• Korean Journal of Poultry Science
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• v.26 no.1
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• pp.1-25
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• 1999

Concerns about meat quality, including chicken meat, for the human diet has led to many attempts to manipulate the carcass fat and increase the eating quality. For actual eating quality, the birds must be grown and finished in a manner that results in meat that are tender, succulent and of good flavor, as well as being free from any foreign taint, flavor or safety hazard. Tenderization treatment with high voltage(820V) electrical stimulation and prechill muscle tensioning would improve the tenderness of chicken meat. Proper programs for the withdrawal of feed and water require a team approach for maximizing yield of meat and minimizing carcass contamination. Also effding of supplemental levels of-tocopherol to poultry with vegetable or fish oils increases of desirable polyunsaturated fatty acid(PUFA) content and stablizes the meat against rancidity and fish off-flavors. The nutritional effects of varying dietary ingredients on broiler carcass fat content are also important. Increasing the levels of energy in the ration increases the carcass fat content, while increasing the proteing levels decreases carcass fat content. Supplement-tation of poultry diets with amino acids such as methionine, lysine, glycine and tryptophan as well as amino acid such as well as amino acid mixtures can reduce body fat deposition. Normal stress leads to chicken muscular damage resulting in reduced meat quality, but this can be controlled by preslaughter management practices. Feed manufactures can utilize ntilize nutrient modulation to control pale soft exudative(PSE)syndrome. Finally, the success in poultry meat production depends on the consistent achievement of carefully selected levels of quality. Quality assurance should be the wider function of incorporating quality into the production system and the combination of motivating quality into actions and operations.

• Clinical Nutrition Research
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• v.12 no.1
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• pp.40-53
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• 2023

Differential bitterness perception associated with genetic polymorphism in the bitter taste receptor gene taste 2 receptor member 38 (TAS2R38) may influence an individual's food preferences, nutrition consumption, and eventually chronic nutrition-related disorders including cardiovascular disease. Therefore, the effect of genetic variations on nutritional intake and clinical markers needs to be elaborated for health and disease prevention. In this study, we conducted sex-stratified analysis to examine the association between genetic variant TAS2R38 rs10246939 A > G with daily nutritional intake, blood pressure, and lipid parameters in Korean adults (males = 1,311 and females = 2,191). We used the data from the Multi Rural Communities Cohort, Korean Genome and Epidemiology Study. Findings suggested that the genetic variant TAS2R38 rs10246939 was associated with dietary intake of micronutrients including calcium (adjusted p = 0.007), phosphorous (adjusted p = 0.016), potassium (adjusted p = 0.022), vitamin C (adjusted p = 0.009), and vitamin E (adjusted p = 0.005) in females. However, this genetic variant did not influence blood glucose, lipid profile parameters, and other blood pressure markers. These may suggest that this genetic variation is associated with nutritional intake, but its clinical effect was not found. More studies are needed to explore whether TAS2R38 genotype may be a potential predictive marker for the risk of metabolic diseases via modulation of dietary intake.

• Journal of Animal Science and Technology
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• v.64 no.6
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• pp.1092-1104
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• 2022

Using antibiotics as growth promoter has been banned in poultry feed industry, thus various researchers try to seek an alternative to replace the growth-promoting antibiotics. In this study, we aimed to evaluate the growth performance via intestinal nutrient utilization and cecal microbial composition of broiler after dietary supplementation with most commonly using antibiotics, zinc bacitracin, and sophorolipid. A total of 180 1-day-old chicks were randomly assigned, and dietary treatment was as follow: CON, basal diet; ZB, 100 ppm of zinc bacitracin supplemented diet; and SPL, 250 ppm of sophorolipid supplemented diet. Their growth performance was evaluated and the samples of blood, small intestine, and ileal and cecal digesta were collected for biochemical, histological, and genomic analyses. The body weight and average daily gain of 7-day-old chicks were higher in ZB and those in overall experimental period were improved by ZB and SPL supplementation (p < 0.05). Their intestinal characteristics were not affected by dietary treatments in duodenum and ileum. Nonetheless, villus height was increased by SPL supplementation in jejunum (p < 0.05). Moreover, dietary SPL supplementation could down-regulate the expression level of pro-inflammatory cytokine, IL-1β (p < 0.05). mRNA levels of lipid and protein transporters did not differ among the treatments, however, relative expression levels of carbohydrate transporters, GLUT2 and SGLT1 were increased in broiler chicken's jejumum fed zinc bacitracin and sophorolipid supplemented diets (p < 0.05). Dietary zinc bacitracin supplementation could increase the population of Firmicutes in phylum level, and the portion of Turiciacter in genus level. On the other hands, the portion of Faecalibacterium was increased by dietary SPL supplementation compared to the other treatments. Our findings suggest that SPL supplementation improves growth performance through enhanced carbohydrate utilization capacity via improvement of gut morphological status and modulation of the cecal microbial population of broilers.

• Molecules and Cells
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• v.41 no.1
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• pp.11-17
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• 2018

Autophagy is critical for the maintenance of organelle function and intracellular nutrient environment. Autophagy is also involved in systemic metabolic homeostasis, and its dysregulation can lead to or accelerate the development of metabolic disorders. While the role of autophagy in the global metabolism of model organisms has been investigated mostly using site-specific genetic knockout technology, the impact of dysregulated autophagy on systemic metabolism has been unclear. Here, we review recent papers showing the role of autophagy in systemic metabolism and in the development of metabolic disorders. Also included are data suggesting the role of autophagy in human-type diabetes, which are different in several key aspects from murine models of diabetes. The results shown here support the view that autophagy modulation could be a new modality for the treatment of metabolic syndrome associated with lipid overload and human-type diabetes.

• Nutrition Research and Practice
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• v.15 no.sup1
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• pp.1-21
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• 2021

The coronavirus disease 2019 (COVID-19) pandemic has put focus on the importance of a healthy immune system for recovery from infection and effective response to vaccination. Several nutrients have been under attention because their nutritional statuses showed associations with the incidence or severity of COVID-19 or because they affect several aspects of immune function. Nutritional status, immune function, and viral infection are closely interrelated. Undernutrition impairs immune function, which can lead to increased susceptibility to viral infection, while viral infection itself can result in changes in nutritional status. Here, we review the roles of vitamins A, C, D, and E, and zinc, iron, and selenium in immune function and viral infection and their relevance to COVID-19.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.27 no.3
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• pp.137-145
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• 2024

Stunting, a condition characterized by impaired growth and development in children, remains a major public health concern worldwide. Over the past decade, emerging evidence has shed light on the potential role of gut microbiota modulation in stunting. Gut microbiota dysbiosis has been linked to impaired nutrient absorption, chronic inflammation, altered short-chain fatty acid production, and perturbed hormonal and signaling pathways, all of which may hinder optimal growth in children. This review aims to provide a comprehensive analysis of existing research exploring the bidirectional relationship between stunting and the gut microbiota. Although stunting can alter the gut microbial community, microbiota dysbiosis may exacerbate it, forming a vicious cycle that sustains the condition. The need for effective preventive and therapeutic strategies targeting the gut microbiota to combat stunting is also discussed. Nutritional interventions, probiotics, and prebiotics are among the most promising approaches to modulate the gut microbiota and potentially ameliorate stunting outcomes. Ultimately, a better understanding of the gut microbiota-stunting nexus is vital for guiding evidence-based interventions that can improve the growth and development trajectory of children worldwide, making substantial strides toward reducing the burden of stunting in vulnerable populations.

• Childhood Kidney Diseases
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• v.21 no.1
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• pp.1-7
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• 2017

Mitogen-activated protein kinases (MAPKs) play important roles in various cellular functions including proliferation, differentiation, and apoptosis. We showed that MAPKs are developmentally regulated in the rat kidney. p38 MAPK (p38) and extracellular signal-regulated kinase (ERK) were strongly expressed in the fetal kidney, whereas c-Jun N-terminal kinase (JNK) was detected predominantly in the adult kidney. The inhibition of p38 or ERK in organ culture resulted in reduced nephron formation with or without reduced kidney size. On the other hand, persistent fetal expression pattern of MAPKs, i.e., upregulation of p38 and ERK and downregulation of JNK, was observed in the cyst epithelium of human renal dysplasia, ovine fetal obstructive uropathy, and pcy mice, a model of polycystic kidney disease. Furthermore, activated p38 and ERK induced by cyclic stretch mediated proliferation and $TGF-{\beta}1$ expression in ureteric bud cells, probably leading to cyst formation and dysplastic changes. Inhibition of ERK slowed the disease progression in pcy mice. Finally, ERK and p38 were inactivated in the early embryonic kidney subjected to maternal nutrient restriction, characterized by reduced ureteric branching and nephron number. Thus, MAPKs mediate the development of normal and diseased kidney. Their modulation may result in novel therapeutic strategies against developmental abnormalities of the kidney.

• Proceedings of the Korean Society of Plant Pathology Conference
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• 2005.10a
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• pp.15-20
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• 2005

Locations of silicon accumulation in rice leaves and its possible association with resistance to rice blast were investigated by analytical electron microscopy and atomic force microscopy. A blast-susceptible cultivar, Jinmi, and partially resistant cultivars, Hwaseong and Suwon345, were grown under a hydroponic culture system with modified Yoshida's nutrient solution. Electron-dense silicon layers were frequently found beneath the cuticle in epidermal cell walls of silicon-treated plants. Increasing levels of silicon were detected in the outer regions of epidermal cell walls. Silicon was present mainly in epidermal cell walls, middle lamella, and Intercellular spaces within subepidermal tissues. Furthermore, silicon was prevalent throughout the leaf surface with relatively small deposition on stomatal guard cells in silicon-treated plants. Force-distance curve measurements revealed relative hardness and smaller adhesion force in silicon-treated plants (18.65 uN) than control plants (28.39 uN). Moreover, force modulation microscopy showed higher mean height values of elastic Images In silicon-treated plants(1.26 V) than in control plants (0.44 V), implying the increased leaf hardness by silicon treatment. These results strongly suggest that silicon-induced cell wall fortification of rice leaves may be closely associated with enhanced host resistance to blast.

• Parasites, Hosts and Diseases
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• v.38 no.3
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• pp.195-199
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• 2000

The 27 kDa cathepsin L-like cysteine protease of Spirometra erinocei plerocercoid is known to play an important function in tissue penetration, nutrient uptake and immune modulation in human sparganosis. In the present study, the expression of this enzyme was examined at different developmental stages of S. erinacei including immature egg, coracidium, plerocercoid in tadpole and rat, and adult Proteolytic activity against carboxybenzoyl-phenylalanyl-arginyl-7-amino-4-rnethylcournarin was do tooted in the extracts of coracidia and plerocercoid while no activity was observed in those of immature egg and adult. The specific activity in coraridial extracts was lower than that in the plerocercoid. Reverse transcription-polymerase chain reaction and Northern biol analysis demonstrated that the gene was expressed in the coracidium and plerocercoid but not in immature egg and adult. These results suggest that the 27 kDa cysteine protease is only expressed in the stages involving active migration of the parasite in the host tissue.

• Nutrition Research and Practice
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• v.17 no.4
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• pp.597-615
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• 2023

Healthy aging can be defined as an extended lifespan and health span. Nutrition has been regarded as an important factor in healthy aging, because nutrients, bioactive food components, and diets have demonstrated beneficial effects on aging hallmarks such as oxidative stress, mitochondrial function, apoptosis and autophagy, genomic stability, and immune function. Nutrition also plays a role in epigenetic regulation of gene expression, and DNA methylation is the most extensively investigated epigenetic phenomenon in aging. Interestingly, age-associated DNA methylation can be modulated by one-carbon metabolism or inhibition of DNA methyltransferases. One-carbon metabolism ultimately controls the balance between the universal methyl donor S-adenosylmethionine and the methyltransferase inhibitor S-adenosylhomocysteine. Water-soluble B-vitamins such as folate, vitamin B6, and vitamin B12 serve as coenzymes for multiple steps in one-carbon metabolism, whereas methionine, choline, betaine, and serine act as methyl donors. Thus, these one-carbon nutrients can modify age-associated DNA methylation and subsequently alter the age-associated physiologic and pathologic processes. We cannot elude aging per se but we may at least change age-associated DNA methylation, which could mitigate age-associated diseases and disorders.