT FROM AUTHOR]

Maternal nutrition during pregnancy influences postnatal life of animals; nevertheless, few studies have investigated its effects on the productive performance and reproductive development of heifers. This study evaluated the performance, reproductive development, and correlation between reproduction × fat thickness and performance × ribeye area (REA) traits of heifers. We also performed an exploratory genomic association during the rearing period in heifers submitted to fetal programming. The study comprised 55 Nellore heifers born to dams exposed to one of the following nutritional planes: control, without protein-energy supplementation; PELT, protein-energy last trimester, protein-energy supplementation offered in the final third of pregnancy; and PEWG, protein-energy whole gestation, protein-energy supplementation upon pregnancy confirmation. Protein-energy supplementation occurred at the level of 0.3% live weight. After weaning, heifers were submitted to periodic evaluations of weight and body composition by ultrasonography. From 12 to 18 months, we evaluated the reproductive tract of heifers to monitor its development for sexual precocity and ovarian follicle population. The treatments had no effect (p > 0.05) on average daily gain; however, the weight of the animals showed a significant difference over time (p = 0.017). No differences were found between treatments for REA, backfat, and rump fat thickness, nor for puberty age, antral follicular count, and other traits related to reproductive tract development (p > 0.05). The correlation analysis between performance traits and REA showed high correlations (r > 0.37) between REA at weaning and year versus weight from weaning until yearling; however, no correlation was found for reproductive development traits versus fat thickness (p > 0.05). The exploratory genomic association study showed one single-nucleotide polymorphism (SNP) for each treatment on an intergenic region for control and PEWG, and the one for PELT on an intronic region of RAPGEF1 gene. Maternal nutrition affected only the weight of the animals throughout the rearing period. [ABSTRACT FROM AUTHOR]

Maternal nutrition during pregnancy influences postnatal life of animals; nevertheless, few studies have investigated its effects on the productive performance and reproductive development of heifers. This study evaluated the performance, reproductive development, and correlation between reproduction × fat thickness and performance × ribeye area (REA) traits of heifers. We also performed an exploratory genomic association during the rearing period in heifers submitted to fetal programming. The study comprised 55 Nellore heifers born to dams exposed to one of the following nutritional planes: control, without protein-energy supplementation; PELT, protein-energy last trimester, protein-energy supplementation offered in the final third of pregnancy; and PEWG, protein-energy whole gestation, protein-energy supplementation upon pregnancy confirmation. Protein-energy supplementation occurred at the level of 0.3% live weight. After weaning, heifers were submitted to periodic evaluations of weight and body composition by ultrasonography. From 12 to 18 months, we evaluated the reproductive tract of heifers to monitor its development for sexual precocity and ovarian follicle population. The treatments had no effect (p > 0.05) on average daily gain; however, the weight of the animals showed a significant difference over time (p = 0.017). No differences were found between treatments for REA, backfat, and rump fat thickness, nor for puberty age, antral follicular count, and other traits related to reproductive tract development (p > 0.05). The correlation analysis between performance traits and REA showed high correlations (r > 0.37) between REA at weaning and year versus weight from weaning until yearling; however, no correlation was found for reproductive development traits versus fat thickness (p > 0.05). The exploratory genomic association study showed one single-nucleotide polymorphism (SNP) for each treatment on an intergenic region for control and PEWG, and the one for PELT on an intronic region of RAPGEF1 gene. Maternal nutrition affected only the weight of the animals throughout the rearing period.

Metabolic Syndrome (MetS) is a complex condition associated with cardiovascular risk factors and diabetes. The weight gain, especially the accumulation of central adipose tissue, may be the first leading cause of the MetS. It is important to highlight that the lifestyle choices considered as modifiable risk factors contribute to the increase in the incidence of the MetS in the population, such as sedentarism and food intake. There is evidence in the literature concerning the benefits associated with the Mediterranean diet, which is rich in polyphenols. Therefore, the flavonoids are a class of non-nutrient that can be extensively studied mainly to elucidate the mechanisms related to the action of these compounds in the modulation of the microbiota, DNA methylation and health improvement. Thus, this review summarized evidence linking flavonoid intake to obesity, insulin resistance, T2DM and cardiovascular diseases.

Summary Objective Genetics contribute to variability in individual response to weight‐loss interventions. The objective of this study was to determine the efficacy of a commercially available exercise and weight‐loss program and whether alignment of diet to genotype related to lipid metabolism promotes greater success. Design Sedentary women with obesity (n = 63) had genotype (FABP2rs1799883, PPARG2rs1801282, ADRB3rs4994C3, ADRB2rs1042713, rs1042714) determined using a direct‐to‐consumer genetic screening kit purported to promote greater weight‐loss success through dietary recommendations based on these genes. Participants were randomly assigned to follow a moderate carbohydrate (MC) or lower carbohydrate (LC) hypo‐energetic diet that aligned (A) or did not align (NA) with genotype for 24 weeks while participating in a resistance training and walking program. Data were analysed by general linear model repeated measures adjusted for baseline variables and are presented as mean (95% confidence interval) changes from baseline. Results Participants in the LC group experienced greater improvements (p = 0.051, ηp2 = 0.025) in per cent changes in body composition (weight: MC −3.32 [−1.4, −5.2], LC −5.82 [−4.1, −7.6]; fat mass: MC −7.25 [−3.2, −11.2], LC −10.93 [−7.3, −14.5]; fat‐free mass: MC −0.32 [1.4, −2.0], LC −1.48 [0.7, −3.0]; and body fat percentage: MC −4.19 [−1.6, −6.8], LC −5.60 [−3.3, −7.9] %). No significant differences were observed between genotype groups (weight: A −5.00 [−3.3, −6.7], NA −4.14 [−2.2, −6.1]; fat mass: A −10.15 [−7.0, −13.6], NA −8.02 [−4.0, −12.0]; fat‐free mass: A −1.23 [0.3, −2.8], NA −0.56 [1.12, −2.3]; and body fat: A −5.28 [−3.0, −7.6], NA −4.51 [−1.9, −7.1] %). Conclusions Adherence to this exercise and weight‐loss program promoted improvements in body composition and health outcomes. While individuals following the LC diet experienced greater benefits, alignment of these diets to this genetic profile did not promote greater health outcomes.

Purpose: The interactions between lifestyle and genetic factors play an important role in obesity development. Mutations in melanocortin-4-receptor (MC4R) gene are one of the most common cause of monogenic obesity, however, the functional effects of polymorphic variants near MC4R gene in general populations remain uncertain. The aim of our study was to analyze whether the common single nucleotide polymorphisms (SNPs) of MC4R gene influence the food preferences, physical activity, body fat content and distribution, as well as fasting and postprandial energy expenditure and substrates utilization. Methods: We genotyped previously identified MC4R SNPs: rs17782313, rs633265, rs1350341, rs12970134 in 927 subjects, who underwent anthropometric, total body fat content, visceral (VAT) and subcutaneous adipose tissue (SAT) measurements, and daily physical activity and dietary intake analysis. In randomly selected 47 subjects the energy expenditure, carbohydrate and lipid utilizations were evaluated in fasting state and after high-carbohydrate and control meals intake. Results: We found the significant associations between studied SNPs of MC4R gene and VAT and VAT/SAT ratio. Moreover, the GG genotype carriers of rs1350341, who had the lowest VAT accumulation (p = 0.012), presented higher relative increase in postprandial carbohydrate utilization (p = 0.013, p = 0.024). Conclusions: We have observed that common SNPs of the MC4R gene influence the body fat content and distribution, as well as relative increase in postprandial carbohydrate utilization. We believe that our study may help to understand better the impact of MC4R gene on obesity development, and to help to provide personalized prevention/treatment strategies to fight against obesity and its metabolic consequences. [ABSTRACT FROM AUTHOR]

Summary: Objective: Genetics contribute to variability in individual response to weight‐loss interventions. The objective of this study was to determine the efficacy of a commercially available exercise and weight‐loss program and whether alignment of diet to genotype related to lipid metabolism promotes greater success. Design Sedentary women with obesity (n = 63) had genotype (FABP2rs1799883, PPARG2rs1801282, ADRB3rs4994C3, ADRB2rs1042713, rs1042714) determined using a direct‐to‐consumer genetic screening kit purported to promote greater weight‐loss success through dietary recommendations based on these genes. Participants were randomly assigned to follow a moderate carbohydrate (MC) or lower carbohydrate (LC) hypo‐energetic diet that aligned (A) or did not align (NA) with genotype for 24 weeks while participating in a resistance training and walking program. Data were analysed by general linear model repeated measures adjusted for baseline variables and are presented as mean (95% confidence interval) changes from baseline. Results: Participants in the LC group experienced greater improvements (p = 0.051, ηp2 = 0.025) in per cent changes in body composition (weight: MC −3.32 [−1.4, −5.2], LC −5.82 [−4.1, −7.6]; fat mass: MC −7.25 [−3.2, −11.2], LC −10.93 [−7.3, −14.5]; fat‐free mass: MC −0.32 [1.4, −2.0], LC −1.48 [0.7, −3.0]; and body fat percentage: MC −4.19 [−1.6, −6.8], LC −5.60 [−3.3, −7.9] %). No significant differences were observed between genotype groups (weight: A −5.00 [−3.3, −6.7], NA −4.14 [−2.2, −6.1]; fat mass: A −10.15 [−7.0, −13.6], NA −8.02 [−4.0, −12.0]; fat‐free mass: A −1.23 [0.3, −2.8], NA −0.56 [1.12, −2.3]; and body fat: A −5.28 [−3.0, −7.6], NA −4.51 [−1.9, −7.1] %). Conclusions: Adherence to this exercise and weight‐loss program promoted improvements in body composition and health outcomes. While individuals following the LC diet experienced greater benefits, alignment of these diets to this genetic profile did not promote greater health outcomes. [ABSTRACT FROM AUTHOR]

Objective Leptin is an adipokine released mainly by adipose tissue, with many functions including regulation of energy balance. However, little is known about the effect of LEPR polymorphism on orexigenic and anorexigenic neuropeptides. Thus, the aim of the present study is to verify the influence of LEPR polymorphism (rs2767485) on serum orexigenic (NPY, MCH and AgRP) and anorexigenic (Leptin and α-MSH) neuropeptides levels among obese adolescents submitted to 1 year of multicomponent weight loss therapy. Methods Seventy-six adolescents with obesity were enrolled in 1 year of weight loss therapy including clinical, nutritional, psychological and exercise-related. Blood samples were collected to analyze neuropeptides (NPY, MCH, AgRP and leptin) and LEPR genotyping. Visceral fat was measured by ultrasound and body composition was measured by plethysmography. The parameters were measured at baseline and after one year. Adolescents were grouped according to genotype (TT or CT + CC group). Effect of the weight loss therapy was analyzed through ANOVA and Wilcox, according to normality. Statistic value was set at < 0.05. Results C-allele carriers have the orexigenic neuropeptides (NPY, AgRP and MCH) levels statistically higher when compared with TT group, at baseline. Furthermore, TT group seems to respond better to the therapy by a greater delta on BMI. Indeed, the data suggest a concomitant increased of AgRP levels in CT + CC genotypes, after weight loss therapy. Conclusion Both groups responded to the weight loss intervention, however wildtypes (TT) appear to respond to the intervention most optimally with C carries, where post intervention reduction in BMI was significantly greater in wildtypes. The leptin receptor polymorphism seems to affect neuroendocrine regulation of energy balance among adolescents with obesity. [ABSTRACT FROM AUTHOR]

Consistent evidence from both experimental and human studies indicates that Type 2 diabetes mellitus (T2DM) is a complex disease resulting from the interaction of genetic, epigenetic, environmental, and lifestyle factors. Nutrients and dietary patterns are important environmental factors to consider in the prevention, development and treatment of this disease. Nutritional genomics focuses on the interaction between bioactive food components and the genome and includes studies of nutrigenetics, nutrigenomics and epigenetic modifications caused by nutrients. There is evidence supporting the existence of nutrient-gene and T2DM interactions coming from animal studies and family-based intervention studies. Moreover, many case-control, cohort, cross-sectional cohort studies and clinical trials have identified relationships between individual genetic load, diet and T2DM. Some of these studies were on a large scale. In addition, studies with animal models and human observational studies, in different countries over periods of time, support a causative relationship between adverse nutritional conditions during in utero development, persistent epigenetic changes and T2DM. This review provides comprehensive information on the current state of nutrient-gene interactions and their role in T2DM pathogenesis, the relationship between individual genetic load and diet, and the importance of epigenetic factors in influencing gene expression and defining the individual risk of T2DM. [ABSTRACT FROM AUTHOR]

It is known that our physiology changes throughout the day and that several physiological hormones display circadian rhythmicity. The alteration of this normal pattern is called chronodisruption (CD). In recent years, it has been demonstrated that CD is related to obesity. Although several factors may be causing CD, one important aspect to consider is the failure in our internal clock. Indeed, studies performed in mutant animals have demonstrated that mutations in clock genes are related to obesity. In human subjects, mutations are rare (<1 % of the population). Nevertheless, it is rather common to have genetic variations in one SNP, which underlie differences in our vulnerability to disease. Several SNP in clock genes are related to obesity and weight loss. Taking into account that genetics is behind CD, as has already been demonstrated in twins’ models, the question is: Are we predestinated? We will see along these lines that nutrigenetics and epigenetics answer: ‘No, we are not predestinated’. Through nutrigenetics we know that our behaviours may interact with our genes and may decrease the deleterious effect of one specific risk variant. From epigenetics the message is even more positive: it is demonstrated that by changing our behaviours we can change our genome. Herein, we propose modifying ‘what, how, and when we eat’ as an effective tool to decrease our genetic risk, and as a consequence to diminish CD and decrease obesity. This is a novel and very promising area in obesity prevention and treatment. [ABSTRACT FROM PUBLISHER]

The intake of tomatoes and tomato products, which constitute the main dietary source of the red pigment lycopene (LYC), has been associated with a reduced risk of prostate cancer and cardiovascular disease, suggesting a protective role of this carotenoid. However, LYC bioavailability displays high interindividual variability. This variability may lead to varying biological effects following LYC consumption. Based on recent results obtained with two other carotenoids, we assumed that this variability was due, at least in part, to several single nucleotide polymorphisms (SNPs) in genes involved in LYC and lipid metabolism. Thus, we aimed at identifying a combination of SNPs significantly associated with the variability in LYC bioavailability. In a postprandial study, 33 healthy male volunteers consumed a test meal containing 100 g tomato puree, which provided 9.7 mg all- trans LYC. LYC concentrations were measured in plasma chylomicrons (CM) isolated at regular time intervals over 8 h postprandially. For the study 1885 SNPs in 49 candidate genes, i.e., genes assumed to play a role in LYC bioavailability, were selected. Multivariate statistical analysis (partial least squares regression) was used to identify and validate the combination of SNPs most closely associated with postprandial CM LYC response. The postprandial CM LYC response to the meal was notably variable with a CV of 70%. A significant ( P =0.037) and validated partial least squares regression model, which included 28 SNPs in 16 genes, explained 72% of the variance in the postprandial CM LYC response. The postprandial CM LYC response was also positively correlated to fasting plasma LYC concentrations ( r =0.37, P <0.05). The ability to respond to LYC is explained, at least partly, by a combination of 28 SNPs in 16 genes. Interindividual variability in bioavailability apparently affects the long-term blood LYC status, which could ultimately modulate the biological response following LYC supplementation. [ABSTRACT FROM AUTHOR]

Nutritional genomics, defined as the study of reciprocal interactions among nutrients, metabolic intermediates, and the genome, along with other closely related nutritional -omic fields (eg, epigenomics, transcriptomics, and metabolomics) have become vital areas of nutrition study and knowledge. Utilizing results from human metabolic research on the essential nutrient choline, this article illustrates how nutrigenetic, nutrigenomic, and inter-related -omic research has provided new insights into choline metabolism and its effect on physiologic processes. Findings from highlighted choline research are also discussed in the context of translation to clinical and public health nutrition applications. Overall, this article underscores the utility of -omic research methods in elucidating nutrient metabolism as well as the potential for nutritional -omic concepts and discoveries to be broadly applied in nutritional practice. [ABSTRACT FROM AUTHOR]

Conjugated linoleic acids (CLAs) are natural PPARγ ligands, which showed conflicting effects on metabolism in humans. We examined metabolic effects of different isomers of CLA in subjects with PPARγ2 Pro12Ala polymorphisms. A total of 35 men underwent four intervention periods in a crossover study design: subjects with either genotypes received c9, t11 CLA or t10, c12 CLA, a commercially available 1:1 mix of both isomers or reference oil (linoleic acid (LA)). Adipocytokines, insulin, glucose and triglycerides were assessed in the fasting state and after a standardized mixed meal. Across all genotypes, there was a significant ( p = 0.025) CLA treatment effect upon postprandial (pp) HOMA-IR values, with c9, t11 CLA and CLA isomer mix improving, but t10, c12 CLA isomer worsening. In Ala12Ala subjects, the t10, c12 isomer caused weight gain ( p = 0.03) and tended to increase postprandial insulin levels ( p = 0.05). In Pro12Pro subjects, t10, c12 resulted in reduction in waist circumference ( p = 0.03). The comparison of the different genotype groups revealed statistically different changes in fasting and postprandial insulin, HOMA-IR and leptin after intervention. c9, t11 CLA and the commercial CLA mix showed beneficial effects on insulin sensitivity compared with LA, while t10, c12 CLA adversely affects body weight and insulin sensitivity in different PPAR genotypes. CLA isomers have different effects on metabolism in Ala and Pro carriers. [ABSTRACT FROM AUTHOR]

Epidemiological nutrition research has established the correlation between dietary intake and chronic diseases. Today, several years after the mapping of the human genome, vast amounts of knowledge generated from genetics and health research have prompted a new evolutionary field in nutrition: nutrigenetics and nutrigenomics. Much is being revealed about the way genes affect dietary intake (nutrigenetics) and how foods influence one’s genetics (nutrigenomics). This article looks at this new “frontier” in nutrition science. [ABSTRACT FROM AUTHOR]

• Flavonoids intake modulate positively the oxidative, glucose and lipid metabolisms. • Flavonoids may exert regulatory effects on gene expression in metabolic disorders. • Health benefits of flavonoids depend of their bioaccessibility and bioavailability. • Flavonoids or their metabolites modulate the composition of the gut microbiota. Metabolic Syndrome (MetS) is a complex condition associated with cardiovascular risk factors and diabetes. The weight gain, especially the accumulation of central adipose tissue, may be the first leading cause of the MetS. It is important to highlight that the lifestyle choices considered as modifiable risk factors contribute to the increase in the incidence of the MetS in the population, such as sedentarism and food intake. There is evidence in the literature concerning the benefits associated with the Mediterranean diet, which is rich in polyphenols. Therefore, the flavonoids are a class of non-nutrient that can be extensively studied mainly to elucidate the mechanisms related to the action of these compounds in the modulation of the microbiota, DNA methylation and health improvement. Thus, this review summarized evidence linking flavonoid intake to obesity, insulin resistance, T2DM and cardiovascular diseases. [ABSTRACT FROM AUTHOR]

(1) Background: Eating is fundamental to survival. Animals choose when to eat depending on food availability. The timing of eating can synchronize different organs and tissues that are related to food digestion, absorption, or metabolism, such as the stomach, gut, liver, pancreas, or adipose tissue. Studies performed in experimental animal models suggest that food intake is a major external synchronizer of peripheral clocks. Therefore, the timing of eating may be decisive in fat accumulation and mobilization and affect the effectiveness of weight loss treatments. (2) Results: We will review multiple studies about the timing of the three main meals of the day, breakfast, lunch and dinner, and its potential impact on metabolism, glucose tolerance, and obesity-related factors. We will also delve into several mechanisms that may be implicated in the obesogenic effect of eating late. Conclusion: Unusual eating time can produce a disruption in the circadian system that might lead to unhealthy consequences. [ABSTRACT FROM AUTHOR]

Human nutrition is a branch of medicine based on foods biochemical interactions with the human body. The phenotypic transition from health to disease status can be attributed to changes in genes and/or protein expression. For this reason, a new discipline has been developed called "-omic science". In this review, we analyzed the role of "-omics sciences" (nutrigenetics, nutrigenomics, proteomics and metabolomics) in the health status and as possible therapeutic tool in chronic degenerative diseases. In particular, we focused on the role of nutrigenetics and the relationship between eating habits, changes in the DNA sequence and the onset of nutrition-related diseases. Moreover, we examined nutrigenomics and the effect of nutrients on gene expression. We perused the role of proteomics and metabolomics in personalized nutrition. In this scenario, we analyzed also how dysbiosis of gut microbiota can influence the onset and progression of chronic degenerative diseases. Moreover, nutrients influencing and regulating gene activity, both directly and indirectly, paves the way for personalized nutrition that plays a key role in the prevention and treatment of chronic degenerative diseases. [ABSTRACT FROM AUTHOR]