Gene-Diet Interaction and Precision Nutrition in Obesity

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Insulin 8 endocrinologydiseasesdrugs
childhood obesity 3 endocrinologydiseases
obesity 62 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Insulin 27582 VariantsOutcomesDiabetes genetic risk score [[85]]Glycemic traitsDiabetes genetic risk score [[72]] Insulin resitence; Insulin secretion IRS1 rs1522813, rs2943641 [[81],[83]]Insulin resistance; Metabolic syndrome;
Insulin 27601 VariantsOutcomesDiabetes genetic risk score [[85]]Glycemic traitsDiabetes genetic risk score [[72]]Insulin resitence; Insulin secretion IRS1 rs1522813, rs2943641 [[81],[83]]Insulin resistance; Metabolic syndrome; Body weight;DHCR7
Insulin 27656 genetic risk score [[72]]Insulin resitence; Insulin secretion IRS1 rs1522813, rs2943641 [[81],[83]] Insulin resistance; Metabolic syndrome; Body weight;DHCR7 rs12785878 [[84]]Insulin resitenceFTO rs1558902 [[93]]Insulin
Insulin 27731 rs1522813, rs2943641 [[81],[83]]Insulin resistance; Metabolic syndrome; Body weight;DHCR7 rs12785878 [[84]] Insulin resitenceFTO rs1558902 [[93]]Insulin resistanceFTO rs9939609, rs1558902 [[73],[90]]Body composition
Insulin 27768 resistance; Metabolic syndrome; Body weight;DHCR7 rs12785878 [[84]]Insulin resitenceFTO rs1558902 [[93]] Insulin resistanceFTO rs9939609, rs1558902 [[73],[90]]Body composition and fat distribution; Appetite GIPR rs2287019
Insulin 27908 rs1558902 [[73],[90]]Body composition and fat distribution; Appetite GIPR rs2287019 [[80]]Glycemic traits; Insulin resistance CRY2 rs11605924, MTNR1B rs10830963 [[79]]Energy expenditureTCF7L2 rs12255372 [[78]]Body compositionPCSK7
Insulin 28047 MTNR1B rs10830963 [[79]]Energy expenditureTCF7L2 rs12255372 [[78]]Body compositionPCSK7 rs236918 [[71]] Insulin resistanceAPOA5 rs964184 [[88]]Lipid profilesLIPC rs2070895 [[86]]Lipid profiles CETP rs3764261 [[82]]Lipid
Insulin 28226 profiles CETP rs3764261 [[82]]Lipid profilesNPY rs16147 [[89]]Blood pressure PPM1K rs1440581 [[87]] Insulin resistance; body weightFGF21 rs838147 [[70]]Body compositionAdiponectin GRS [[75]]Appetit
Select Disease Character Offset Disease Term Instance
childhood obesity 11323 In line with evidence in adults, studies have shown that FTO rs9939609 genotype was associated with childhood obesity [[59],[60],[61],[62]], and also suggested an association of the FTO variant and dietary intake and preference
childhood obesity 12059 studies [[63]]. A study suggests an interaction between the FTO SNP rs9939609 and socioeconomic status on childhood obesity [[64]], and some other studies reported gene–environment interactions in childhood obesity [[53],[65],[66]].
childhood obesity 12152 status on childhood obesity [[64]], and some other studies reported gene–environment interactions in childhood obesity [[53],[65],[66]]. In a population-based longitudinal study in Brazil, Vitamin D status significantly
obesity 523 02115, USAPublication date (epub): 4/2017Publication date (collection): 4/2017AbstractThe rapid rise of obesity during the past decades has coincided with a profound shift of our living environment, including unhealthy
obesity 730 unhealthy dietary patterns, a sedentary lifestyle, and physical inactivity. Genetic predisposition to obesity may have interacted with such an obesogenic environment in determining the obesity epidemic. Growing
obesity 813 predisposition to obesity may have interacted with such an obesogenic environment in determining the obesity epidemic. Growing studies have found that changes in adiposity and metabolic response to low-calorie
obesity 989 metabolic response to low-calorie weight loss diets might be modified by genetic variants related to obesity , metabolic status and preference to nutrients. This review summarized data from recent studies of gene-diet
obesity 1307 potential application of the findings in precision nutrition.1. IntroductionThe increasing epidemic of obesity has coincided with a profound shift of our living environment, such as unhealthy dietary patterns, a
obesity 1627 background [[1]]. In a recent study of the US national cohort, the magnitude of association between obesity , as assessed by body mass index (BMI) and genetic risk of obesity was stronger in more recent birth
obesity 1693 magnitude of association between obesity, as assessed by body mass index (BMI) and genetic risk of obesity was stronger in more recent birth cohorts than in earlier years of birth cohorts, suggesting that such
obesity 1830 birth cohorts than in earlier years of birth cohorts, suggesting that such genetic predisposition to obesity may have a greater effect in more recent obesogenic environments [[2]]. Although the environmental risk
obesity 1996 environments [[2]]. Although the environmental risk factors are largely modifiable and the development of obesity would be essentially preventable, genetic variants associated with adiposity may also influence behavioral
obesity 2378 carbohydrate consumption) [[7],[8]] would partly be genetically determined.The genetic contribution to obesity has been extensively investigated in genome-wide association studies (GWAS) [[9],[10],[11]], which successfully
obesity 3252 will provide new insights into the roles of gene–environment interaction in complex traits including obesity , and contribute to a precision prevention and management of obesity. Here, we highlighted data from
obesity 3320 interaction in complex traits including obesity, and contribute to a precision prevention and management of obesity . Here, we highlighted data from recent studies of gene–diet interactions on obesity, and discussed
obesity 3406 management of obesity. Here, we highlighted data from recent studies of gene–diet interactions on obesity , and discussed how these findings may inform understanding of more complex architecture of interactions
obesity 3559 understanding of more complex architecture of interactions between genes and environment factors in obesity and associated diseases.2. Studying Gene–Environment InteractionsMore and more genetic bases of complex
obesity 3700 Studying Gene–Environment InteractionsMore and more genetic bases of complex metabolic diseases such as obesity and type 2 diabetes have been revealed [[9],[10],[11],[20],[21]], however the genetic variants identified
obesity 4338 of studying gene–environment interaction has been well recognized, and the missing heritability of obesity could be partly due to interactions between the genetic variations and environmental factors such as
obesity 4600 section of our review, we showed several studies on lifestyle and dietary factors that magnified risk of obesity among individuals genetically at high risk. Genes can trigger the occurrence of diseases when a person
obesity 5343 characterized by different body shapes and considerable heterogeneity within the spectrum of clinical obesity may exist [[28],[29],[30],[31],[32],[33],[34],[35],[36],[37]]. A recent GWAS identified genetic variants
obesity 5618 multiple anthropometric traits [[38]]. To support gene–diet interaction and precision nutrition in obesity , considering different body shapes and subtypes of obesity would be necessary.3. Dietary and Lifestyle
obesity 5677 gene–diet interaction and precision nutrition in obesity, considering different body shapes and subtypes of obesity would be necessary.3. Dietary and Lifestyle Factors Interact with Genetic Variants on ObesityEpidemiological
obesity 5882 ObesityEpidemiological studies have consistently shown that particular diets and lifestyles accentuate risk of obesity among adults genetically at high risk (Table 1). For example, replicable evidence has shown that sugar-sweetened
obesity 6181 and sedentary lifestyles [[43],[44],[45]] are interacted with genetic variants in the association of obesity .Intake of free sugars or sugar sweetened beverages is a determinant of body weight [[48],[49]]. We previously
obesity 6367 weight [[48],[49]]. We previously reported significant interactions between genetic factors linked to obesity (as assessed by genetic risk score (GRS) based on 32 BMI-associated loci) and intake of sugar-sweetened
obesity 6632 Study (NHS) and the Health Professionals Follow-up Study (HPFS) [[39]]. The genetic association with obesity was stronger among individuals with higher intake of sugar-sweetened beverages as compared with those
obesity 6945 association of sugar-sweetened beverages with BMI was stronger in people genetically predisposed to obesity [[40]]. Further, another recent study reported similar interactions between a GRS for obesity and soft
obesity 7039 predisposed to obesity [[40]]. Further, another recent study reported similar interactions between a GRS for obesity and soft drinks consumption in relation to changes in BMI [[41]]. In a Hispanic population living in
obesity 7472 risk [[50]]. Consumption of sugar-sweetened beverages has been implicated in driving the epidemic of obesity [[51]]; recent reproducible evidence from these studies in the US and European populations suggests
obesity 7774 intake, is considered as one of unhealthy dietary factors that influence risks of general and central obesity [[52]]. We previously reported for the first time that fried food consumption interacted with genetic
obesity 7910 reported for the first time that fried food consumption interacted with genetic background in relation to obesity in the NHS and HPFS cohorts, highlighting the importance of reducing fried food consumption among individuals
obesity 8055 highlighting the importance of reducing fried food consumption among individuals genetically predisposed to obesity [[42]]. Our study indicated that FTO genotype showed the strongest interaction (Pinteraction < 0.001)
obesity 8175 study indicated that FTO genotype showed the strongest interaction (Pinteraction < 0.001) among all obesity predisposing variants [[42]]. In addition to fried food, among participants of the Genetics of Lipid
obesity 8507 saturated fatty acids was associated with higher BMI among individuals at a genetically high risk of obesity [[46]]. In a study of three US cohorts, association of the APOA2 − 265T > C polymorphism and BMI was
obesity 9539 sugar-sweetened beverages and fried potatoes) modified associations of genetic variants associated with obesity using GRSs based on 32 BMI- and 14 waist–hip ratio (WHR)-associated single nucleotide polymorphisms
obesity 9741 polymorphisms (SNPs) [[54]]. Their results suggested that associations between genetic predisposition and obesity traits were stronger among individuals with healthier diet scores [[54]].A number of studies investigated
obesity 9897 healthier diet scores [[54]].A number of studies investigated a gene–physical-activity interaction on obesity [[43],[44],[45],[55],[56]]. A meta-analysis has shown that physical activity attenuated the influence
obesity 10026 [[43],[44],[45],[55],[56]]. A meta-analysis has shown that physical activity attenuated the influence of FTO variants on obesity in adults [[55]]. Whereas greater leisure time physical activity attenuated the genetic association,
obesity 10564 recent study of the UK Biobank study also provides similar results, and the effect of genetic risk of obesity on BMI was stronger for people watching at least four hours of TV per day compared with those watching
obesity 11131 of genetic risk and adiposity was exacerbated by adverse sleeping characteristics [[47]].Childhood obesity is a strong risk factor for metabolic abnormalities in later adulthood [[57],[58]]. In line with evidence
obesity 11333 with evidence in adults, studies have shown that FTO rs9939609 genotype was associated with childhood obesity [[59],[60],[61],[62]], and also suggested an association of the FTO variant and dietary intake and preference
obesity 12069 A study suggests an interaction between the FTO SNP rs9939609 and socioeconomic status on childhood obesity [[64]], and some other studies reported gene–environment interactions in childhood obesity [[53],[65],[66]].
obesity 12162 childhood obesity [[64]], and some other studies reported gene–environment interactions in childhood obesity [[53],[65],[66]]. In a population-based longitudinal study in Brazil, Vitamin D status significantly
obesity 12929 Controlled Trial (DIRECT) [[69]], we have performed a series of analyses on gene–diet interactions in obesity and metabolic risk factors (Table 2) [[70],[71],[72],[73],[74],[75],[76],[77],[78],[79],[80],[81],[82],[83],[84],[85],[86],[87],[88],[89],[90],[91],[92],[93]].
obesity 15438 were significantly influenced by several other individual genetic variants, such as those relating obesity (FTO and NPY), and type 2 diabetes (TCF7L2 and IRS1, etc.). Also, a genetic variant in FGF21 region
obesity 15622 variant in FGF21 region determining preference to carbohydrate intake was associated with improving obesity in the POUNDS Lost trial [[70]]. Our series of studies through assessing gene–diet interaction support
obesity 16969 bariatric surgery is also considered to be an effective treatment for patients with severe and complex obesity [[106],[107],[108]]. There is a significant genetic contribution to weight loss after Roux-en-Y gastric
obesity 18852 concentrations have been consistently associated with metabolic abnormalities like type 2 diabetes and obesity -associated insulin resistance [[27],[114],[118],[119]]. Also, taurine metabolism disturbance is closely
obesity 18974 insulin resistance [[27],[114],[118],[119]]. Also, taurine metabolism disturbance is closely linked to obesity , insulin resistance and diabetes, and we recently reported that effects of diabetes genetic risk (assessed
obesity 19741 and these variants would be useful to investigate effects of genetic determinant of metabolites on obesity . According to the Mendelian randomization principle, genetic variants can be a better marker than biomarkers
obesity 20062 causation. We previously examined relations between a genetic variant determining amino acid metabolites and obesity in the POUNDS Lost trial [[87]]. We identified significant interactions between dietary fat and a genetic
obesity 20779 Interactions of Diet with Gut MicrobiomeGut microbiota may be a potential factor for the treatment of obesity and related metabolic diseases [[120],[121]], and a study has also shown that obese individuals with
obesity 22419 intake [[16]]. In a study of elderly Mediterranean population, an association of the LCT variant and obesity was significantly modified by dairy lactose and milk intake [[129]], suggesting that changes in the
obesity 22654 LCT genotype might be involved in differences in caloric extraction of ingested food and the risk of obesity [[129]]. Further studies considering gut-microbiome, those related genetic variants, and dietary habit
obesity 23041 replicable in other populations [[23],[24],[25]]. In previous publications on gene–diet interactions on obesity , results from different populations are presented to demonstrate that the findings are replicable in
obesity 23404 perform more detailed analyses including different types of dietary factors, phenotypes, and different obesity GRSs. Within the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium, authors
obesity 24923 individuals, and these differences in BMI may create false positive evidence of interaction.8. ConclusionsThe obesity epidemic during the past decades has coincided with a profound shift of unhealthy dietary patterns,
obesity 25105 unhealthy dietary patterns, a sedentary lifestyle, and physical inactivity. Genetic predisposition to obesity may have interacted with such an obesogenic environment in determining the obesity epidemic. Increasing
obesity 25188 predisposition to obesity may have interacted with such an obesogenic environment in determining the obesity epidemic. Increasing evidence has shown the potential effects of gene–environment interactions on
obesity 25296 epidemic. Increasing evidence has shown the potential effects of gene–environment interactions on obesity . Data from dietary intervention trials suggest that changes in adiposity and metabolic response to low-calorie
obesity 25514 weight-loss diets could be significantly modified by genetic variants, especially those related to obesity , type 2 diabetes, metabolism and food preference. While further external replication and a large-scale
obesity 26494 and gut microbiome that may act at the interface of genetic variation and environment in affecting obesity and health. Research integrating data on genes, dietary habits, metabolites and gut-microbiome in investigation
obesity 26815 future.ijms-18-00787-t001_Table 1Table 1Unfavorable lifestyle and dietary factors that may accelerate risk of obesity among individuals genetically at high risk.FactorsReferencesHigh intake of sugar-sweetened beverages[[39],[40],[41]]High
obesity 27288 2Genetic variant that may alter effect of low-fat/high-carbohydrate and high-protein weight-loss diets on obesity and metabolic risk factors among overweight and obese individuals.Low-Fat/High-Carbohydrate Diet or

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