Journal of Nutrigenetics and Nutrigenomics最新文献

Background/aim: Amaranth is a source of several bioactive compounds, among which peptides with inhibitory activity upon dipeptidyl peptidase IV (DPP-IV) have been reported. However, there is no information about the action of amaranth DPP-IV-inhibitory peptides using in vivo models. The aim of this work was to evaluate the effect of amaranth consumption on plasma and kidney DPP-IV activity as well the changes in plasma proteome profile of streptozotocin (STZ)-induced hyperglycemic rats.

Methods: Rats were fed for 12 weeks with a diet containing 20% popped amaranth grain. Kidneys and blood samples were collected for lipid profile, DPP-IV activity and expression, and proteomic analysis.

Results: Total cholesterol and DPP-IV activity in plasma was increased in hyperglycemic rats, but this effect was reverted by amaranth consumption. Triacylglycerols were increased in the hyperglycemic group fed amaranth, and the highest levels of high-density lipoproteins were also observed in this group. These data correlated with the accumulation of apolipoprotein A-II in plasma. Accumulation of the antioxidant protein paraoxonase/arylesterase 1 in STZ-induced hyperglycemic rats was observed when amaranth was supplied in the diet.

Conclusion: This study provides new insights into the molecular mechanisms by which amaranth exerts its beneficial health action in a hyperglycemic state.

Background/aims: Picky eating is prevalent among preschoolers and is associated with risk of both underweight and overweight. Although differences in taste perception may be due to genetic variation, it is unclear whether these variations are related to picky eating behavior. The aim of this study was to investigate the association of 6 single nucleotide polymorphisms (SNPs) in 5 candidate genes related to chemosensory perception with picky eating behavior and adiposity in a cohort of preschool-aged children.

Methods: Parents of 2- to 5-year-old non-Hispanic white preschoolers (n = 153) responded to survey questions on demographics, and information regarding their child's breastfeeding history and picky eating behavior. Height and weight were measured to calculate body mass index (BMI) z-scores using standard growth charts, and saliva was collected for genotyping. Generalized linear models were used to examine associations between picky eating behavior and BMI z-scores with genetic variation.

Results: When controlling for child age, sex, breastfed status, and parent education level, SNPs in TAS2R38 (rs713598) and CA6 (rs2274327) were associated with picky eating behavior in children. There was no association between SNPs and BMI z-scores.

Conclusion: Genes related to chemosensory perception may play a role in children's picky eating behavior.

Background/aims: It is possible that carnosinase (CNDP1) and cellular nonspecific dipeptidase (CNDP2) have important roles in protecting cells and tissues against the damage of oxidative stress. Oxidative stress and subsequent inflammation are key factors in the development of common chronic metabolic diseases, such as obesity. We aimed to investigate the combined effects of genetic variations in CNDP1 and CNDP2 and dietary carbohydrate and carotene intake on obesity risk.

Methods: A total of 1,059 Japanese men were randomly selected from participants who visited a medical center for routine medical checkups. We analyzed the relationships between the genotypes of 4 single-nucleotide polymorphisms (SNPs) (rs12605520, rs7244647, rs4891558, and rs17089368) in the CNDP1/CNDP2 locus and body mass index or prevalence of obesity/overweight taking into account dietary carbohydrate and carotene intake.

Results: We found that 2 SNPs (rs7244647 in CNDP1 and rs4891558 in CNDP2) were associated with obesity risk. In addition, these associations were observed only in the group with high carbohydrate and low carotene intake but not in the group with low carbohydrate and high carotene intake.

Conclusions: Our findings indicate that the combination of genetic variations in CNDP1 and CNDP2 and dietary carbohydrate/carotene intake modulate obesity risk.

Background: Numerous studies have reported on the influence of diet on insulin resistance. Our study provides insight into the effect of germinated brown rice (GBR) and γ-aminobutyric acid (GABA) on early environment-driven programming and susceptibility to insulin resistance in rat offspring.

Methods: Male rat offspring from female Sprague-Dawley rats fed with a high-fat diet (HFD) alone, HFD + GBR, or HFD + GABA extract throughout pregnancy and lactation were weaned 4 weeks after delivery and followed up for 8 weeks. A biochemical analysis and an assessment of the hepatic expression of insulin signaling genes were performed.

Results: The results showed that intrauterine exposure to HFD caused metabolic perturbations in rat offspring which gravitated towards insulin resistance even though the rat offspring did not consume an HFD. GBR and GABA attenuated the HFD-induced changes by underlying regulation of the insulin signaling genes.

Conclusions: The results suggest that intake of GBR and GABA during pregnancy and lactation can influence the programming of genes in rat offspring, thereby enhancing insulin sensitivity.

Aims: The objective of this study was to determine whether vitamin D and genistein supplementation had an additive beneficial effect on levels of vitamin D and bone markers and whether this effect was mediated by genes regulating isoflavone metabolism.

Materials and methods: We carried out a prospective study in postmenopausal women randomized to calcium and vitamin D supplementation or calcium, vitamin D, and genistein supplementation. Vitamin D, parathyroid hormone (PTH), cross-linked C-telopeptide (CTX), and procollagen 1 N-terminal (P1NP) were determined by electrochemiluminescence. Three SNPs - rs2231142 (ABCG2), rs358231 (cytosolic β-glucosidase [CBG]), and rs2273697 (ABCC2) - were determined.

Results: We included 102 women. The effects on bone remodeling were similar: rises in vitamin D were significantly associated with reductions in PTH, CTX, and P1NP. Pharmacogenomic analysis of the genotypes showed that, in AT heterozygotes of the CBG1368T>A polymorphism, CTX and P1NP were not reduced.

Conclusion: Genistein added to calcium and vitamin D supplementation had no additional effect. The supplementation of individual AT heterozygotes of the CBG1368T>A polymorphism had no effect on markers of bone remodeling.

Background and aims: ApaI, FokI, TaqI, and BsmI polymorphisms in the vitamin D receptor (VDR) gene have been reported to be associated with the risk of coronary artery disease (CAD), although the results of previous studies have been inconsistent. The aim of this study was to explore whether these polymorphisms play a role in the genetic susceptibility to CAD.

Methods: A comprehensive search of Medline and Embase databases was conducted for studies evaluating the association between the VDR polymorphisms and CAD risk. Odds ratios with 95% confidence intervals were calculated to assess the strength of association in the dominant model, recessive model, allelic model, and genotypes contrast.

Results: Nine studies involving a total of 5,259 cases and 1,981 controls were finally included in this meta-analysis. Overall, no significant associations were found between ApaI, FokI, TaqI, and BsmI polymorphisms and the risk of CAD in any of the genetic models (all p ˃ 0.05). Moreover, a subgroup analysis by ethnicity did not reveal a significant relationship between any of the examined polymorphisms and CAD risk in Caucasians and East-Asians for any model (all p ˃ 0.05).

Conclusion: Current evidence suggests that the ApaI, FokI, TaqI, and BsmI polymorphisms of the VDR gene might not be associated with genetic susceptibility to CAD. Further well-designed studies with large sample sizes are needed to confirm our results.

Background: The role of brain-derived neurotrophic factor (BDNF) variants on change in body weight and cardiovascular risk factors after weight loss remains unclear in obese patients.

Objective: Our aim was to analyze the effects of the rs10767664 BDNF gene polymorphism on body weight, cardiovascular risk factors, and serum adipokine levels after a high monounsaturated fatty acids (MUFAs) hypocaloric diet (diet M) versus a high polyunsaturated fatty acids (PUFAs) hypocaloric diet (diet P).

Methods: A Caucasian population of 361 obese patients was enrolled. Subjects who met the inclusion criteria were randomly allocated to one of two diets for a period of 3 months.

Results: Two hundred and sixteen subjects (59.8%) had the genotype AA (wild-type group), and 145 (40.2%) patients had the genotypes AT (122 patients, 33.8%) or TT (23 patients, 6.4%) (mutant-type group). After weight loss with diet P and diet M and in both genotype groups, body mass index, weight, fat mass, waist circumference, systolic blood pressure, serum leptin levels, low-density lipoprotein cholesterol, and total cholesterol decreased in a significant way. Secondary to weight loss with diet M and only in the wild-type group, insulin levels (-2.1 ± 2.0 vs. -0.7 ± 2.9 IU/L, p < 0.05) and homeostatic model assessment of insulin resistance (-0.7 ± 0.9 vs. -0.3 ± 1.0 U, p < 0.05) decreased.

Conclusion: Our data show that the rs10767664 variant of the BDNF gene modifies insulin resistance and insulin levels after weight loss with a hypocaloric diet enriched with MUFAs.

Diversity in the genetic profile between individuals and specific ethnic groups affects nutrient requirements, metabolism and response to nutritional and dietary interventions. Indeed, individuals respond differently to lifestyle interventions (diet, physical activity, smoking, etc.). The sequencing of the human genome and subsequent increased knowledge regarding human genetic variation is contributing to the emergence of personalized nutrition. These advances in genetic science are raising numerous questions regarding the mode that precision nutrition can contribute solutions to emerging problems in public health, by reducing the risk and prevalence of nutrition-related diseases. Current views on personalized nutrition encompass omics technologies (nutrigenomics, transcriptomics, epigenomics, foodomics, metabolomics, metagenomics, etc.), functional food development and challenges related to legal and ethical aspects, application in clinical practice, and population scope, in terms of guidelines and epidemiological factors. In this context, precision nutrition can be considered as occurring at three levels: (1) conventional nutrition based on general guidelines for population groups by age, gender and social determinants; (2) individualized nutrition that adds phenotypic information about the person's current nutritional status (e.g. anthropometry, biochemical and metabolic analysis, physical activity, among others), and (3) genotype-directed nutrition based on rare or common gene variation. Research and appropriate translation into medical practice and dietary recommendations must be based on a solid foundation of knowledge derived from studies on nutrigenetics and nutrigenomics. A scientific society, such as the International Society of Nutrigenetics/Nutrigenomics (ISNN), internationally devoted to the study of nutrigenetics/nutrigenomics, can indeed serve the commendable roles of (1) promoting science and favoring scientific communication and (2) permanently working as a 'clearing house' to prevent disqualifying logical jumps, correct or stop unwarranted claims, and prevent the creation of unwarranted expectations in patients and in the general public. In this statement, we are focusing on the scientific aspects of disciplines covering nutrigenetics and nutrigenomics issues. Genetic screening and the ethical, legal, social and economic aspects will be dealt with in subsequent statements of the Society.

Background: The effect of the rs10767664 variant of the brain-derived neurotrophic factor gene on weight loss after bariatric surgery has not been evaluated. We decided to investigate the role of the rs10767664 variant on outcomes after biliopancreatic diversion surgery.

Materials and methods: A sample of 90 patients with morbid obesity without diabetes mellitus was operated. Biochemical and anthropometric evaluation were realized at basal visit and at each visit during 3 years (at 1, 2 and 3 years).

Results: Initial percentage excess weight loss, body mass index, weight, waist circumference, fat mass, blood pressure, low-density lipoprotein cholesterol, total cholesterol, triglyceride levels, insulin and homeostasis model assessment for insulin resistance (HOMA-IR) improved. No differences in these changes were detected between the two genotypes (wild-type group AA vs. mutant group AT plus TT) in a dominant model. The improvement of insulin levels was lower in T-allele carriers than non-T-allele carriers (-2.8 ± 0.7 vs. -7.1 ± 0.9 UI/dl; p = 0.02). The decrease of fasting glucose (-13.4 ± 7.4 vs. -24.2 ± 5.2 mg/dl; p = 0.01) and HOMA-IR (-1.1 ± 0.3 vs. -0.5 ± 0.4 units; p = 0.02) were lower in T-allele carriers than non-T-allele carriers.

Conclusion: Our data showed an association between the rs10767664 variant and metabolic response after weight loss. Non-T-allele carriers have a better improvement in glucose, insulin and HOMA-IR levels than T-allele carriers.

Background/aim: This study hypothesized an association between healthy dietary patterns, hypermethylation of the tumor necrosis factor-α (TNF-α) promoter and decreased risk of metabolic changes.

Methods: Forty normal-weight young women were involved in this cross-sectional study. DNA was isolated from white blood cells, and CpG site methylation in TNF-α was analyzed by Sequenom EpiTyper. The quality of the diet was assessed by Healthy Eating Index (HEI-2005).

Results: Contradicting our hypothesis, HEI-2005 score was negatively associated with CpG5 (r = -0.460, p = 0.003) and TNF-α total methylation (r = -0.355, p = 0.026). A higher intake of fruits was related to lower insulin, HOMA-IR, and TNF-α methylation. No other dietary pattern was related to TNF-α methylation. TNF-α total methylation correlated positively with systolic blood pressure (r = 0.323; p = 0.042) and CpG5 methylation with body mass index (r = 0.333, p = 0.036). Furthermore, fiber intake was negatively associated with the CpG5 (r = -0.324, p = 0.041) and TNF-α total methylation (r = -0.434, p = 0.005), whereas vitamin C intake was negatively associated with TNF-α total methylation (r = -0.411, p = 0.009). Intakes of apples and citrus fruits were negatively associated with TNF-α total methylation.

Conclusion: A healthy dietary pattern and higher fruit intake (particularly apples and citrus fruits) were related to better glucose tolerance in healthy subjects, which could be mediated by lower TNF-α methylation.