• Journal of Life Science
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• v.21 no.1
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• pp.155-158
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• 2011

Uncoupling protein (UCP) 3 has a number of proposed roles in the regulation of fatty acid metabolism. A number of polymorphisms in the human UCP3 gene have been identified, and the correlation with obesity related phenotypes evaluated. The objective of this study was to identify SNP in porcine UCP3 gene and to investigate the effect of the SNP on economic traits. The sequencing analysis method was used to identify nucleotide polymorphisms at position 1405 bp (Genebank accession No : AY739704) in porcine UCP3 gene. The SNP (G150R), located in the exon 3, changed the amino acid to glycine (GGG) from arginine (AGG). This G150R showed three genotypes - GG, GR and RR - by digestion with the restriction enzyme Sma Ⅰ using the PCR-RFLP method. The G150R showed significant effects only on back fat (P<0.05). Animals with the genotype GG had significantly higher back fat thickness (1.358 cm) than animals with the genotype GR (1.288 cm, P<0.05) and RR (1.286 cm, P<0.05). However, the genotypes had no significant association with ADG and days to 90kg. According to results of this study, a G allele of the G150R was found to have a significant effect on back fat thickness. It will be possible to use SNP markers on selected pigs to improve backfat thickness, an important economic trait.

• Reproductive and Developmental Biology
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• v.33 no.3
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• pp.163-169
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• 2009

Many biological systems are regulated by an intricate set of feedback loops that oscillate with a circadian rhythm of roughly 24 h. This circadian clock mediates an increase in body temperature, heart rate, blood pressure, and cortisol secretion early in the day. Recent studies have shown changes in the amplitude of the circadian clock in the hearts and livers of streptozotocin (STZ)-treated rats. It is therefore important to examine the relationships between circadian clock genes and growth factors and their effects on diabetic phenomena in animal models as well as in human patients. In this study, we sought to determine whether diurnal variation in organ development and the regulation of metabolism, including growth and development during the juvenile period in rats, exists as a mechanism for anticipating and responding to the environment. Also, we examined the relationship between changes in growth factor expression in the liver and clock-controlled protein synthesis and turnover, which are important in cellular growth. Specifically, we assessed the expression patterns of several clock genes, including Per1, Per2, Clock, Bmal1, Cry1 and Cry2 and growth factors such as insulin-like growth factor (IGF)-1 and -2 and transforming growth factor (TGF)-${\beta}1$ in rats with STZ-induced diabetes. Growth factor and clock gene expression in the liver at 1 week post-induction was clearly increased compared to the level in control rats. In contrast, the expression patterns of the genes were similar to those observed after 5 weeks in the STZ-treated rats. The increase in gene expression is likely a compensatory change in response to the obstruction of insulin function during the initial phase of induction. However, as the period of induction was extended, the expression of the compensatory genes decreased to the control level. This is likely the result of decreased insulin secretion due to the destruction of beta cells in the pancreas by STZ.

• Journal of Veterinary Clinics
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• v.19 no.3
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• pp.342-349
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• 2002

Vitamin D is one of important factors involved in the regulation of bone metabolism. In osteoporosis, the therapeutic effect of vitamin D on the healing process has still been controversial. To conform the effect of $1{\alpha}$, 25 dihydroxy-vitamin $D_3$ on osteoporosis, the change of serum calcium, serum phosphorus, serum alkaline phosphatase, bone mineral density and bone mineral content of osteoporotic tibia were examined comparatively in normal control group(positive control), CFA control(negative control), CFA+$1{\alpha}$, 25 dihydroxy-vitamin $D_3$ 0.01 ug/kg group and CFA+$1{\alpha}$, 25 dihydroxy-vitamin $D_3$ 0.1 ug/kg group after osteoporosis was induced by single injection of complete Freund's adjuvant(CFA) in rats. In change of serum calcium. the significantly increased value was shown on 2nd and 5th week(P< 0.05) after treatment in $1{\alpha}$, 25 dihydroxy-vitamin D$_3$ 0.01 ug/kg group and on 3rd week(P<0.05) after treatment in $1{\alpha}$, 25 dihydroxy-vitamin $D_3$ 0.1 ug/kg group than CFA control. In change of serum phosphorus, the significantly increased value was shown on 2nd week(P<0.05) after treatment in $1{\alpha}$, 25 dihydroxy-vitamin $D_3$ 0.01 ug/kg group and on 3rd and 4th week(P<0.05) after treatment in $1{\alpha}$, ,25 dihydroxy-vitamin $D_3$ 0.1 ug/kg group than CFA control. The value of bone mineral density and bone mineral content of tibia was increased in both $1{\alpha}$,25 dihydroxy-vitamin $D_3$ 0.01 ug/kg group and $1{\alpha}$, 25 dihydroxy-vitamin $D_3$ 0.1 ug/kg group than CFA control, and the increase rate of that was higher in $1{\alpha}$, 25 dihydroxy-vitamin $D_3$ 0.1 ug/kg group than $1{\alpha}$, 25 dihydroxy-vitamin $D_3$ 0.01 ug/kg group. Considering above findings collectively, it was considered that $1{\alpha}$, 25 dihydroxy-vitamin $D_3$ was effective in preventing the complete Freund's adjuvant-induced osteoporotic decrease of bone mass.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.1
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• pp.93-97
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• 2006

To investigate whether GyeongshinhaeGihwan 1(GGT1), an anti-obesity herbal medicine widely used in oriental medicine, regulates the expression of obesity-related genes, we measured the changes in mRNA levels of these genes by GGT1 in human growth hormone transgenic (hGHTg) obese male rats, and these effects by GGT1 were compared with those of reductil (RD), an anti-obesity drug approved by FDA. Rats received once daily oral administrations of autoclaved water, RD, or GGT1 for 8 weeks. At the end of study, rats were sacrificed and tissues were harvested. Total RNA from adipose tissue, liver and kidney was prepared and the mRNA levels for LPL (lipoprotein lipase), PPAR $\gamma$ (peroxisome proliferator activated receptor-gamma), PPAR$\delta$ (peroxisome proliferator activated receptor-delta), leptin, TNF$\alpha$ (tumor necrosis factor-alpha), and internal standard G3PDH (glyceraldehyde-3- phosphate dehydrogenase) were analyzed by RT-PCR. PPAR$\gamma$ mRNA levels of liver and kidney were decreased in drug-treated groups compared with control group and the decrease of PPAR$\gamma$ expression was more prominent in GGT1 group than in RD group, suggesting that GGT1 is effective in the inhibition of adipogenesis and lipid storage by decreasing the PPAR$\gamma$ expression. In contrast, PPAR$\delta$ mRNA levels of adipose tissue and kidney were increased by RD and GGT1 , and the magnitudes of increase were higher in GGT1 group than in RD group, indicating that GGT1 stimulates fatty acid oxidation and energy metabolism by activating PPAR$\delta$ expression, Compared with control and RD groups, GGT1 group had higher concentrations of serum leptin, a well-known inhibitor of appetite. However, The mRNA levels of leptin, LPL, and TNF$\alpha$ were not changed by GGT1 and RD, compared with DW. These results demonstrate that GGT1 not only decreases PPAR$\gamma$ expression of liver and kidney, but also increases PPAR$\delta$ expression of adipose tissue and kidney, leading to the regulation of obesity and that these effects were more pronounced in GGT1 group compared with RD group. In addition, GGT1 seems to prevent obesity by increasing the serum leptin levels.

• Journal of Life Science
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• v.17 no.3 s.83
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• pp.305-311
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• 2007

Glucocorticoids (GCs) alter metabolism, synaptogenesis, apoptosis, neurogenesis, and dendritic morphology in the hippocampus. To better understand how glucocorticoids regulate these aspects of hippocampal biology, we studied gene expression patterns in the CA3 (Hippocampal pyramidal cell field CA3) and dentate gyrus (DG). Litter-matched Lewis inbred rats treated for 20 days with either 9.5 mg per day sustained-release corticosterone or placebo pellets were compared with high-density oligonucleotide microarray analysis (Rat Neurobiology U34 Arrays, Affymetrix). In placebo-treated rats, 32 genes were expressed at greater levels in CA3 than DG, whereas 3 genes were expressed at great levels in DC than CA3. Regional differences were also apparent in corticosterone-induced changes in the hippocampal transcriptome. Six genes in CA3 and 41 genes in DC were differentially regulated by corticosterone. As per the glucocorticoid effects on gene transcription in the brain, forty three of these genes were upregulated, and 4 genes were downregulated. Genes differentially expressed in hippocampus included those for 13 neurotransmitter proteins, 5 ion channel related proteins, 4 transcription factors, 3 neurotrophic factors, 1 cytokine, 1 apoptosis related protein, and 5 genes involved in synaptogenesis. Interestingly, GCs can have suppressive effects on brain BDNF mRNA transcription, one of the neurotrophic factors. These results indicate the diversity of targets affected by chronic exposure to corticosterone and highlight important regional differences in hippocampal neurobiology.

• Molecules and Cells
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• v.28 no.5
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• pp.431-439
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• 2009

Rice Oryza sativa accelerated cell death and resistance 1 (OsACDR1) encodes a putative Raf-like mitogen-activated protein kinase kinase kinase (MAPKKK). We had previously reported upregulation of the OsACDR1 transcript by a range of environmental stimuli involved in eliciting defense-related pathways. Here we apply biochemical, gain and loss-of-function approaches to characterize OsACDR1 function in rice. The OsACDR1 protein showed autophosphorylation and possessed kinase activity. Rice plants overexpressing OsACDR1 exhibited spontaneous hypersensitive response (HR)-like lesions on leaves, upregulation of defense-related marker genes and accumulation of phenolic compounds and secondary metabolites (phytoalexins). These transgenic plants also acquired enhanced resistance to a fungal pathogen (Magnaporthe grisea) and showed inhibition of appressorial penetration on the leaf surface. In contrast, loss-of-function and RNA silenced OsACDR1 rice mutant plants showed downregulation of defense-related marker genes expressions and susceptibility to M. grisea. Furthermore, transient expression of an OsACDR1:GFP fusion protein in rice protoplast and onion epidermal cells revealed its localization to the nucleus. These results indicate that OsACDR1 plays an important role in the positive regulation of disease resistance in rice.

• Journal of Life Science
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• v.29 no.11
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• pp.1294-1303
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• 2019

Perchlorate is an anionic pollutant that is very soluble and stable in water. It has been detected not only in soil/ground water but also in surface water, drinking water, food, fish, and crops. Perchlorate inhibits iodine uptake by the thyroid gland and reduces production of thyroid hormones that are primarily responsible for regulation of metabolism. Although various technologies have been developed to remove perchlorate from the environment, biodegradation is the method of choice since it is economical and environmentally friendly. However there is limited information on perchlorate biodegradation in salt environment such as salt water. Therefore this paper reviews biodegradation of perchlorate in salt water and related microorganisms. Most biodegradation research has employed heterotrophic perchlorate removal using organic compounds such as acetate as electron donors. Biodegradation research has focused on perchlorate removal from spent brine generated by ion exchange technology that is primarily employed to clean up perchlorate-contaminated ground water. Continuous removal of perchlorate at up to 10% NaCl was shown when bioreactors were inoculated with enriched salt-tolerant perchlorate-reducing bacteria. However the reactors did not show long-term stable removal of perchlorate. Microorganisms belonging to ${\beta}$- and ${\gamma}$-Proteobacteria were dominant in bioreactors used to remove perchlorate from salt water. This review will help our understanding of perchlorate removal from salt water to develop a decent biotechnology for the process.

• Nutrition Research and Practice
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• v.15 no.6
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• pp.673-685
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• 2021

BACKGROUND/OBJECTIVES: Obesity is associated with the impaired regulation of T cells characterized by increased numbers of Th1 and Th17 cells and the dysregulation of vitamin D metabolism. Both obesity and vitamin D have been reported to affect autophagy; however, a limited number of studies have investigated the effects of vitamin D on T cell autophagy in obese mice. Therefore, we aimed to determine whether in vitro treatment with vitamin D affects the proliferation, function, and autophagy of T cells from obese and control mice. MATERIALS/METHODS: Five-week-old male C57BL/6 mice were fed control or high-fat diets (10% or 45% kcal fat: CON or HFDs, respectively) for 12 weeks. Purified T cells were stimulated with anti-CD3 and anti-CD28 monoclonal antibodies and cultured with either 10 nM 1,25(OH)₂D₃ or 0.1% ethanol (vehicle control). The proliferative response; expression of CD25, Foxp3, RORγt, and autophagy-related proteins (LC3A/B, SQSTM1/P62, BECLIN-1, ATG12); and the production of interferon (IFN)-γ, interleukin (IL)-4, IL-17A, and IL-10 by T cells were measured. RESULTS: Compared with the CON group, T cell proliferation tended to be lower, and the production of IFN-γ was higher in the HFD group. IL-17A production was reduced by 1,25(OH)2D₃ treatment in both groups. The LC3 II/I ratio was higher in the HFD group than the CON group, but P62 did not differ. We observed no effect of vitamin D treatment on T cell autophagy. CONCLUSIONS: Our findings suggest that diet-induced obesity may impair the function and inhibit autophagy of T cells, possibly leading to the dysregulation of T cell homeostasis, which may be behind the aggravation of inflammation commonly observed in obesity.

• Korean Journal of Microbiology
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• v.55 no.2
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• pp.160-163
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• 2019

Senegalimassilia sp. KGMB 04484 was isolated from fecal samples obtained from a healthy Korean. The whole-genome sequence of Senegalimassilia sp. KGMB 04484 was analyzed using the PacBio Sequel platform. The genome comprises a 2,748,041 bp chromosome with a G+C content of 61.18%, 2,300 total genes, 2,139 protein-coding gene, 21 rRNA genes, and 51 tRNA genes. Also, we found that strain KGMB 04484 had some genes for hydrolysis enzyme, fatty acid biosynthesis and metabolism in its genome based on the result of genome analysis. Those genes of KGMB 04484 may be related to regulation of human health and digest.

• Journal of Life Science
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• v.29 no.9
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• pp.1034-1046
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• 2019

The mitochondria is the major cellular organelle of energy metabolism for the supply of cellular energy; it also plays an important role in controlling calcium regulation, reactive oxygen species (ROS) production, and apoptosis. Mitochondrial dysfunction causes various diseases, such as neurodegenerative diseases, Lou Gehrig's disease, cardiovascular disease, mental disorders, diabetes, and cancer. Most of the diseases are age-related diseases. In this review, we focus on the roles of mitochondrial dysfunction in cancer. Mitochondrial dysfunction induces carcinogenesis and is found in many cancers. The factors that cause mitochondrial dysfunction differ depending on the types of carcinoma, and those factors could cause cancer malignancy, such as resistance to therapy and metastasis. Mitochondrial dysfunction is caused by a lack of mitochondria, an inability to provide key substances, or a dysfunction in the ATP synthesis machinery. The main factor associated with cancer malignancy is mtDNA depletion. Mitochondrial dysfunction would leads to malignancy through changes in molecular activity or expression, but it is not known in detail which changes lead to cancer malignancy. In order to explore the relationship between mitochondrial dysfunction and cancer malignancy in detail, mitochondria dysfunctional cell lines are constructed using chemical methods such as EtBr treatment or gene editing methods, including shRNA and CRISPR/Cas9. Those mitochondria dysfunctional cell lines are used in the study of various diseases caused by mitochondrial dysfunction, including cancer.