• Journal of Preventive Medicine and Public Health
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• 제42권6호
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• pp.360-370
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• 2009

Genetic factors clearly play a role in carcinogenesis, but migrant studies provide unequivocal evidence that environmental factors are critical in defining cancer risk. Therefore, one may expect that the lower availability of substrate for biochemical reactions leads to more genetic changes in enzyme function; for example, most studies have indicated the variant MTHFR genotype 677TT is related to biomarkers, such as homocysteine concentrations or global DNA methylation particularly in a low folate diet. The modification of a phenotype related to a genotype, particularly by dietary habits, could support the notion that some of inconsistencies in findings from molecular epidemiologic studies could be due to differences in the populations studied and unaccounted underlying characteristics mediating the relationship between genetic polymorphisms and the actual phenotypes. Given the evidence that diet can modify cancer risk, gene-diet interactions in cancer etiology would be anticipated. However, much of the evidence in this area comes from observational epidemiology, which limits the causal inference. Thus, the investigation of these interactions is essential to gain a full understanding of the impact of genetic variation on health outcomes. This report reviews current approaches to gene-diet interactions in epidemiological studies. Characteristics of gene and dietary factors are divided into four categories: one carbon metabolism-related gene polymorphisms and dietary factors including folate, vitamin B group and methionines; oxidative stress-related gene polymorphisms and antioxidant nutrients including vegetable and fruit intake; carcinogen-metabolizing gene polymorphisms and meat intake including heterocyclic amins and polycyclic aromatic hydrocarbon; and other gene-diet interactive effect on cancer.

• Journal of Microbiology and Biotechnology
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• 제27권12호
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• pp.2228-2236
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• 2017

During menopausal transition, the imbalance of estrogen causes body weight gain. Although gut microbiome dysbiosis has been reported in postmenopausal obesity, it is not clear whether there is any difference in the microbiome profile between dietary-induced obesity and postmenopausal obesity. Therefore, in this study, we analyzed intestinal samples from ovariectomized mice and compared them with those of mice with high-fat diet-induced obesity. To further evaluate the presence of menopause-specific bacteria-gene interactions, we also analyzed the liver transcriptome. Investigation of the 16S rRNA V3-V4 region amplicon sequence profile revealed that menopausal obesity and dietary obesity resulted in similar gut microbiome structures. However, Bifidobacterium animalis was exclusively observed in the ovariectomized mice, which indicated that menopausal obesity resulted in a different intestinal microbiome than dietary obesity. Additionally, several bacterial taxa (Dorea species, Akkermansia muciniphila, and Desulfovibrio species) were found when the ovariectomized mice were treated with a high-fat diet. A significant correlation between the above-mentioned menopause-specific bacteria and the genes for female hormone metabolism was also observed, suggesting the possibility of bacteria-gene interactions in menopausal obesity. Our findings revealed the characteristics of the intestinal microbiome in menopausal obesity in the mouse model, which is very similar to the dietary obesity microbiome but having its own diagnostic bacteria.

• Asian-Australasian Journal of Animal Sciences
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• 제25권9호
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• pp.1285-1293
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• 2012

The aim of the present study was to evaluate the effect of commercial monostrain and multistrain probiotics in diets on growth performance, intestinal morphology and mucin gene (MUC2) expression in broiler chicks. Three hundred seventy-eight 1-d-old male Arian broiler chicks were allocated in 3 experimental groups for 6 wk. The birds were fed on a corn-soybean based diet and depending on the addition were labeled as follows: control-unsupplemented (C), birds supplemented with Bacillus subtilis (BS) and lactic acid bacteria (LAB) based probiotics. Each treatment had 6 replicates of 21 broilers each. Treatment effects on body weight, feed intake, feed conversion ratio and biomarkers such as intestinal goblet cell density, villus length, villus width, and mucin gene expression were determined. Total feed intake did not differ significantly between control birds and those fed a diet with probiotics (p>0.05). However, significant differences in growth performance were found. Final body weight at 42 d of age was higher in birds fed a diet with probiotics compared to those fed a diet without probiotic (p<0.05). Inclusion of Bacillus subtilis based probiotic in the diets also significantly affected feed conversion rate (FCR) compared with control birds (p<0.05). No differences in growth performance were observed in birds fed different types of probiotic supplemented diets. Inclusion of lactic acid bacteria based probiotic in the diets significantly increased goblet cell number and villus length (p<0.05). Furthermore, diets with Bacillus subtilis based probiotics significantly increased gene expression (p<0.05), with higher intestinal MUC2 mRNA in birds fed diet with probiotics compared to those fed the control diet. In BS and LAB probiotic fed chicks, higher growth performance may be related to higher expression of the MUC2 gene in goblet cells and/or morphological change of small intestinal tract. The higher synthesis of the mucin gene after probiotic administration may positively affect bacterial interactions in the intestinal digestive tract, intestinal mucosal cell proliferation and consequently efficient nutrient absorption.

• Genomics & Informatics
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• 제8권3호
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• pp.116-121
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• 2010

The association between adiponectin concentration and obesity have been reported and genetic variations of the ADIPOQ gene are known to influence the plasmatic concentration of adiponectin. Therefore, we investigated the effect of AIPOQ single nucleotide polymorphism (SNP) on obesity-related variables, and their modulation by dietary intakes in Korean women. The subjects consisted of 3,217 Korean women aged 40-59 years participating in the Korean Genome Epidemiology Study (KoGES). The general characteristics, anthropometric variables, serum blood profiles were measured. Dietary intake was analyzed using the Food Frequency Questionnaire. Subjects with the T allele of AIPOQ rs182052 showed significantly higher obesity-related variables such as weight (p=0.005), BMI (p<0.000), fat body mass (p=0.005), and waist-hip ratio (p=0.007) than those with the C allele. Moreover, the rs182052 T allele was associated with an increased risk of obesity prevalence (p=0.019). However, there were not any significant interactions observed between the genotype of ADIPOQ rs182052 and dietary intake on BMI and fat body mass. These findings suggest that the obesity-related variables may be more dominantly affected by the genotype of ADIPOQ rs182052 than dietary intake in middle aged Korean women.

• Journal of Korean Biological Nursing Science
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• 제25권1호
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• pp.73-85
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• 2023

Purpose: This study focused on identifying the interaction effects of genetic and lifestyle-environmental factors on the development of type 2 diabetes mellitus (T2D). Methods: Study subjects were selected from the Korean Genome and Epidemiology Study (KoGES) from 2001 to 2014. Data on genetic variations, anthropometric measurements, biochemical data, and seven lifestyle factors (diet, physical activity, alcohol drinking, smoking, sleep, depression, and stress) were obtained from 4,836 Koreans aged between 40 and 59 years, including those with T2D at baseline (n = 1,209), newly developed T2D (n= 1,298) and verified controls (n = 3,538). The genetic risk score (GRS) was calculated by using 11 single-nucleotide polymorphisms (SNPs) related to T2D development and the second quartile was used as the reference category. A Cox proportional hazards regression model was used to evaluate the associations of GRS and lifestyle factors with T2D risk, controlling for covariates. Results: Multivariate regression analysis revealed that GRS was the strongest risk factor for T2D, and body mass index (BMI), smoking, drinking, and spicy food preference also increased the risk. Lifestyle/environmental factors that showed significant interactions with GRS were BMI, current smoking, current drinking, fatty food preference, and spicy food preference. Conclusions: Interactions between genetic factors and lifestyle/environmental factors were associated with an increased risk of T2D. The results will be useful to provide a new perspective on genetic profiling for the earlier detection of T2D risk and clues for personalized interventions, which might be more effective prevention strategies or therapies in individuals with a genetic predisposition to T2D.

• Preventive Nutrition and Food Science
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• 제20권1호
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• pp.1-7
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• 2015

Obesity has become one of the major public health problems all over the world. Recent novel eras of research are opening for the effective management of obesity though gene and nutrient intake interactions because the causes of obesity are complex and multifactorial. Through GWASs (genome-wide association studies) and genetic variations (SNPs, single nucleotide polymorphisms), as the genetic factors are likely to determine individuals' obesity predisposition. The understanding of genetic approaches in nutritional sciences is referred as "nutrigenomics". Nutrigenomics explores the interaction between genetic factors and dietary nutrient intake on various disease phenotypes such as obesity. Therefore, this novel approach might suggest a solution for the effective prevention and treatment of obesity through individual genetic profiles and help improve health conditions.

• Animal Bioscience
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• 제35권2호
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• pp.247-259
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• 2022

Objective: This study was conducted to investigate the effects of age and diet forms on growth-development patterns, serum metabolism indicators, and parameters of body fat deposition in Cherry Valley ducks. Methods: According to the hatching age and initial weight, a total of 150 1-day-old male SM3 Cherry Valley ducks were randomly assigned to two diet forms (pellet vs powder form). Each treatment had with 5 replicates per treatment and 15 meat ducks per replicate. The study lasted 42 d, which was divided into two periods (1 to 21 vs 22 to 42 d). Results: Our results showed that compared with powder group, ducks in pellet group had greater growth performance during different period (p<0.05). The inflection point was 24 d and was not numerically affected by diet forms. Increasing age (42 vs 21 d) significantly increased the weight of body fat and hepatic fat metabolism related enzyme activities in ducks (p<0.05), meanwhile, increasing age (42 vs 21 d) improved serum metabolism indicators and decreased mRNA expression levels of fat metabolism-related genes in liver (p<0.05). Ducks fed different diets (pellet vs powder form) increased growth performance as well as the weight of body fat and improved serum metabolism indicators (p<0.05). In addition, interactions were found between age and diet forms on the levels of serum metabolism indicators in ducks (p<0.05). Conclusion: In conclusion, powder feed reduced growth performance of ducks, and the day of inflection point was 24 days old. Ducks with higher age or fed with pellet diet showed higher fat deposition. The effect of age and feed forms on body fat deposition might result from changes in the contents of serum metabolism indicators, key enzyme activity of lipid production, and hepatic gene expressions.

• 한국식품위생안전성학회지
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• 제22권1호
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• pp.1-14
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• 2007

The term, "food safety", has traditionally been viewed as a practical science aimed at assuring the prevention acute illnesses caused by biological microorganisms, and only to a minor extent, chronic diseases cause by chronic low level exposures to natural and synthetic chemicals or pollutants. "food safety" meant to prevent microbiological agents/toxins in/on foods, due to contamination any where from "farm to Fork", from causing acute health effects, especially to the young, immune-compromised, genetically-predisposed and elderly. However, today a broader view must also include the fact that diet, perse (nutrients, vitamins/minerals, calories), as well as low level toxins and pollutant or supplemented synthetic chemicals, can alter gene expressions of stem/progenitor/terminally-differentiated cells, leading to chronic inflammation and other mal-functions that could lead to diseases such as cancer, diabetes, atherogenesis and possibly reproductive and neurological disorders. Understanding of the mechanisms by which natural or synthetic chemical toxins/toxicants, in/on food, interact with the pathogenesis of acute and chronic diseases, should lead to a "systems" approach to "food safety". Clearly, the interactions of diet/food with the genetic background, gender, and developmental state of the individual, together with (a) interactions of other endogenous/exogenous chemicals/drugs; (b) the specific biology of the cells being affected; (c) the mechanisms by which the presence or absence of toxins/toxicants and nutrients work to cause toxicities; and (d) how those mechanisms affect the pathogenesis of acute and/or chronic diseases, must be integrated into a "system" approach. Mechanisms of how toxins/toxicants cause cellular toxicities, such as mutagenesis; cytotoxicity and altered gene expression, must take into account (a) irreversible or reversal changes caused by these toxins or toxicants; (b)concepts of thresholds or no-thresholds of action; and (c) concepts of differential effects on stem cells, progenitor cells and terminally differentiated cells in different organs. This brief Commentary tries to illustrate this complex interaction between what is on/in foods with one disease, namely cancer. Since the understanding of cancer, while still incomplete, can shed light on the multiple ways that toxins/toxicants, as well as dietary modulation of nutrients/vitamins/metals/ calories, can either enhance or reduce the risk to cancer. In particular, diets that alter the embryo-fetal micro-environment might dramatically alter disease formation later in life. In effect "food safety" can not be assessed without understanding how food could be 'toxic', or how that mechanism of toxicity interacts with the pathogenesis of any disease.

• Asian-Australasian Journal of Animal Sciences
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• 제20권5호
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• pp.789-794
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• 2007

A PCR-aided monitoring of verotoxin-producing Escherichia coli (VTEC) was performed over the period of 12 months by using fresh feces collected monthly from 5 dairy cows that had been identified as VTEC carriers. The PCR products were confirmed to be verotoxin genes by Southern hybridization using a gene fragment of verotoxin 2 as a probe. Although seasonal variation of VTEC shedding seemed to depend on each cow, several factors may have influenced the frequency of detection. Shedding of VTEC tended to be reduced during grazing from the middle of May up to the beginning of October. Only one cow was positive for VTEC in August. Dry-off was also suggested to have a depressive effect on VTEC shedding, i.e. 3 of 4 dry cows showed no shedding of VTEC. Contrary to these factors, winter or indoor rearing tended to increase VTEC with only 5/24 samples being negative during the period from November to April. Total VFA concentration was higher (p<0.05) in VTEC-positive feces than in VTEC-negative feces, while fecal pH and VFA proportions were not different. Partial sequences of verotoxin genes from feces of 4 VTEC-positive cows were nearly identical (99-100%), suggesting that gut bacteria sharing the same gene were distributed among the cows. The present results indicate that grazing and dry-off could be factors which reduce VTEC shedding, while winter/indoor rearing may be a factor which increases the shedding, possibly through on-farm interactions.

• Asian Pacific Journal of Cancer Prevention
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• 제16권4호
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• pp.1591-1597
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• 2015

Background: Korea has experienced rapid economic development in a very short period of time. A mixture of traditional and modern risk factors coexists and the rapid change in non-genetic factors interacts with genetic constituents. With consideration of these unique aspects of Korean society, a large-scale genomic cohort study-the Health Examinees (HEXA) Study-has been conducted to investigate epidemiologic characteristics, genomic features, and gene-environment interactions of major chronic diseases including cancer in the Korean population. Materials and Methods: Following a standardized study protocol, the subjects were prospectively recruited from 38 health examination centers and training hospitals throughout the country. An interview-based questionnaire survey was conducted to collect information on socio-demographic characteristics, medical history, medication usage, family history, lifestyle factors, diet, physical activity, and reproductive factors for women. Various biological specimens (i.e., plasma, serum, buffy coat, blood cells, genomic DNA, and urine) were collected for biorepository according to the standardized protocol. Skilled medical staff also performed physical examinations. Results: Between 2004 and 2013, a total of 167,169 subjects aged 40-69 years were recruited for the HEXA study. Participants are being followed up utilizing active and passive methods. The first wave of active follow-up began in 2012 and it will be continued until 2015. The principal purpose of passive follow-up is based on data linkages with the National Death Certificate, the National Cancer Registry, and the National Health Insurance Claim data. Conclusions: The HEXA study will render an opportunity to investigate biomarkers of early health index and the chronological changes associated with chronic diseases.