• The Korea Journal of Herbology
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• v.32 no.1
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• pp.15-23
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• 2017

Objectives : It is well known that Sibjotang (Shizaotang), traditional herbal medicine formula, regulates the body fluid blood pressure homeostasis. This study is to investigate whether Sibjotang improves diabetic renal dysfunction in type II diabetes mellitus animal model, db/db mice. Methods : The animals model were divided into three groups at the age of 8 weeks; control group (C57BLKS/J-db/m mice), diabetic group [(C57BLKS/J+Lepr)-db/db mice], and Sibjotang group [(C57BLKS/J+Lepr)-db/db mice + Sibjotang 100 mg/kg/day]. During 8 weeks of treatment, blood glucose and urinary albumin excretion were checked in metabolic chamber at 8, 12, and 16 weeks of age, respectively. Results : Body weight and food intake of diabetic group were significantly higher than control group after 8 weeks administration. However, there were not significant different between the diabetic group and Sibjotang group. Urinary albumin excretion was significantly decreased in the Sibjotang group than the diabetic group. In addition, supplementation with Sibjotang significantly lowered levels of blood glucose, insulin, and homeostatic model assessment-insulin resistance (HOMA-IR), suggesting reduced insulin resistance. The ratio of mesangial matrix/glomerular area was markedly larger in diabetic group than control group, whereas Sibjotang significantly reduced this expansion. Moreover, immunohistological study revealed that Sibjotang attenuated the increase of transforming growth $factor(TGF)-{\beta}$ expression in kidney. Conclusion : Sibjotang ameliorates diabetes-associated renal injury through the improvement of the blood glucose and insulin sensitivity, and inhibiting the $TGF-{\beta}1$ expression. Therefore, Sibjotang may be a new therapeutic formula for the treatment of diabetic-associated renal dysfunction.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.5
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• pp.459-466
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• 2016

Adipogenic differentiation of mesenchymal stem cells (MSCs) is critical for metabolic homeostasis and nutrient signaling during development. However, limited information is available on the pivotal modulators of adipogenic differentiation of MSCs. Adaptor protein Lnk (Src homology 2B3 [SH2B3]), which belongs to a family of SH2-containing proteins, modulates the bioactivities of different stem cells, including hematopoietic stem cells and endothelial progenitor cells. In this study, we investigated whether an interaction between insulin-like growth factor-1 receptor (IGF-1R) and Lnk regulated IGF-1-induced adipogenic differentiation of MSCs. We found that wild-type MSCs showed greater adipogenic differentiation potential than $Lnk^{-/-}$ MSCs. An ex vivo adipogenic differentiation assay showed that $Lnk^{-/-}$ MSCs had decreased adipogenic differentiation potential compared with wild-type MSCs. Interestingly, we found that Lnk formed a complex with IGF-1R and that IGF-1 induced the dissociation of this complex. In addition, we observed that IGF-1-induced increase in the phosphorylation of Akt and mammalian target of rapamycin was triggered by the dissociation of the IGF-1R-Lnk complex. Expression levels of a pivotal transcription factor peroxisome proliferator-activated receptor gamma ($PPAR-{\gamma}$) and its adipogenic target genes (LPL and FABP4) significantly decreased in $Lnk^{-/-}$ MSCs. These results suggested that Lnk adaptor protein regulated the adipogenesis of MSCs through the $IGF-1/Akt/PPAR-{\gamma}$ pathway.

• Journal of Nutrition and Health
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• v.7 no.2
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• pp.37-51
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• 1974

This Study was carried out to observe the effect of nutritional condition on the change of protein metabolism in the animal body by feeding on imbalanced protein diet. A total 242 growing male albino rats, weighing $115{\sim}120$ gm, were used for the experimental animals. The rats were fed on the standard diet(st), protein flee diet(pf) and imbalanced protein diet(ib) for twelve weeks respectively. Hemoglobin, packed cell volume in blood, and total nitrogen, amino acid nitrogen, urea-nitrogen, creatinine, transaminases(GPT, GOT) in liver and serum, and total nitrogen in small intestine, and total nitrogen, urea-nitrogen In small intestine, and total nitrogen, urea-nitrogen, creatinine, urea-nitrogen/creatinine ratio in urine were measured. The results obtained are as follows; 1. The gained body weight were lower in pf group and ib group than those of st group. The gained body weight fed for 12 weeks, were 80% lower in pf group than those of st group, and the body weight of pf group for $50{\sim}75$ days feeding were $40{\sim}60%$ decreased, compared with the stating weight, and then all of them died. 2. The change of the brain, liver, kidney, spleen and small intestine by feeding on imbalanced diet for 12 weeks were no remarkable difference with the starting weight, but those of protein free diet group were half or more decrease and those were significantly lower in spleen and small intestine especially than the other organ 3. The contents of hemoglobin in pf group for 8 weeks feeding, and the packed cell volume in pf group for 8 weeks feeding and in ib group for 12 weeks feeding were decreased. but those of the other feeding group were almost same value. 4. The total nitrogen in the liver, small intestine and serum of each diet group were no remarkable difference respectively. The contents of amino acid nitrogen in pf group for 2 and 6 weeks feeding were increased. 5. On transaminases: a) The cycle of increase and decrease of GPT activities were come periodically and the interval of cycle were fast in the early stage of feeding and slow there-after. b) The GPT activities were decreased gradually in pf group after feeding and those were increased in ib group for 6 weeks feeding but decreased there-after. The frequency of cycle were more GPT than GOT and specially those of GPT in early stage of feeding were two or three times while GOT was one. c) The interval of increase and decrease in GOT and amino acid nitrogen cycle were similar tendency. 6. The contents of total nitrogen, creatinine and urea-nitrogen of pf group in urine were decreased very sharply from sharting feeding to one week but increased dully from six weeks to eight weeks feeding. The contents of urea-nitrogen of ib group were increased dully by feeding on ten weeks but decreased by feeding on twelve weeks. From the above results, it is concluded that the trend of the metabolic change is maintained equally by homeostatic mechanism using the endogenous protein source during a certain period by imbalanced protein diet feeding. The homeostatic mechanism is come peridically, very fast in early stage of feeing and than slow there-after.

• Korean Journal of Poultry Science
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• v.46 no.3
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• pp.185-191
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• 2019

Nucleoporin 210 (Nup210) is associated with several physiological processes including muscle and neural cell differentiation, autoimmune diseases, and peripheral T cell homeostasis. Chicken Nup210 (chNup210) gene was originally identified as one of the differentially expressed genes (DEGs) in the kidney tissues of chicken. To elucidate the role of Nup210 in metabolic disease of chicken, we studied the molecular characteristics of chNup210 and analyzed its gene expression under the stimulation of Toll-like receptor 3 (TLR3) ligands. The Nup210 genomic DNA and amino acid sequences of various species including fowls, fishes, and mammals were retrieved from the Ensemble database and subjected to bioinformatics analyses. The expression of Nup210 from several chicken tissues was probed through qRT-PCR, and chicken fibroblast DF-1 cell line was used to determine the change in expression of chNup210 after stimulation with TLR3 ligand, polyinosinic-polycytidylic acid (poly (I:C)). The chNup210 gene was highly expressed in chicken lung and spleen tissues. Although highly conserved among the species, chNup210 was evolutionary clustered in the same clade as that of duck compared to other mammals. Furthermore, this study revealed that chNup210 is expressed in TLR3 signaling pathway and provides fundamental information on Nup210 expression in chicken. Future studies that offer insight into the involvement of chNup210 in the chicken innate immune response against viral infection are recommended.

• Journal of Life Science
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• v.32 no.1
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• pp.63-69
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• 2022

The thioredoxin reductase (TrxR) system is essential for cell survival and function by playing a pivotal role in maintaining homeostasis of cellular redox and regulating signal transduction pathways. The TrxR system comprises thioredoxin (Trx), TrxR, and nicotinamide adenine dinucleotide phosphate. Trx reduced by the catalytic reaction of the TrxR enzyme reduces downstream proteins, resulting in protection against oxidative stress and regulation of cell differentiation, growth, and death. Cancer cells survive by improving their intracellular antioxidant capacity to eliminate excessively generated reactive oxygen species (ROS) due to infinite cell proliferation and a high metabolic rate. Therefore, cancer cells have high dependence and sensitivity to antioxidant systems, suggesting that focusing on TrxR, a representative antioxidant system, is a potential strategy for cancer therapy. Several studies have revealed that TrxR is expressed at high levels in various types of cancers, and research on anticancer activity targeting the TrxR system is increasing. In this review, we discuss the feasibility and value of the TrxR system as a strategy for anticancer activity research by examining the relationship between the function of the intracellular TrxR system and the development and progression of cancer, considering the anticancer activity and mechanism of TrxR inhibitors.

• Journal of Life Science
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• v.31 no.4
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• pp.442-451
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• 2021

Microplastics are fragments of any type of plastic with a size less than 5 mm. Ocean pollution by microplastics is now a worldwide concern in relation to marine ecosystems and human health. The widespread contamination by microplastics means that they can be ingested by and accumulated in diverse species of wildlife, such as fish, mussels, oysters, clams, and scallops. Once ingested, the microplastics can be observed in the intestines, liver, and kidney, and even in the brain. Seafood is one of the major sources of protein intake in humans; therefore, seafood consumption could be pathway for human microplastics exposure. Accumulating evidence indicates that repeated oral exposure to microplastics induces pathologic and functional changes in the reproductive, cardiac, gastrointestinal, endocrine, and even nervous systems of rodents. Maternal exposure to microplastics during gestation and lactation alters metabolic homeostasis in the offspring. Given that seafood provides more than 20% of the total protein intake by over 310 million people worldwide, a reasonable assumption is that microplastics could be substantially accumulated in the human body and impair physiological function. In this review, we have summarized the current status of microplastics contamination in the ocean, their accumulation and toxicities in marine animals and rodents, their exposure to humans, and their potential impacts on human health.

• Journal of Life Science
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• v.32 no.5
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• pp.391-410
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• 2022

Human microbiota is a community of microorganisms, including bacteria, fungi, and viruses, that inhabit various locations of the body, such as the gut, oral, and skin. Along with the development of metabolomic analysis and next-generation sequencing techniques for 16S ribosomal RNA, it has become possible to analyze the population for subtypes of microbiota, and with these techniques, it has been demonstrated that bacterial microbiota are involved in the metabolic and immunological processes of the hosts. While specific bacteria of microbiota, called commensal bacteria, positively affect hosts by producing essential nutrients and protecting hosts against other pathogenic microorganisms, dysbiosis, an abnormal microbiota composition, disrupts homeostasis and thereby has a detrimental effect on the development and progression of various types of diseases. Recently, several studies have reported that oral and gut bacteria of microbiota are involved in the carcinogenesis of gastrointestinal tumors and the therapeutic effects of anticancer therapy, such as radiation, chemotherapy, targeted therapy, and immunotherapy. Studying the complex relationships (bacterial microbiota-cancer-immunity) and microbiota-related carcinogenic mechanisms can provide important clues for understanding cancer and developing new cancer treatments. This review provides a summary of current studies focused on how bacterial microbiota affect gastrointestinal cancer and anticancer therapy and discusses compelling possibilities for using microbiota as a combinatorial therapy to improve the therapeutic effects of existing anticancer treatments.

• Journal of Ginseng Research
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• v.47 no.3
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• pp.376-384
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• 2023

Background: Hepatic lipid disorder impaired mitochondrial homeostasis and intracellular redox balance, triggering development of non-alcohol fatty liver disease (NAFLD), while effective therapeutic approach remains inadequate. Ginsenosides Rc has been reported to maintain glucose balance in adipose tissue, while its role in regulating lipid metabolism remain vacant. Thus, we investigated the function and mechanism of ginsenosides Rc in defending high fat diet (HFD)-induced NAFLD. Methods: Mice primary hepatocytes (MPHs) challenged with oleic acid & palmitic acid were used to test the effects of ginsenosides Rc on intracellular lipid metabolism. RNAseq and molecular docking study were performed to explore potential targets of ginsenosides Rc in defending lipid deposition. Wild type and liver specific sirtuin 6 (SIRT6, 50721) deficient mice on HFD for 12 weeks were subjected to different dose of ginsenosides Rc to determine the function and detailed mechanism in vivo. Results: We identified ginsenosides Rc as a novel SIRT6 activator via increasing its expression and deacetylase activity. Ginsenosides Rc defends OA&PA-induced lipid deposition in MPHs and protects mice against HFD-induced metabolic disorder in dosage dependent manner. Ginsenosides Rc (20mg/kg) injection improved glucose intolerance, insulin resistance, oxidative stress and inflammation response in HFD mice. Ginsenosides Rc treatment accelerates peroxisome proliferator activated receptor alpha (PPAR-α, 19013)-mediated fatty acid oxidation in vivo and in vitro. Hepatic specific SIRT6 deletion abolished ginsenoside Rc-derived protective effects against HFD-induced NAFLD. Conclusion: Ginsenosides Rc protects mice against HFD-induced hepatosteatosis by improving PPAR-α-mediated fatty acid oxidation and antioxidant capacity in a SIRT6 dependent manner, and providing a promising strategy for NAFLD.

• Journal of Nutrition and Health
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• v.57 no.1
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• pp.16-26
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• 2024

Purpose: Type 2 diabetes mellitus is a metabolic condition marked by persistent elevated blood sugar levels resulting from insulin resistance. The effective management of diabetes mellitus involves strict regulation of the blood glucose levels. This study examined the effects of Autumn olive (Elaeagnus umbellata Thunb.) berry (AOB) on insulin resistance and hyperglycemia using a type 2 diabetes mellitus animal model. Methods: Eight-week-old C57BL/6J mice were divided into four groups. The control group received a basal diet, while the high-fat, high-sucrose (HFHS) group was fed a HFHS diet containing 27% sucrose and 33% lard for 12 weeks. The low AOB (LAOB) and high AOB (HAOB) groups were offered a HFHS diet with a 0.5% and 1.0% AOB extract, respectively. Results: The HAOB group showed significantly lower epididymal fat pad weight than the HFHS group. The LAOB and HAOB groups showed lower serum glucose levels and homeostasis model assessment for insulin resistance values than the HFHS group, and the HAOB group has lower serum insulin levels than the HFHS group. Supplementation with HAOB decreased serum cholesterol levels significantly compared with the HFHS group. The consumption of LAOB and HAOB reduced the serum triglyceride and hepatic total lipids and triglyceride levels compared to the HFHS group. In addition, LAOB and HAOB consumption in mice fed a HFHS diet increased adenosine monophosphate-activated protein kinase protein expression. Insulin receptor substrate-2 protein expression in the HAOB group was significantly higher than the HFHS group. Conclusion: AOB can alleviate hyperglycemia in type 2 diabetes mellitus partly by mitigating insulin resistance.

• Journal of Nutrition and Health
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• v.41 no.7
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• pp.602-611
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• 2008

We compared antiobese, hypocholesterolemic, antiplatelet and antioxidant effect of 10% green tea powder and 3% green tea extract in rats pair fed 5% cholesterol diets. The final body weight was decreased significantly compared with the control (p < 0.05). Plasma and liver total cholesterol were lower in group of green tea powder or extract, but not statistically different. HDL cholesterol was increased significantly in group of green tea powder compared with the control or green tea extract (p < 0.05). Plasma triglyceride was significantly decreased in group of green tea extract compared with green tea powder, and green tea powder compared with the control respectively (p < 0.05). Liver triglyceride was significantly decreased in group of green tea powder or green tea extract compared with the control (p < 0.01). Platelet aggregations in the maximum and initial slope were not different among groups. Hemolysis was significantly lower in group of green tea powder compared with the control (p < 0.05). Plasma TBARS production was decreased in group of green tea extract compared with the control (p < 0.05). Na passive leak in intact cells was not different, but Na leak in AAPH treated cell was significantly decreased in group of green tea powder than the control (p < 0.05). The leak increase (${\Delta}Na$ Leak) after AAPH treatment was significantly decreased in groups of green tea powder and extract compared with the control (p < 0.05). Isotope excretion after $^{14}C$-cholesterol ingestion was significantly increased in group of green tea extract compared with the control or the green tea powder (p < 0.05). Consumption of green tea in powder or extract may give beneficial effects in weight control and plasma lipid profiles, impeding metabolic syndrome. More studies are needed to clarify what component of green tea and what mechanism are involved in antiobese and hypolipedemic actions of green tea.