• KSBB Journal
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• v.21 no.6 s.101
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• pp.466-473
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• 2006

Impaired insulin secretion from pancreatic beta-cells in response to glucose is an important feature in the pathology of non-insulin-dependent diabetes mellitus (NIDDM). In the course of screening for useful insulin secretagogues, we have isolated and identified YHB-2017 (Genistein) as a insulin secretion potentiator from fermentation broths of our in-house microbial library. The insulinotropic activity of YHB-2017 in isolated rat pancreatic islets was exerted only at high concentration of glucose (8.3-16 mM) but not at low concentration of glucose (3.3-5.5 mM). Also, in perifusion study with isolated rat pancreatic islets, YHB-2017 stimulated insulin secretion in a time-dependent manner when YHB-2017 was added to KRB buffer containing 16 mM glucose. In the presence of $200\;{\mu}M$ diazoxide and 35 mM KCI, which stimulates maximum $Ca^{2+}$ influx independently of KATP channel, YHB-2017 enhanced KATP channel-independent insulin secretion at high concentration glucose (16 mM). To elucidate the mechanisms of the glucose-dependent potentiation effect of YHB-2017, pharmacologic inhibitors for protein kinase A, protein kinase C and calcium/calmodulin kinase II were pre-treated and then the potentiation effect of YHB-2017 on insulin secretion was investigated. Pre-treatment of H89 as a PKA inhibitor had a significant inhibitory effect on YHB-2017-induced potentiation effect. Furthermore, western immunoblotting analyses revealed that YHB-2017 increased phosphorylation of PKA substrates and cAMP response element-binding protein (CREB) under high concentration of glucose. These results demonstrated that the insulinotropic effect of YHB-2017 is mediated through PKA signal pathway and activated amplifying $K_{ATP}$ channel-independent insulin secretion pathway.

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.3
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• pp.255-261
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• 2014

Essential fatty acid (EFA) is known to be required for the body to function normally and healthily. However, the effect of EFA on glucose uptake in skeletal muscle has not yet been fully investigated. In this study, we examined the effect of two EFAs, linoleic acid (LA) and ${\alpha}$-linolenic acid (ALA), on glucose uptake of C2C12 skeletal muscle cells and investigated the mechanism underlying the stimulatory effect of polyunsaturated EFAs in comparison with monounsaturated oleic acid (OA). In palmitic acid (PA)-induced insulin resistant cells, the co-treatment of EFAs and OA with PA almost restored the PA-induced decrease in the basal and insulin-stimulated 2-NBDG (fluorescent D-glucose analogue) uptake, respectively. Two EFAs and OA significantly protected PA-induced suppression of insulin signaling, respectively, which was confirmed by the increased levels of Akt phosphorylation and serine/threonine kinases ($PKC{\theta}$ and JNK) dephosphorylation in the western blot analysis. In PA-untreated, control cells, the treatment of $500{\mu}M$ EFA significantly stimulated 2-NBDG uptake, whereas OA did not. Phosphorylation of AMP-activated protein kinase (AMPK) and one of its downstream molecules, acetyl-CoA carboxylase (ACC) was markedly induced by EFA, but not OA. In addition, EFA-stimulated 2-NBDG uptake was significantly inhibited by the pre-treatment of a specific AMPK inhibitor, adenine 9-${\beta}$-D-arabinofuranoside (araA). These data suggest that the restoration of suppressed insulin signaling at PA-induced insulin resistant condition and AMPK activation are involved at least in the stimulatory effect of EFA on glucose uptake in C2C12 skeletal muscle cells.

• Korean Journal of Food Science and Technology
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• v.28 no.6
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• pp.1001-1008
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• 1996

Staphylococcal food poisoning is the major cause of bacterial food poisoning occurring in this country. Therefore government regulates commercial foods through Official Dictionary of Food that there should be free of enterotoxigenic Staphylococcus aureus in Korean rice cakes, bread, and a box lunch. Since at least 5 days are required to identify the S. aureus by the official method in the Dictionary it is difficult to prevent the food poisoning and the investigation of the outbreaks. In this report an improved determination method of the S. aureus has been developed using polymerase chain reaction (PCR) technique. Sense and antisense primers for specific amplification of genes encoding staphylococcal enterotoxins were designed and synthesized for the PCR. Rapid chromosomal DNA isolation method was also developed from S. aureus using lysostaphin. The PCR condition was developed as follows. Reaction solution $(50\;{\mu}l)$ consisted of target DNA $2\;{\mu}l$ (about 20ng), 10X buffer $5\;{\mu}l$, primer 100pmole, dNTP (10 mM) $4\;{\mu}l$ and Taq DNA polymerase 2.5 unit in a thin-wall tube. Operation condition of the PCR was 5 min pre-denaturation at $94^{\circ}C$, 15 sec denaturation at $94^{\circ}C$, 15 sec annealing at $50^{\circ}C$, 20 sec extension at $72^{\circ}C$, and 5 min post-extension at $72^{\circ}C$, and 30 cycles of denaturation-annealing- extension. Using the PCR with Perkin Elmer GeneAmp PCR system 2400, types of enterotoxigenic S. aureus could be identified from Ddok or bread in a day.

• Nutrition Research and Practice
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• v.12 no.6
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• pp.494-502
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• 2018

BACKGROUND/OBJECTIVES: Reducing the number of adipocytes by inducing apoptosis of mature adipocytes as well as suppressing differentiation of preadipocytes plays an important role in preventing obesity. This study examines the anti-adipogenic and pro-apoptotic effect of red pepper seed water extract (RPS) prepared at $4^{\circ}C$ (RPS4) in 3T3-L1 cells. MATERIALS/METHODS: Effect of RPS4 or its fractions on lipid accumulation was determined in 3T3-L1 cells using oil red O (ORO) staining. The expressions of AMP-activated protein kinase (AMPK) and adipogenic associated proteins [peroxisome proliferator-activated receptor-${\gamma}$ ($PPAR-{\gamma}$), CCAAT/enhancer-binding proteins ${\alpha}$ (C/EBP ${\alpha}$), sterol regulatory element binding protein-1c (SREBP-1c), fatty acid synthase (FAS), and acetyl-CoA carboxylase (ACC)] were measured in 3T3-L1 cells treated with RPS4. Apoptosis and the expression of Akt and Bcl-2 family proteins [B-cell lymphoma 2 (Bcl-2), Bcl-2-associated death promoter (Bad), Bcl-2 like protein 4 (Bax), Bal-2 homologous antagonist/killer (Bak)] were measured in mature 3T3-L1 cells treated with RPS4. RESULTS: Treatment of RPS4 ($0-75{\mu}g/mL$) or its fractions ($0-50{\mu}g/mL$) for 24 h did not have an apparent cytotoxicity on pre and mature 3T3-L1 cells. RPS4 significantly suppressed differentiation and cellular lipid accumulation by increasing the phosphorylation of AMPK and reducing the expression of $PPAR-{\gamma}$, C/EBP ${\alpha}$, SREBP-1c, FAS, and ACC. In addition, all fractions except ethyl acetate fraction significantly suppressed cellular lipid accumulation. RPS4 induced the apoptosis of mature adipocytes by hypophosphorylating Akt, increasing the expression of the pro-apoptotic proteins, Bak, Bax, and Bad, and reducing the expression of the anti-apoptotic proteins, Bcl-2 and p-Bad. CONCLUSIONS: These finding suggest that RPS4 can reduce the numbers as well as the size of adipocytes and might useful for preventing and treating obesity.

• Journal of the Korean Applied Science and Technology
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• v.36 no.3
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• pp.995-1007
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• 2019

The purpose of this study was to investigate the effects of 12-week elastic band exercise on body composition, blood lipids and AMPK in 24 elderly female volunteers aged 65-75 years, and they were divided into the combined exercise group(n=12) and the control group(n=12). The elastic band exercise method was to do exercise 3 times a week for 60 minutes per session, 1-4 weeks for low intensity of OMNI-RES 3-4, 5-8 weeks for medium intensity of OMNI-RES 5-6, 9-12 weeks for OMNI-RES 7-8 of high intensity. In order to compare the differences in the groups before and after the elastic band exercise, two-way repeated measures ANOVA was used to verify the interaction between group and time. The difference in the groups of the measured data was paired t-test, the difference between the groups was paired independent t-test, and analysis of covariance ANCOVA was performed to minimize the inter-group error. The statistical significance level of each item was set to .05. As a result, body fat percentage of exercise group significantly decreased (p<.05), and skeletal muscle volume was significantly increased (p<.01). TC, TG and LDL-C were not significantly different between the exercise and control groups, and HDL-C was significantly decreased in the control group (p<.05). AMPK was significantly decreased in the exercise group (p<.001), but there was no significant difference in the control group. According to the covariance analysis to minimize the error of difference between the pre-exercise groups (p<.05), there was significant difference in AMPK of groups after exercise. These results suggest that the 12-week elastic band exercise has a positive effect on the body composition and AMPK of the elderly women.

• Journal of Life Science
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• v.31 no.11
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• pp.987-994
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• 2021

Our previous studies have reported that antimicrobial peptides (AMPs) derived from the larvae of white-spotted flower chafer (Protaetia brevitarsis seulensis) exert anti-inflammatory and neuroprotective activities. This study explored the anti-inflammatory effects of protaetiamycine 9 (CVLKKAYFLTNLKLRG-NH₂), a novel AMP, derived from P. b. seulensis against lipopolysaccharide (LPS)-mediated inflammatory response in RAW264.7 macrophage cells. Protaetiamycine 9 (25, 50, 75, and 100 ㎍/ml) did not cause cytotoxic effects against RAW264.7 cells. The RAW264.7 cells were pre-treated with various concentrations of protaetiamycine 9 (25-100 ㎍/ml) for 1 hr and then exposed to LPS (100 ng/ml) for 24 hr. Protaetiamycine 9 treatments decreased the LPS-induced secretion of inflammatory mediators, such as nitric oxide (NO), in a dose-dependent manner. Protaetiamycine 9 (25-100 ㎍/ml) effectively downregulated the LPS-induced increase in mRNA and the protein expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2), which are involved in the production of inflammatory mediators. Protaetiamycine 9 also suppressed the production and gene expression of pro-inflammatory cytokines, including interleukin (IL)-6 and IL-1β, compared to the presence of LPS alone. Furthermore, protaetiamycine 9 inhibited the degradation of inhibitory kappa B alpha (IκB-α) and the phosphorylation of mitogen-activated protein kinases (MAPKs), such as extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38. In conclusion, these results suggest that protaetiamycine 9 exhibits LPS-mediated inflammatory responses by blocking IκB-α degradation and MAPK phosphorylation.

• Korean Journal of Plant Resources
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• v.35 no.4
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• pp.417-427
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• 2022

In this study, we investigated in vitro immuno-stimulatory and anti-obesity activity of fruit (LIF), leaves (LIL) and stems (LIS) from Lonicera insularis Nakai in mouse macrophages RAW264.7 cells and mouse pre-adipocytes 3T3-L1 cells. LIF, LIL and LIS increased the production of immunostimulatory factors such as nitric oxide (NO), inducible nitric oxide synthase (iNOS), interleukin-1β (IL-1β), cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α) and activated phagocytosis in RAW264.7 cells. Inhibition of toll-like receptor 2/4 (TLR2/4) partly blocked LIF, LIL and LIS mediated production of immunostimulatory factors. In addition, inhibition of mitogen-activated protein kinases (MAPK) signaling attenuated the production of immunostimulatory factors induced by LIF, LIL and LIS. Based on these results of this study, LIF, LIL and LIS is thought to activate macrophages the production of immunostimulatory factors and phagocytosis through toll-like receptor 2/4 (TLR2/4) and MAPKs signaling pathway. In anti-obesity study, LIF reduced the lipid accumulation in 3T3-L1 cells. LIF increased the protein phosphorylation expressions such as AMP-activated protein kinase (AMPK), hormone sensitive lipase (HSL), adipose triglyceride lipase (ATGL) related to the lipolysis of the adipocytes. In addition, LIF increased the expression of proteins involved in energy metabolism and brown adipose tissues differentiation such as peroxisome proliferator-activated receptor gamma coativator 1α (PGC-1α) and PR domain-containing16 (PRDM16). These results suggest that LIF is involved in lipid accumulation inhibition through expressing the proteins such as lipolysis and differentiation of white adipocytes to brown adipocytes.

• Journal of Life Science
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• v.34 no.7
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• pp.509-519
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• 2024

A previous study showed that krill oil improved recognition and memory through anti-oxidative effects in an amyloid β model, but the authors noted that further investigations are necessary of alterations to neurotransmitters' states and of serum lipid profile improvements related to serum lipid peroxidation. Accordingly, in this study, ICR mice were pre-treated intraperitoneally with scopolamine prior to induced neurotransmission impairment, and the effects of krill oil provision on their capabilities of cognition were tested by performing a passive avoidance test (PAT), water maze test (WMT), and novel object recognition test. Then, parameters including the acetylcholine (ACh) concentration, acetylcholinesterase activity (AChE), lipid peroxidation, serum lipid levels, and nerve cell proliferation were investigated. The results showed that krill oil improved the mice's abilities in recognition and memory as the times taken to complete the PAT and WMT were reduced compared to the mice in a comparison scopolamine-treated group. Krill oil produced an increased concentration of Ach, and this was accompanied by a decrease in AChE. As shown in a scopolamine-treated SH-SY5Y cell line, krill oil reduced the activity of AChE. Moreover, the suppression of lipid peroxidation-reflected in the finding that malondialdehyde was decreased with krill oil provision-is speculated to affect the recorded serum triglyceride and cholesterol decreases and LDL cholesterol increase. The intake of krill oil was also found to produce an improvement in brain-derived neurotrophic factor expression by stimulating the activation of cyclic AMP response element binding protein in the brain tissue. Overall, the current results imply that the provision of krill oil raises the cognition and memory by elevating neurotransmitters and by improving the serum lipid profile and nerve cell proliferation, which occur as lipid peroxidation is suppressed in the brain tissue.