The effect of vitamin d supplementation on glycaemic control in women with gestational interacrions mellitus: A systematic review and meta-analysis of randomised controlled trials. Maternal vitamin B12 status and risk of neural tube defects in a population with high neural tube defect prevalence and no folic acid fortification. Antony, K. Persistent influence of maternal obesity on offspring health: mechanisms from animal models and clinical studies. Associations of maternal BMI and gestational weight gain with neonatal adiposity in the Healthy Start study. SN carriers if also including p.
Diabetol Metab Syndr 11, 37 Maternal smoking during pregnancy and child overweight: systematic review and meta-analysis.
Genotype-environment interactions arise when the response of a phenotype eg, fat mass to environmental changes eg, dietary intervention is modulated by the genotype of the individual. Efforts are needed to identify among these genes those responsible for modulating the response to diet.
Obesity-induced down-regulation of the mitochondrial translocator protein TSPO impairs placental steroid production. This highlights the need for an early nutritional management intervention, which theoretically includes the couple from pre-conceptional stages, and which subsequently involves the mother from conception to birth, to ensure the prevention and treatment of any metabolic imbalances.
The measured genotype approach uses genetic variation in random genetic markers or in candidate genes and attempts to evaluate the effect of variation at the DNA level on the quantitative phenotype under study. In addition, gene-diet interactions in children need to be investigated to determine whether the genes involved are the same as those found in adults. Lissner LHeitmann BL.
Reprinted from [ obesit ] by permission of Oxford University Press. Placentas from mothers with Gene diet interactions in obesity and pregnancy are frequently larger, with an increased placental weight and placental-weight to birth-weight ratio irrespective of glycemic control Differences between BMS and AMS offspring were tested using analysis of variance general linear model, type III sum of squares and adjusted for the effects of sex and puberty. A possible explanation is that the effect of a single gene on GWG is minimal. Ther Drug Monit — Mothers, Babies, and Health in Later Life. Download other formats More.
This review summarized data from recent studies of gene-diet interactions, and discussed integration of research of metabolomics and gut microbiome, as well as potential application of the gne in precision nutrition. J Clin Invest ; 94 : — 6. The risk factor represents one of the many risk factors associated with the disease and may itself be influenced by genetic and environmental agents. Effect of dietary fat content on total and regional adiposity in men and women. Despite the limited number of studies, the data reviewed in this article suggest that genetic factors play an important role in determining the response of body mass and body fat stores to chronic alterations in energy balance.
Sorli et al.
Seven pairs of young, adult, male identical twins completed a negative energy balance protocol during which they exercised on cycle ergometers twice a day, 9 of 10 d, over a period of 93 d while maintaining constant daily energy and macronutrient intakes
Article Google Scholar 4. Diet-induced changes in maternal gut microbiota and metabolomic profiles influence programming of offspring obesity risk in rats.
Three modifiable postnatal factors during infancy that influence weight in later life include.
The role of dietary fat in the etiology of obesity was addressed in several studies but remains controversial 10 — There is strong evidence that this variability in the response to diet is partly determined by genetic factors, especially for lipid and lipoprotein phenotypes.
Article Google Scholar Download references. S1 Fig. Landau et al. Maternal—Fetal nutrient transport in pregnancy pathologies: The role of the placenta.
Abstract The rapid rise inferactions obesity during the past decades has coincided with a profound shift of our living environment, including unhealthy dietary patterns, a sedentary lifestyle, and physical inactivity. Interestingly, neither apo E phenotype nor lipoprotein a concentrations, either independently or interactively with changes in dietary lipids, were found to influence changes in plasma lipids 6. Dietary fat and obesity: an unconvincing relation. Publication types Review.
A guide for authors and readers of the American Society for Nutrition Journals obewity the proper use of P values and strategies that promote transparency and improve research reproducibility. Examination of the segregation of this trait in the progeny of crosses between the sensitive and the resistant strains showed a polygenic pattern of inheritance with a minimum of 3 loci determining the response to dietary lipids Uptake of cancer risk management strategies among women who undergo cascade genetic testing for breast cancer susceptibility genes. The results of the long-term overfeeding 27 and negative energy balance 29 experiments are reviewed here.
Obese pregnant women were more likely to have inadequate levels of 25 Ln D vitamin in pregnancy We should be aware that specific maternal conditions during the pre- and peri-conceptional period particularly obesity and excessive weight gain during pregnancy are associated with higher risk of maternal complications and LGA infants, with obesity and impaired glucose metabolism in children and, subsequently, with increased cardiometabolic risk in adults. Methods and Materials 2. In humans, however, it remains challenging to unravel the complex interaction between genetics, epigenetics, and pre- and postnatal environmental influences [ 6 ]. Placenta —9.
C Venn diagram illustrating gene diet interactions in obesity and pregnancy of differentially methylated and hydroxymethylated loci. Programming of host metabolism by the gut microbiota. Dietary Data Dietary intake was collected during the following preghancy periods of pregnancy: 16—22 weeks, 24—29 weeks, and 32—37 weeks. This original seeding of the microbiome from maternal transmission may play profound roles in influencing development of human diseases in later life. The DOHaD hypothesis conceptualized the intra-uterine basis of long-term metabolic programming in progeny: it has become increasingly evident how this developmental plasticity allows the fetus to arrange anticipatory responses to the external environment, already altering the cell differentiation pathway and acquiring adaptive advantages to the challenges of adult life. Placentas from mothers with HIP are frequently larger, with an increased placental weight and placental-weight to birth-weight ratio irrespective of glycemic control Capturing functional epigenomes for insight into metabolic diseases.
DNA methylation analysis: choosing the right method. The mediation effect of dietary intake during pregnancy on GWG was not conclusive. I27L rs, p. Circulating levels of leptin gradually increase throughout gestation.
Obesity during pregnancy
Global gene expression analysis of amniotic fluid cell-free fetal RNA identified lipid apolipoprotein D and transcriptional regulators FOS and STAT3 as well as apoptotic cell death-related genes among differentially expressed genes between fetuses of obese vs. Nucleic Acids Res 1— However, the analysis of a replication cohort performed by Martin et al. Diabetic pregnant women did not show correlation between the changes in PGH levels and insulin levels Dudley, K.
Subcutaneous fat mm 5. On the basis of indian diet for heart disease reversal programs model, the accumulation of the amino acid phenylalanine from dietary origin in the blood causes mental retardation because individuals affected by this inherited disease lack the enzyme responsible for the degradation of phenylalanine into tyrosine. Major gene with sex-specific effects influences fat mass in Mexican Americans. Dietary fat and obesity: an epidemiologic perspective. Finally, data on children are needed to allow assessment of the tracking of nutrient intake between childhood and adulthood. There is strong evidence that this variability in the response to diet is partly determined by genetic factors, especially for lipid and lipoprotein phenotypes.
Growing studies have found that changes in adiposity and gene diet interactions response to low-calorie weight loss diets might be modified by obesity variants related to obesity, metabolic status and preference to nutrients. A major gens is the lack of data on children. Despite the limited number of studies, the data reviewed in this article suggest that genetic factors play an important role in determining the response of body mass and body fat stores to chronic alterations in energy balance. The mean loss in body weight was 5. Five hypothetical models describing the relations between genetic susceptibility to disease and risk factors for disease in an epidemiologic framework. Eur J Clin Nutr ; 49 : 79 —
Toxic Food Environment
Adapted from reference Phenylketonuria is the classic case fitting model A. Am J Physiol ; : R — Willett WC. Despite the limited number of studies, the data reviewed in this article suggest that genetic factors play an important role in determining the response of body mass and body fat stores to chronic alterations in energy balance.
Intfractions is well-established that the maternal diet may have a long-term impact on offspring gene diet interactions in obesity and pregnancy outcome in adulthood. Ala98Valp. Epigenetic alterations in the offspring of obese mothers It is well known that metabolic diseases such as obesity have a multifactorial etiology, with genetic and environmental factors contributing to disease development. In conclusion, our results indicate that dietary macronutrients, especially fat intake, may modify the effect of the KCTD15 gene on GWG. Exposure to maternal obesity during development is associated with increased white adipose tissue in the progeny [ 28 ]. Fraser, C.
In our participants, fat intake was correlated with carbohydrate intake, which could potentially explain why this SNP interacted with both fat and carbohydrate intake. S1 Fig. BsmI rsp. Fowles, and B. Expression values means relative to common homozygotes from the BMS group.
Therapeutic interventions based on a dietary approach, physical activity or both, are able to reduce the risk pfegnancy excessive weight gain, with a consequent reduced incidence of pregnancy complications. Institute of Medicine. These can lead to increased body fat, which generally manifests as larger size at birth. Challenges and progress in interpretation of non-coding genetic variants associated with human disease. Zurawek et al.
The aim of this ahd was to summarize the evidence currently available about the role of gene-nutrient interactions in human obesity. Download all slides. Major gene with sex-specific effects influences fat mass gene diet interactions in obesity and pregnancy Mexican Americans. The restoration of fertility of LepRloxTB was performed by stereotaxic delivery of adeno-associated virus-Cre into the hypothalamic ventral premammillary nucleus. In this experiment, 12 pairs of healthy, male, monozygotic twins with no familial history of obesity, hyperlipidemia, or diabetes were submitted to a 4. The role of dietary fat in the etiology of obesity was addressed in several studies but remains controversial 10 —
FokI [ 23 ], p. References 1. Gregory TR. Elbers, R. A meta-analysis by Yamamoto and collaborators defined the Medical Nutritional Therapy MNT for GDM as the effective intervention to achieve maternal euglycemia and optimal neonatal weight, through an early intervention that also affects fetal programming. Midthune, K. Circulating vitamin D and the risk of gestational diabetes: a systematic review and dose-response meta-analysis.
Although gene diet interactions in obesity and pregnancy gastrointestinal system functions to absorb and excrete food and nutrition we consume everyday, it is also considered to be the most important habitation for the indigenous intersctions microbiota. Epigenetics in human disease and prospects for epigenetic therapy. Maternal GDM and obesity have been reported to alter placental fatty acid transfer, although further progress will be need in understanding the mechanisms of specific placental alterations on lipid transport and metabolism The System A amino acid transporter facilitates uptake of small non-essential neutral amino acids such as alanine, glycine, and serine against their concentration gradient. Pre-pregnancy weight, weight at delivery, and GWG were similar between p. Nat Rev Genet —
Journal of Nutrition and Metabolism
Perinatal exposure to high-fat diet programs energy balance, metabolism and behavior in adulthood. Horm Mol Biol Clin Invest — J Hepatol. PubMed Article Google Scholar 4. Table 2.
The results of the long-term overfeeding 27 and negative energy balance 29 experiments are reviewed here. This review summarized data from recent studies of gene-diet interactions, and yene integration of research of metabolomics and gut microbiome, as well as potential application of the findings in precision nutrition. Segregation analysis of fat mass and fat-free mass with age and sex-dependent effects: the Stanislas Family Study. However, as indicated in Figure 2 left panelthis heterogeneity in the response was not randomly distributed across genotypes.
Second, genotype-environment interaction effects could also be involved in the susceptibility of obese individuals to develop comorbidities associated with obesity eg, diabetes, hyperlipidemia, hypertension, gene diet interactions in obesity and pregnancy coronary heart prwgnancy or in response to treatment. These findings suggest the existence of a putative gene that affects body mass or body fat, the effects of which are dependent on the sex and the age of the individual, which represents a special case of genotype-environment interaction effect. Hepcidin-regulating iron metabolism genes and pancreatic ductal adenocarcinoma: a pathway analysis of genome-wide association studies. It is important to understand the tracking of key nutrients before developing new dietary recommendations for children.
Using data from our intervention studies in monozygotic twins, we found that a BamHI restriction an fragment polymorphism in the lipoprotein lipase gene was associated with the response to overfeeding The risk factor represents one of the many risk factors associated with the disease and may itself be influenced by genetic and environmental agents. Arterioscler Thromb Vasc Biol ; 15 : — Email alerts Article activity alert. Willett WC.
The consequences were different according to the different gestational ages affected by nutritional deficiency. Lond ;
However, only approximately one third of the human population is able to metabolize daidzein to equol and this difference is grne due to different composition of the intestinal microbiome, which may play an important role in metabolizing soy isoflavones. Numerous human studies have shown that maternal obesity likely leads to detrimental pregnancy outcomes such as increased risks of gestational diabetes, gestational hypertension, preeclampsia and cesarean section compared to pregnancy with normal weight Gaillard et al.
Also, we did not control our data for confounding variables such as nutrition, education, smoking and parity. Gene diet interactions in obesity and pregnancy pregnant women did not show correlation between the changes in PGH levels jn insulin levels Among children with optimal levels of all four those whose mothers did not smoke and did not gain too much weight during pregnancy, who were breastfed for at least one year, and who got at least 12 hours of sleep on an average nightthe predicted probability of overweight was 6 percent. Glucose transport and system A activity in syncytiotrophoblast microvillous and basal plasma membranes in intrauterine growth restriction.
However, most maternal and neonatal complications correlate with maternal BMI; therefore dietary-behavioural intervention is an essential strategy in obese women, but it should begin in the pre-conception period. Trujillo, D. Liang, H. Nutrients 7, —
Differences in the implications of maternal lipids on fetal metabolism and growth between gestational diabetes mellitus and control pregnancies. Substantial human and animal studies have shown the altered composition and diversity of the gut microbiota in obese populations Kvit and Kharchenko, The P values of the analysis of covariance are provided.
The impact of probiotic supplementation during pregnancy on DNA methylation of obesity-related genes in mothers and their children.
Abbey M. Permissions Icon Permissions.
Are the Institute of Medicine weight gain targets applicable in women with gestational diabetes mellitus? Adaptation of plasma membrane amino acid transport mechanisms to physiological demands.
Open in new tab.
For this dlet, QTL identified from animal models probably represent the most promising approach. In a study by Dixon et al 6the response of plasma lipids to dietary modifications elicited by means of a nutrition education program was investigated in children aged 4—10 y with elevated LDL-cholesterol concentrations at baseline. Dietary fat intake and weight gain in women genetically predisposed for obesity. This review summarizes the evidence currently available regarding the role of gene-diet interactions for phenotypes related to obesity.
The MspI polymorphism of the apolipoprotein A-II gene as a modulator of the dyslipidemic state found in visceral obesity. The mean loss in body weight was 5. Sign In. N Engl J Med ; : — Using data from our intervention studies in monozygotic twins, we found that a BamHI restriction length fragment polymorphism in the lipoprotein lipase gene was associated with the response to overfeeding
These obesity phenotypes were adjusted for age and sex and were tested for linkage with the sibpair linkage method. These loci— Dob1Dob2and Dob3 —were located on mouse chromosomes 4, 9, and 15, respectively. Evidence from both genetic epidemiology and molecular epidemiology studies suggests that genetic factors are involved in determining the susceptibility to gaining or losing fat in response to diet or the risk of developing some of the comorbidities generally observed in obese individuals.
Jirtle, R. Also, vene two genes directly interacted in a mouse hypothalamus-derived cell line. Maternal pre-pregnancy obesity, offspring cord blood DNA methylation, and offspring cardiometabolic health in early childhood: an epigenome-wide association study. The origins of the developmental origins theory. View at: Google Scholar T. Astrup, A. Using PLINK we analyzed interactions between offspring gene variations and maternal surgical status on offspring gene expression levels.
Genet Epidemiol ; 14 : 51 — Issue Section:. The mean body mass gain was 8. Genet Epidemiol ; 12 : —
Clin Genet. Mamm Genome. When pre-pregnancy insulin resistance in obese women superimposes to the pregnancy-related insulin resistance, it leads to an increased insulin response, which affects early placental growth and gene expression.
Inflamm Bowel Dis —
J Nutr Biochem
The established epigenetic landmarks are relatively stable and heritable through mitosis, allowing a faithful differentiation process and the propagation of lineage-specific transcription profiles over many cell divisions during the whole lifetime in the organisms. Pregnant women have biologic, behavioral, and hormonal changes throughout pregnancy [ 11 ].
Obesity-risk genes have been associated with dietary intake, appetite regulation, and gestational weight gain GWG. I27L rs, p. Association of maternal prepregnancy BMI and plasma folate concentrations with child metabolic health. To date, consistent data confirm the pivotal role of maternal nutritional status and diet for the fetal epi-genotype and the resulting phenotype 9 — The association between the polymorphism rs, close to the MC4R gene, and the percentage of energy intake from fat was significant at the nominal level but not after adjusting for multiple testing. I27L TT carriers. A trained technician interviewed participants either face to face or via telephone.
Hepcidin-regulating iron metabolism genes and obesity ductal adenocarcinoma: a and pregnancy analysis of genome-wide association studies. It is possible that the effect of some genes on the response may differ between adults and children. Livestrong best diet pills to lose weight Res ; 2 : — In gene diet interactions, these studies showed that, for a given amount of energy from fat 18 or a given percentage point reduction in the percentage of energy from fat 15there was marked heterogeneity in the response of body mass. The second method involves a comparison of the effect of a gene on a phenotype of interest between subgroups of individuals within the same population, but categorized on the basis of variables that can potentially affect the phenotype, eg, the amount of fat in the diet. The response to exercise with constant energy intake in identical twins.
Sexual dimorphism in gene expression was only apparent in placentas from obese LepRloxTB det. New issue alert. This is especially true for dietary fat, which is known to be associated with obesity at the population level. Arterioscler Thromb Vasc Biol ; 15 : — The influence of apolipoprotein polymorphism on the response to dietary fat and cholesterol.
The phenotypes investigated included BMI, subcutaneous fat assessed by the sum of 6 skinfold-thickness measures, and percentage body fat and fat mass derived from underwater weighing Pregmancy WC. Receive exclusive offers and updates from Oxford Academic. Other data suggest that the apo A-II MspI polymorphism is associated with lower HDL 2 -cholesterol concentrations, but only in men with high amounts of abdominal visceral fat or with evidence of an insulin-resistance state Fat intake and short-term energy balance. However, as indicated in Figure 2 left panelthis heterogeneity in the response was not randomly distributed across genotypes.
At the same time, the placenta is thought to contribute to excessive neonatal fat already in early pregnancy.
No data are available to determine whether consumption of a high-fat diet early in life increases the risk of exhibiting the same pattern of nutrient intake during adulthood.
However, this adaptation could also have negative effects on fetal development, since maternal hyperketonemia has been associated with increased incidence of fetal malformations, impaired neurophysiologic development, as well as still birth 46 ,
However, the impact of individual genes on GWG remains uncertain. Maternal—Fetal nutrient transport in pregnancy pathologies: The role of the placenta.
Despite the limited number of studies, the evidence on gene-diet interactions in obesity is convincing.
Supporting Information. Gene expression levels of the 45 offspring analyzed here were obtained from previous studies from our group evaluating differences in gene expression and methylation of genes involved in diabetes, immune and inflammatory pathways [ 1732 ]. Changes in serum adipocyte fatty acid-binding protein in women with gestational diabetes mellitus and normal pregnant women during mid- and late pregnancy. This problem is further aggravated, especially in DNA methylation studies, by a multitude of different methodological approaches in the analysis and quantification of DNA methylation. Furthermore, a short excurse is given on epigenetic mechanisms and emerging data regarding a putative interaction between metabolism and epigenetics.
General linear models were used to assess the genetic effect on GWG and dietary intake. Nat Rev Genet — Childhood cardiometabolic outcomes of maternal obesity during pregnancy: the Generation R Study. Endocrine 70 1 — DNA methylation analysis: choosing the right method. I27L Full size table. PLoS One 6: e
Golay ABobbioni E. A guide for authors and readers of the American Society for Nutrition Journals on the proper use of P values and strategies that promote transparency and improve research reproducibility. Genet Epidemiol ; 12 : —
Sex and gender differences in developmental programming of metabolism. Browse Subject Areas? J Endocrinol — Growth in utero, blood pressure in childhood and adult life, and mortality from cardiovascular disease. Suter, M.
Lancet Diabetes Endocrinol 2 6 —
The aim of this review was to summarize the evidence currently available about the role of gene-nutrient interactions in human obesity. J Clin Invest ; 94 : — 6.
Folate and fetal programming: a play in epigenomics? Only about 1.
Subcutaneous fat mm 5.
J Clin Invest ; 94 : — 6. Skip Nav Destination Article Navigation. The apolipoprotein E polymorphism: a comparison of allele frequencies and imteractions in nine populations. Candidate genes or genomic regions identified in these animal models can be tested in humans by using association or linkage studies with obesity phenotypes or, more interestingly, with the response of these phenotypes to dietary interventions. Indeed, the latter group exhibit the more atherogenic pattern B subclass after consuming a low-fat diet 4. It is generally accepted that high-fat diets induce an overconsumption of energy, which can lead to the development of obesity.
Public Health Nutr — Endocrinology— Folic acid as one of the well-studied methyl donors is crucial for synthesis of S-adenosylmethionine SAMthe universal methyl donor of DNA methylation and synthesis Hoffman et al. Laraia, B.
With advances in molecular genetics, the study of gene-nutrient interactions is now performed at the gene level. Other QTL from the same cross were reported, but only in abstract forms. Ignoring existing genotype-environment interaction effects was shown to reduce the power to detect major gene effects 21 ,
The early-life maternal diets, microbiome and epigenome may interact with each other and establish a complicated crosstalk mechanism that contributes to initiation of developmental plasticity in response to the environmental factors Figure 1. Google Scholar. Metrics details. The effect of gene-diet interactions on GWG is presented in Table 3.
Thus, several biomolecules including glucose, fatty acids, ketone bodies, hormones and adipokines maintain a proper balance, in which the placenta plays a central role. Most importantly, butyrate is a histone deacetylase HDAC that can influence histone modification processes.
Other data suggest that the apo A-II MspI polymorphism is associated with lower HDL 2 -cholesterol concentrations, but only in men with high amounts of abdominal visceral fat or with evidence of an insulin-resistance state
Nonetheless, we assessed gene expression as representative of systemic biological differences between BMS and AMS offspring to which multiple organs and tissues have contributed. Interactions between offspring gene variations and maternal surgical status were tested on offspring gene expression levels in whole blood using PLINK.
After 7 weeks, pregnant women randomized to LGID had lower fasting and post-prandial blood sugar levels, lower insulin resistance, and less need for insulin therapy.
Epigenetic mechanisms regulate the accessibility of DNA for transcription factor complexes, the efficiency of gene transcription, and the stability of messenger RNA mRNA.
Ethics declarations Gene diet interactions in obesity and pregnancy of interest The author declares no competing interests. Although debate lingers over whether breastfeeding protects against childhood obesity, breastfeeding has many other proven health benefits for infants and their prgnancy, and it should be promoted regardless of its relationship to childhood obesity. Linking fat intake, the intestinal microbiome, and necrotizing enterocolitis in premature infants. Int J Obes Lond. Impact on DNA methylation in cancer prevention and therapy by bioactive dietary components. Moreover, this low-level insulin resistance drives endogenous glucose production and utilization of fat stores, leading to further increases in blood glucose and free fatty acids [ 7 ]. Maternal high-fat diet promotes body length increases and insulin insensitivity in second-generation mice.
Int J Obes ; 14 : — And pregnancy data from the Quebec Family Study, we tested for linkage obesity markers syntenic to Dob1 on human chromosome 1 and various obesity phenotypes. Another gene diet interactions znd requires investigation concerns the tracking of dietary intake, especially fat intake. Placentas of resorbed embryos from obese mice displayed necrosis and inflammatory infiltrate in the labyrinth and changes in the expression of genes associated with angiogenesis and inflammation e. Although we assume that the response to diet in children is characterized by a degree of variability similar to that observed in young adults, studies are needed to investigate this issue specifically in children. Article Navigation.
Impact of dietary fat content and fat oxidation on energy intake in humans. An example of such a model is the major gene model, which is characterized by the segregation of a single locus that has a large effect on the phenotype. Using data from the Quebec Family Study, we tested for linkage between markers syntenic to Dob1 on human chromosome 1 and various obesity phenotypes. Permissions Icon Permissions.
Effects of family ohesity of heart disease, apolipoprotein E phenotype, and lipoprotein a on the response of children's plasma indian diet to change in obesityy lipids. Obes Res ; 2 : — Hepcidin-regulating iron metabolism genes and pancreatic ductal adenocarcinoma: a pathway analysis of genome-wide association studies. Second, genotype-environment interaction reversal programs could also be involved in the susceptibility of obese individuals to develop comorbidities associated with obesity eg, diabetes, hyperlipidemia, hypertension, and coronary heart disease or in response to treatment. In contrast, placentas from embryos of females on HFD showed changes in a different set of genes, mostly associated with cellular growth and response to stress e. Evidence from both genetic epidemiology and molecular epidemiology studies suggests that genetic factors are involved in determining the susceptibility to gaining or losing fat in response to diet or the risk of developing some of the comorbidities generally observed in obese individuals. The human obesity gene map: the update.
However, this traditional practice may raise a concern since adverse pregnabcy may occur. Thus, early increased lipids, due to maternal obesity or HFD, probably accumulate in the fetal liver, establishing an inflammatory and lipotoxic environment and priming Kupffer cell and hepatic stellate cell to fibrosis, inflammation and non-alcoholic fatty liver diseases NAFLD later in life Qorbani, S. It is well demonstrated that nutrition as one of the most important environmental factors influences adult-onset disease. Moreover, metastable epialleles refer to epialleles in which the degree of DNA methylation can be altered by environmental factors [ 54 ].
AB Increased DNA methylation and reciprocally decreased DNA hydroxymethylation at obeskty gene clusters in placentas of obese gene diet interactions in obesity and pregnancy to lean mothers. The impact of maternal nutrition on the offspring guts microbiome and the associated health outcomes can extend beyond pregnancy into the postnatal period through breastfeeding. Pompei, A. In a prospective cohort study of children, infants who slept fewer than 12 hours a day had double the odds of being overweight at age 3, compared with infants who slept more than 12 hours a day.
These findings suggest the existence of a putative gene that affects body mass or body fat, the effects of which are dependent on the sex and the age of the individual, which represents a special case of genotype-environment interaction effect. Low density lipoprotein subclass patterns and lipoprotein response to a reduced fat diet in men. Influence of genetic polymorphisms on responsiveness to dietary fat and cholesterol.
Among children with optimal levels of all four those whose mothers did not smoke and did not gain too much weight during prengancy who were breastfed for at least one obesitu, gene diet who got at least 12 hours of interactions obesity on an average nightthe predicted probability of overweight was gene diet interactions in obesity and pregnancy percent. Other transporters for cationic and anionic amino acids have been detected in the human placenta, although their specific role in determining the fetal growth is less well studied Causality of identified variants cannot be determined: identified variants might be markers of genomic regions or loci in which causal variants lie and allelic heterogeneity cannot be ruled out, together necessitating much larger population studies than our unique but relatively small cohort study. Am J Reprod Immunol. The AG carriers gained more weight during pregnancy than the AA carriers. Linking fat intake, the intestinal microbiome, and necrotizing enterocolitis in premature infants. Energy adaptations in human pregnancy: Limits and long-term consequences.
The relation between dietary fat and obesity is reviewed briefly first. Seidell JC. Am J Clin Nutr ; 43 : — Adapted from reference Recent evidence suggests that quantitative trait loci identified from animal models of diet-induced obesity could influence body fat in humans.
J Lipid Res — Educational attainment was the highest grade completed at the time of enrollment. The first-trimester of pregnancy — A window of opportunity interatcions prediction and prevention of pregnancy complications and future life. We suggest that the adiposity-related gene FTO was associated with increased risk of GDM by increasing pre-pregnancy obesity. Proc Natl Acad Sci U. Although these durable effects were not replicated quantitatively or qualitatively by other current bariatric operations, they add critical insight into molecular mechanisms associated with the gene expression levels presented here.
The norbert freinkel award lecture. Similarly, p. Studies have shown that transplantation of gut microbiome from diet-induced obese mice to lean germ-free recipients resulted in a significant increased body fat deposition suggesting an important role for the intestinal microbiome in development of obesity Turnbaugh et al. Inhibition of cephalic neural tube closure by 5-azacytidine in neurulating rat embryos in vitro. Arrowheads in the figures indicate marked differences in 5mC and 5hmC distributions.
Rasmussen and A. Differences in promoter methylation indian diet such metastable epialleles can lead to different phenotypes of qnd for heart disease individuals [ reversal programs55 ]. Only about 1. In summary, there is evidence for a rather strong genetic component in the development of obesity, but the heritability of obesity cannot entirely be attributed to genetic variation [ 454649 ].
Herrera E. Also other evidence points toward a connection between metabolism and epigenetics. Nat Genet. Article Google Scholar 2. Gut — A larger effect size is indicated by darker shading regardless of direction.
An epidemiologic approach to gene-environment interaction. The human obesity gene map: the update. These findings indicate that, in response to an energy surplus, some individuals are storing fat predominantly in selected fat depots primarily as a result of undetermined genetic characteristics. Issue Section:.
Downregulation of IRS-1 in adipose tissue of offspring oesity obese mice is programmed cell-autonomously through post-transcriptional mechanisms. In a meta-analysis of 14 studies, maternal smoking during pregnancy was associated with a 50 percent higher risk of childhood obesity. Effects of calcium-vitamin D co-supplementation on glycaemic control, inflammation and oxidative stress in gestational diabetes: A randomised placebo-controlled trial. Environ Epigenet 4 2 :dvy
For example, it obeaity been shown that individuals with a predominance of small, dense LDL particles subclass pattern Ba phenotype that is associated with an increased risk of coronary heart disease, benefit more from a low-fat diet 3 than do those with the subclass pattern A. The restoration of fertility of LepRloxTB was performed by stereotaxic delivery of adeno-associated virus-Cre into the hypothalamic ventral premammillary nucleus. Adapted from reference J Clin Invest ; 94 : — 6.
Genetic predisposition to obesity may have interacted with such an obesogenic environment in determining the obesity epidemic. Gov't, P. The response to exercise with constant energy intake in identical twins. Left panel: Twelve pairs of monozygotic twins were subjected to a MJ kcal surplus over d.
Intriguingly, studies in non-human primates have shown that maternal HFD led to persistently reduced abundance of Campylobacter species in the offspring gut compared to the control diet group even though the primates were weaned and switched to control diet for 6 months Table 2 ; Ma et al. Breast-feeding and childhood obesity-a systematic review.
Using this method, we performed a series of studies to investigate the role of the genotype in determining the response to changes in energy balance by submitting both members of male monozygotic twin pairs either to positive energy balance induced by short-term and long-term overfeeding 2627 or to negative energy balance induced by exercise training in the presence of constant energy intake conditions 28 Significant reductions in plasma total and LDL-cholesterol concentrations were found, but only in children with little evidence of a family history of coronary heart disease CAD as assessed by the occurrence of a myocardial infarction or hypercholesterolemia in none or not more than one first or one second-degree relative.
Gestational weight gain GWG was calculated as the difference between the maternal weight at delivery and pre-pregnancy weight.
Hastie R, Lappas M. Chemoprevention gene diet interactions in obesity and pregnancy dibenzo[a,l]pyrene transplacental carcinogenesis in mice interacyions to mothers administered green tea: primary role of caffeine. In a recent animal study, researchers found that probiotic intake during pregnancy and lactation attenuated maternal HFD-induced detrimental nutritional programming of offspring obesity associated with maternal obesity, indicating that altered maternal gut microbiota through additional microbiota manipulations could be a useful strategy to improve maternal and offspring metabolic outcome with a long-standing impact Paul et al. Stuebe, H. Int J Epidemiol. In fact, newborns of obese women have an increased risk of overgrowth, and maternal obesity accounts for a greater number of LGA infants than pregnancies complicated by GDM 53 Diabetes Care.
Beta-cell dysfunction is more prone to developing impaired glucose tolerance during pregnancy [ 28 ]. A98V rs, p. S1 Fig. View at: Google Scholar L.
This review summarizes the evidence currently available regarding the role of gene-diet interactions for phenotypes related to obesity. Am J Clin Nutr ; 72 : — An example of this approach is provided by the study of Andd et al 30who showed that the effect of apo E polymorphism on total cholesterol concentrations varied among populations with different amounts of fat in their diet. For example, it has been shown that individuals with a predominance of small, dense LDL particles subclass pattern Ba phenotype that is associated with an increased risk of coronary heart disease, benefit more from a low-fat diet 3 than do those with the subclass pattern A.
The indian diet for heart disease reversal programs of energy exchange in man: an analysis. Acta Genet Med Gemellol Roma ; 39 : 85 — 9. Am J Hum Genet ; 49 : — In this experiment, 12 pairs of healthy, male, monozygotic twins with no familial history of obesity, hyperlipidemia, or diabetes were submitted to a 4. Therefore, preventive measures adopted early in life may help reduce the prevalence of these diseases in adulthood. F ratio.
Genomics 20, — Finally, a summary of important findings of animal and clinical studies investigating maternal obesity-related epigenetic effects is presented also addressing current limitations of clinical studies. Int J Obes — Lager S, Powell TL. Int J Obes Lond. These represent 48, unique SNPs 1. Int J Obes.