44 research outputs found
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The influence of one-carbon metabolism gene polymorphisms and gene-environment interactions on homocysteine, vitamin B12, folate and lipids in a Brazilian adolescent population
Background: Several single-nucleotide polymorphisms (SNPs) have been associated with the metabolism of Vitamin B12, folic acid, homocysteine and lipids. However, the interaction between SNPs involved in the one-carbon metabolism pathway and macronutrient intake on cardiovascular risk factors in the Brazilian population has not yet been investigated. Hence, the present study examined whether the association of ten SNPs involved in the one-carbon metabolism pathway with Vitamin B12, folic acid, homocysteine and lipid levels is modified by dietary factors and physical activity in adolescents with cardiovascular risk. Materials and Methods: A total of 113 adolescents (10–19 years old), from a public school in the city of Goiânia, Goiás, Brazil, underwent anthropometric, biochemical and food consumption evaluations and genetic tests. Results: After adjusting for potential confounders, SNPs rs4633 (catechol-O-methyltransferase, COMT), rs602662 (fucosyltransferase 2, FUT2) and rs1801394 (5-methyltetrahydrofolate-homocysteine methyltransferase reductase) showed significant associations with folic acid (P = 0.042), Vitamin B12 (P = 0.009) and oxidised low-density lipoprotein (ox-LDL) (P = 0.041) concentrations, respectively. The COMT SNP rs4680 showed a significant interaction with carbohydrate intake on ox-LDL concentrations (Pinteraction = 0.005). In addition, the FUT2 SNP rs602662 showed a significant interaction with protein intake on homocysteine concentrations (Pinteraction = 0.007). However, after correction for multiple testing, none of these associations and interactions were statistically significant. Conclusions: For the first time, we provide evidence for the interactions between COMT SNP rs4680 and carbohydrate intake on ox-LDL levels and the FUT2 SNP rs602662 and protein intake on homocysteine concentrations. However, replication of our results in a larger sample size is required to confirm our findings
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Vitamin D supplementation and immune-related markers: an update from nutrigenetic and nutrigenomic studies
Vitamin D is both a nutrient and a neurologic hormone that plays a critical role in modulating immune responses. While low levels of vitamin D are associated with increased susceptibility to infections and immune-related disorders, vitamin D supplementation has demonstrated immunomodulatory effects that can be protective against various diseases and infections. Vitamin D receptor is expressed in immune cells that have the ability to synthesise the active vitamin D metabolite. Thus, vitamin D acts in an autocrine manner in a local immunologic milieu in fighting against infections. Nutrigenetics and nutrigenomics are the new disciplines of nutritional science that explore the interaction between nutrients and genes using distinct approaches to decipher the mechanisms by which nutrients can influence disease development. Though molecular and observational studies have proved the immunomodulatory effects of vitamin D, only very few studies have documented the molecular insights of vitamin D supplementation. Until recently, researchers have investigated only a few selected genes involved in the vitamin D metabolic pathway that may influence the response to vitamin D supplementation and possibly disease risk. This review summarises the impact of vitamin D supplementation on immune markers from nutrigenetics and nutrigenomics perspective based on evidence collected through a structured search using PubMed, EMBASE, Science Direct and Web of Science. The research gaps and shortcomings from the existing data and future research direction of vitamin D supplementation on various immune-related disorders are discussed
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Evidence for a causal association between milk intake and cardiometabolic disease outcomes using a two-sample Mendelian Randomization analysis in up to 1,904,220 individuals
Background: High milk intake has been associated with cardio-metabolic risk. We conducted a Mendelian Randomization (MR) study to obtain evidence for the causal relationship between milk consumption and cardio-metabolic traits using the lactase persistence (LCT-13910 C>T, rs4988235) variant as an instrumental variable.
Methods: We tested the association of LCT genotype with milk consumption (for validation) and with cardio-metabolic traits (for a possible causal association) in a meta-analysis of the data from three large-scale population-based studies (1958 British Birth Cohort, Health and Retirement study, and UK Biobank) with up to 417,236 participants and using summary statistics from consortia meta-analyses on intermediate traits (N=123,665 to 697,307) and extended to cover disease endpoints (N=86,995 to 149,821).
Results: In the UK Biobank, carriers of ‘T’ allele of LCT variant were more likely to consume milk (P=7.02x10-14). In meta-analysis including UK Biobank, the 1958BC, the HRS, and consortia-based studies, under an additive model, ‘T’ allele was associated with higher body mass index (BMI) (Pmeta-analysis=4.68x10-12) and lower total cholesterol (TC) (P=2.40x10-36), low-density lipoprotein cholesterol (LDL-C) (P=2.08x10-26) and high-density lipoprotein cholesterol (HDL-C) (P=9.40x10-13). In consortia meta-analyses, ‘T’ allele was associated with a lower risk of coronary artery disease (OR:0.86, 95% CI:0.75-0.99) but not with type 2 diabetes (OR:1.06, 95% CI:0.97-1.16). Furthermore, the two-sample MR analysis showed a causal association between genetically instrumented milk intake and higher BMI (P=3.60x10-5) and body fat (total body fat, leg fat, arm fat and trunk fat; P<1.37x10-6) and lower LDL-C (P=3.60x10-6), TC (P=1.90x10-6) and HDL-C (P=3.00x10-5).
Conclusions: Our large-scale MR study provides genetic evidence for the association of milk consumption with higher BMI but lower serum cholesterol levels. These data suggest no need to limit milk intakes with respect to cardiovascular disease risk, with the suggested benefits requiring confirmation in further studies
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A systematic review of the gene-lifestyle interactions on metabolic disease-related outcomes in Arab populations
The increased prevalence of metabolic diseases in the Arab countries is mainly associated with genetic susceptibility, lifestyle behaviours, such as physical inactivity, and an unhealthy diet. The objective of this review was to investigate and summarise the findings of the gene-lifestyle interaction studies on metabolic diseases such as obesity and type 2 diabetes in Arab populations. Relevant articles were retrieved from a literature search on PubMed, Web of Science, and Google Scholar starting at the earliest indexing date through to January 2024. Articles that reported an interaction between gene variants and diet or physical activity were included and excluded if no interaction was investigated or if they were conducted among a non-Arab population. In total, five articles were included in this review. To date, among three out of twenty-two Arab populations, fourteen interactions have been found between the FTO rs9939609, TCF7L2 rs7903146, MC4R rs17782313, and MTHFR rs1801133 polymorphisms and diet or physical activity on obesity and type 2 diabetes outcomes. The majority of the reported gene-diet/ gene-physical activity interactions (twelve) appeared only once in the review. Consequently, replication, comparisons, and generalisation of the findings are limited due to the sample size, study designs, dietary assessment tools, statistical analysis, and genetic heterogeneity of the studied sample
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A genetic approach to study the relationship between maternal Vitamin D status and newborn anthropometry measurements: the Vitamin D pregnant mother (VDPM) cohort study
Purpose
Adverse effects of maternal vitamin D deficiency have been linked to adverse pregnancy outcomes. We investigated the relationship between maternal vitamin D status and newborn anthropometry measurements using a genetic approach and examined the interaction between genetic variations in involved in vitamin D synthesis and metabolism and maternal vitamin D concentrations on newborn anthropometry.
Methods
The study was conducted in 183 pregnant Indonesian Minangkabau women. Genetic risk scores (GRSs) were created using six vitamin D–related single nucleotide polymorphisms and their association with 25-hydroxyvitamin D [25(OH)D] levels and newborn anthropometry (183 infants) were investigated.
Results
There was no significant association between maternal 25(OH)D concentrations and newborn anthropometry measurements (P > 0.05, for all comparisons). After correction for multiple testing using Bonferroni correction, GRS was significantly associated with 25(OH)D in the third trimester (P = 0.004). There was no association between GRS and newborn anthropometric measurements; however, there was an interaction between GRS and 25(OH)D on head circumference (P = 0.030), where mothers of neonates with head circumference < 35 cm had significantly lower 25(OH)D if they carried ≥4 risk alleles compared to those who carried ≤3 risk alleles.
Conclusion
Our findings demonstrate the impact of vitamin D-related GRS on 25(OH)D and provides evidence for the effect of vitamin D-related GRS on newborn anthropometry through the influence of serum 25(OH)D levels among Indonesian pregnant women. Even though our study is a prospective cohort, before the implementation of vitamin D supplementation programs in Indonesia to prevent adverse pregnancy outcomes, further large studies are required to confirm our findings
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The APOB insertion/deletion polymorphism (rs17240441) influences postprandial lipaemia in healthy adults
BACKGROUND:
Apolipoprotein (apo)B is the structural apoprotein of intestinally- and liver- derived lipoproteins and plays an important role in the transport of triacylglycerol (TAG) and cholesterol. Previous studies have examined the association between the APOB insertion/deletion (ins/del) polymorphism (rs17240441) and postprandial lipaemia in response to a single meal; however the findings have been inconsistent with studies often underpowered to detect genotype-lipaemia associations, focused mainly on men, or with limited postprandial characterisation of participants. In the present study, using a novel sequential test meal protocol which more closely mimics habitual eating patterns, we investigated the impact of APOB ins/del polymorphism on postprandial TAG, non-esterified fatty acids, glucose and insulin levels in healthy adults.
FINDINGS:
Healthy participants (n = 147) consumed a standard test breakfast (0 min; 49 g fat) and lunch (330 min; 29 g fat), with blood samples collected before (fasting) and on 11 subsequent occasions until 480 min after the test breakfast. The ins/ins homozygotes had higher fasting total cholesterol, LDL-cholesterol, TAG, insulin and HOMA-IR and lower HDL-cholesterol than del/del homozygotes (P < 0.017). A higher area under the time response curve (AUC) was evident for the postprandial TAG (P < 0.001) and insulin (P = 0.032) responses in the ins/ins homozygotes relative to the del/del homozygotes, where the genotype explained 35% and 7% of the variation in the TAG and insulin AUCs, respectively.
CONCLUSIONS:
In summary, our findings indicate that the APOB ins/del polymorphism is likely to be an important genetic determinant of the large inter-individual variability in the postprandial TAG and insulin responses to dietary fat intake
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Effect of dietary fat intake and genetic risk on glucose and insulin-related traits in Brazilian young adults
Purpose The development of metabolic diseases such as type 2 diabetes (T2D) is closely linked to a complex interplay between genetic and dietary factors. The prevalence of abdominal obesity, hyperinsulinemia, dyslipidaemia, and high blood pressure among Brazilian adolescents is increasing and hence, early lifestyle interventions targeting these factors might be an efective strategy to prevent or slow the progression of T2D.
Methods We aimed to assess the interaction between dietary and genetic factors on metabolic disease-related traits in 200 healthy Brazilian young adults. Dietary intake was assessed using 3-day food records. Ten metabolic disease-related single nucleotide polymorphisms (SNPs) were used to construct a metabolic-genetic risk score (metabolic-GRS).
Results We found significant interactions between the metabolic-GRS and total fat intake on fasting insulin level (Pinteraction=0.017), insulin-glucose ratio (Pinteraction=0.010) and HOMA-B (Pinteraction=0.002), respectively, in addition to a borderline GRS-fat intake interaction on HOMA-IR (Pinteraction=0.051). Within the high-fat intake category [37.98±3.39% of total energy intake (TEI)], individuals with≥5 risk alleles had increased fasting insulin level (P=0.021), insulin-glucose ratio (P=0.010), HOMA-B (P=0.001) and HOMA-IR (P=0.053) than those with<5 risk alleles.
Conclusion Our study has demonstrated a novel GRS-fat intake interaction in young Brazilian adults, where individuals with higher genetic risk and fat intake had increased glucose and insulin-related traits than those with lower genetic risk. Large intervention and follow-up studies with an objective assessment of dietary factors are needed to confirm our findings
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Aldehydes: magnificent acyl equivalents for direct acylation
From the viewpoint of meeting the current green chemistry challenges in chemical synthesis, there is a need to disseminate how the cocktail of acylation and activation can play a pivotal role in affording bioactive acylated products comprising substituted ketone motifs in fewer reaction steps, with higher atom-economy and improved selectivity. In recent years, a significant number of articles employing the title compounds “aldehydes” as magnificent acylation surrogates which are less toxic and widely applicable have been published. This review sheds light on the compounds use for selective acylation of arene, heteroarene and alkyl (sp3, sp2 and sp) C–H bonds by proficient utilization of the C–H activation strategy. Critical insights into selective acylation of diverse moieties for the synthesis of bioactive compounds are presented in this review that will enable academic and industrial researchers to understand the mechanistic aspects involved and fruitfully employ these strategies in designing novel molecules
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Interaction between TCF7L2 polymorphism and dietary fat intake on high density lipoprotein cholesterol
Recent evidence suggests that lifestyle factors influence the association between the Melanocortin 4 receptor (MC4R) and Transcription Factor 7-Like 2 (TCF7L2) gene variants and cardio-metabolic traits in several populations; however, the available research is limited among the Asian Indian population. Hence, the present study examined whether the association between the MC4R single nucleotide polymorphism (SNP) (rs17782313) and two SNPs of the TCF7L2 gene (rs12255372 and rs7903146) and cardio-metabolic traits is modified by dietary factors and physical activity. This cross sectional study included a random sample of normal glucose tolerant (NGT) (n = 821) and participants with type 2 diabetes (T2D) (n = 861) recruited from the urban part of the Chennai Urban Rural Epidemiology Study (CURES). A validated food frequency questionnaire (FFQ) was used for dietary assessment and self-reported physical activity measures were collected. The threshold for significance was set at P = 0.00023 based on Bonferroni correction for multiple testing [(0.05/210 (3 SNPs x 14 outcomes x 5 lifestyle factors)]. After Bonferroni correction, there was a significant interaction between the TCF7L2 rs12255372 SNP and fat intake (g/day) (Pinteraction = 0.0001) on high-density lipoprotein cholesterol (HDL-C), where the 'T' allele carriers in the lowest tertile of total fat intake had higher HDL-C (P = 0.008) and those in the highest tertile (P = 0.017) had lower HDL-C compared to the GG homozygotes. In a secondary analysis of SNPs with the subtypes of fat, there was also a significant interaction between the SNP rs12255372 and polyunsaturated fatty acids (PUFA, g/day) (Pinteraction<0.0001) on HDL-C, where the minor allele carriers had higher HDL-C in the lowest PUFA tertile (P = 0.024) and those in the highest PUFA tertile had lower HDL-C (P = 0.028) than GG homozygotes. In addition, a significant interaction was also seen between TCF7L2 SNP rs12255372 and fibre intake (g/day) on HDL-C (Pinteraction<0.0001). None of the other interactions between the SNPs and lifestyle factors were statistically significant after correction for multiple testing. Our findings indicate that the association between TCF7L2 SNP rs12255372 and HDL-C may be modified by dietary fat intake in this Asian Indian population
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A nutrigenetic approach for investigating the relationship between vitamin B12 status and metabolic traits in Indonesian women
Purpose: Adverse effects of maternal vitamin B12 deficiency have been linked to major clinical outcomes, including increased body mass index and gestational diabetes, however, less is known about vitamin B12 nutrition in non-pregnant women. Hence, the aim of the present study was to explore the relationships between metabolic traits and vitamin B12 status in a cohort of healthy Indonesian women and to investigate whether these relationships were modified by dietary intake using a genetic approach.
Methods: A total of 117 Minangkabau women (aged 25-60 years), from the city of Padang, West Sumatra underwent anthropometric, biochemical, dietary intake analysis and genetic tests. Genetic risk scores (GRS) based on nine vitamin B12 associated single nucleotide polymorphisms (SNPs) (B12-GRS) and nine metabolic SNPs (metabolic-GRS) were constructed.
Results: The B12-GRS and metabolic-GRS had no effect on vitamin B12 (P>0.160) and metabolic traits (P>0.085). However, an interaction was observed between the B12-GRS and dietary fibre intake (g) on glycated haemoglobin (HbA1C) levels (P interaction=0.042), where among those who consumed a low fibre diet (4.90 ± 1.00 g/day), individuals carrying ≥9 risk alleles for vitamin B12 deficiency had significantly higher HbA1C levels (P=0.025) compared to those carrying ≤8 risk alleles.
Conclusion: Our study showed a significant impact of the B12-GRS on HbA1C concentrations through the influence of a dietary factor, however, our study failed to provide evidence for an impact of metabolic-GRS on lowering B12 concentrations. Further replication studies utilizing larger sample sizes are needed to confirm our findings