• The Journal of Korean Medicine
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• v.33 no.3
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• pp.33-45
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• 2012

Objectives: Recent data have revealed that the plasma concentration of inflammatory mediators is increased in the insulin-resistant states of obesity and type 2 diabetes. The purpose of this study was to investigate the antidiabetic and anti-obesity effect of Massa Medicata Fermentata on obese type 2 diabetes mice. Methods: In order to examine the effects of Massa Medicata Fermentata, obese type 2 diabetes mice induced by Surwit's high fat, high sucrose diet. Mice were divided into 4 groups of ND (normal diet), HFD (high fat and high sucrose diet), Met (high fat and high sucrose diet with metformin) and MMF (high fat and high sucrose diet with Massa Medicata Fermentata) and investigated over 8 weeks. Diabetic and obese clinical markers, including body weight, glucose level, lipid level, leptin concentration, epididymal fat pad and liver weights and adipose tissue macrophage (ATM) were determined. Results: Compared with the HFD group, body weight, fructosamine, triglyceride, epididymal fat pad weight and ATM were significantly reduced in the MMF group. Conclusions: From the above results, the intake of Massa Medicata Fermentata may be effective in anti-hyperglycemia and anti-obesity by the attenuation of glucose and lipid levels and also inflammation state. Massa Medicata Fermentata may be beneficial for controlling diabetes mellitus type 2 in humans.

• The Journal of Internal Korean Medicine
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• v.43 no.4
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• pp.606-624
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• 2022

Objective: The aim of this study was to compare the effects of different doses of Geumnyeonyijin-tang (GNYJT) water extracts with those of metformin (250 mg/kg) in mild diabetic-obese mice. Methods and Results: The 48 mice were divided into 1 normal pellet diet (NFD) group and 5 high-fat diet (HFD) groups. At the end of 12 weeks of oral administration of metformin (250 mg/kg) or GNYJT water extracts (400, 200, or100 mg/kg), the effects were evaluated. The HFD control mice showed noticeable increases in body weight, adipose tissue density, fat pad weight of the periovarian and abdominal wall, and insulin, blood glucose, and HbA1c levels, with decreases in serum HDL levels. Increases in the periovarian and dorsal abdominal fat pad, regions of steatohepatitis, adipocyte hypertrophy, and hepatocyte hypertrophy were also discovered. The HFD group showed a decline in glucose levels and elevation of hepatic gluconeogenesis, suggesting an HFD-induced AMPK downregulation related to glucose dysregulation, as well as lipid metabolism related to obese insulin-resistant type II diabetes, dyslipidemia, and oxidative stress related diabetic hepatopathy (non-alcoholic fatty liver disease, NAFLD). Conclusion: Assessment of the key parameters for inhibition of diabetes and related complications in HFD-fed diabetic-obese mice demonstrated that GNYJT water extracts have favorable ameliorating effects. The effect of GNYJT was manifested through the stimulation of AMPK upregulation of related hepatic glucose enzyme activities and expression of lipid metabolism-related genes. Therefore, appropriate oral dosages of GNYJT could be promising as a new preventive candidate for controlling diabetes and related complications. Further screening of biologically active compounds, elucidation of detailed mechanisms, and more animal studies are warranted.

• Journal of Ginseng Research
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• v.47 no.3
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• pp.420-428
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• 2023

Background: Ginsenoside F2 (GF2), a minor component of Panax ginseng, has been reported to possess a wide variety of pharmacological activities. However, its effects on glucose metabolism have not yet been reported. Here, we investigated the underlying signaling pathways involved in its effects on hepatic glucose. Methods: HepG2 cells were used to establish insulin-resistant (IR) model and treated with GF2. Cell viability and glucose uptake-related genes were also examined by real-time PCR and immunoblots. Results: Cell viability assays showed that GF2 up to 50 μM did not affect normal and IR-HepG2 cell viability. GF2 reduced oxidative stress by inhibiting phosphorylation of the mitogen-activated protein kinases (MAPK) signaling components such as c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase 1/2 (ERK1/2), and p38 MAPK, and reducing the nuclear translocation of NF-κB. Furthermore, GF2 activated PI3K/AKT signaling, upregulated the levels of glucose transporter 2 (GLUT-2) and GLUT-4 in IR-HepG2 cells, and promoted glucose absorption. At the same time, GF2 reduced phosphoenolpyruvate carboxykinase and glucose-6-phosphatase expression as well as inhibiting gluconeogenesis. Conclusion: Overall, GF2 improved glucose metabolism disorders by reducing cellular oxidative stress in IR-HepG2 cells via MAPK signaling, participating in the PI3K/AKT/GSK-3β signaling pathway, promoting glycogen synthesis, and inhibiting gluconeogenesis.

• The korean journal of orthodontics
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• v.35 no.5 s.112
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• pp.351-360
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• 2005

This study aimed to investigate the effects of indomethacin on distribution and expression of COX-2 and IGF-1 in the mandibular condyle ofi growing dogs and to examine the number of chondroclasts around the mineralization zone indomethacin inhibits prostatlandin $E_2$ production in the tissue by inhibiting synthesis of cyclooxygenase 2. Prostaglandin $E_2$ stimulates insulin-like growth factor synthesis. Insulin-like growth factor stimulates growth of mandibular condylar cartilage. Eight mongrel dogs. aged 13-14 weeks, were divided into 4 groups. Group 1 and group 2 were administered indomethacin 2 mg/Kg/day orally two times a day for 7 days and 14 days respectively. Group 3 were administered indomethacin 8mg/Kg/day orally 2 times a day for 14 days, and 4he control group were administered a placebo. The mandibular condyle heads were sectioned in $5{\mu}m$ thickness The specimens were stained with H-E staining. COX-2 immunohistochemical staining and IGF-1 immunohistochemical staining and examined under microscope. After TRAP staining, the number of chondroclasts were calculated The observed results were as follows: Indomethacin inhibited expression and distribution of COX-2 and IGF-1 on the proliferative zone of condylar cartillage. Indomethacin decreased the number of chondroclastes on the mineralization zone by a time-dependent manner (P<0.05). Indomethacin inhibited expression and distribution of IGF-I by a dose and time-dependent manner. These results show that indomethacin inhibited expression and distribution of COX-2 and IGF-1 on the proliferative zone of condylar cartilage and decreased the number of chondroclasts and suggests that when indomethacin is administered for a long time, condyle growth could be delayed.

• Food Science of Animal Resources
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• v.26 no.2
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• pp.257-262
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• 2006

This experiment was carried out to investigate the effect of hypoglycemic yogurt as a clinical test with person both who have diabetes and who don't have diabetes. Diabetes is a disease caused by unused and accumulated glucoses produced via the foods digestion due to the lack of insulin or lower tissue reaction to insulin. Patients with diabetes or complications of diabetes are on the rise annually. For the therapy and prevention of diabetes, a yogurt made from functional materials such as insulin-resistant FK-23 lactic acid bacteria, Pinitol, edible fiber which delays glucose-absorption, extract powder of glucose-absorption-inhibitory white bean and low-caloric Erythritol and banaba extract is effective for reduce or restrain the blood glucose levels. The blood glucose levels after a meal of non-diabetic persons were lower after drinking a hypoglycemic yogurt than they after drinking general yogurt. The blood glucose levels after a meal of 10 diabetic patients were checked after drinking the yoghurt. As a result, 19 mg/dL, 30 mg/dL, 31 mg/dL of blood glucose levels decreased in 30 min, 60 min and 120 min respectively after drinking the yogurt. Blood glucose inhibition rates of 80 % of the tested patients also decreased. The blood glucose level of the diabetic patients having drunk the yogurt for 30 days consistently decreased into 59 mg/dL in 120 min after a meal.

• BMB Reports
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• v.46 no.12
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• pp.606-610
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• 2013

Glucagon like peptide-1 (GLP-1) regulates glucose mediated-insulin secretion, nutrient accumulation, and ${\beta}$-cell growth. Despite the potential therapeutic usage for type 2 diabetes (T2D), GLP-1 has a short half-life in vivo ($t_{1/2}$ <2 min). In an attempt to prolong half-life, GLP-1 fusion proteins were genetically engineered: GLP-1 human serum albumin fusion (GLP-1/HSA), AGLP-1/HSA which has an additional alanine at the N-terminus of GLP-1, and AGLP-1-L/HSA, in which a peptide linker is inserted between AGLP-1 and HSA. Recombinant fusion proteins secreted from the Chinese Hamster Ovary-K1 (CHO-K1) cell line were purified with high purity (>96%). AGLP-1 fusion protein was resistant against the dipeptidyl peptidase-IV (DPP-IV). The fusion proteins activated cAMP-mediated signaling in rat insulinoma INS-1 cells. Furthermore, a C57BL/6N mice pharmacodynamics study exhibited that AGLP-1-L/HSA effectively reduced blood glucose level compared to AGLP-1/HSA.

• Kidney Research and Clinical Practice
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• v.35 no.2
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• pp.69-77
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• 2016

Diabetic nephropathy (DN) is the leading cause of end-stage renal disease, and its pathogenesis is complex and has not yet been fully elucidated. Abnormal glucose and lipid metabolism is key to understanding the pathogenesis of DN, which can develop in both type 1 and type 2 diabetes. A hallmark of this disease is the accumulation of glucose and lipids in renal cells, resulting in oxidative and endoplasmic reticulum stress, intracellular hypoxia, and inflammation, eventually leading to glomerulosclerosis and interstitial fibrosis. There is a growing body of evidence demonstrating that dysregulation of 50 adenosine monophosphate-activated protein kinase (AMPK), an enzyme that plays a principal role in cell growth and cellular energy homeostasis, in relevant tissues is a key component of the development of metabolic syndrome and type 2 diabetes mellitus; thus, targeting this enzyme may ameliorate some pathologic features of this disease. AMPK regulates the coordination of anabolic processes, with its activation proven to improve glucose and lipid homeostasis in insulin-resistant animal models, as well as demonstrating mitochondrial biogenesis and antitumor activity. In this review, we discuss new findings regarding the role of AMPK in the pathogenesis of DN and offer suggestions for feasible clinical use and future studies of the role of AMPK activators in this disorder.

• Clinical and Experimental Pediatrics
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• v.49 no.9
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• pp.946-951
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• 2006

Purpose : The purpose of this study was to demonstrate the effectiveness of combined exercise for 12 weeks on the adiponectin and obesity related variables in overweight and obese children. Methods : Eighteen children in 5th grade in a certain elementary school in Busan were recruited. They were all overweight or obese children(more than 85 percentile in body mass index). Nine children in the experimental group were given exercises consisting of walking and band resistant training for 12 weeks. Auxological data(including height, weight and body fat mass) and laboratory data (fasting blood sugar, insulin, adiponectin) were checked at baseline and at the 1 week, and at the 4 weeks and 12 weeks stages of their exercise program. Insulin resistance and sensitivity were evaluated indirectly using HOMA index and QUICKI index. Results : Adiponectin gradually decreased until the 4 weeks point and gradually increased thereafter to the starting level at the 12 weeks stage. Body weight, body mass index(BMI) and HOMA index significantly decreased more at the 1 week, 4 weeks, and 12 weeks stages in the experimental group than in the control group. Body fat mass significantly decreased at 12 weeks. The change of insulin was significantly correlated with changes of body weight and BMI. But there was no correlation between changes of adiponectin and changes of insulin. Conclusion : Exercise seems to effect the adiponectin concentration. And it might be assumed that exercise increases the adiponectin concentration if it is continued for long time(may be more than 12 weeks). More studies may be necessary to draw that conclusion.

• Journal of the Korean Society of Food Science and Nutrition
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• v.45 no.7
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• pp.929-937
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• 2016

The purpose of this study was to investigate the effect of Acanthopanax senticosus extract (ASE) (ethanol : DW=1:1, v/v) on inhibition of type 2 diabetes using an OLETF rat model via regulation of HbA1c and AGEs levels. Supplementation with ASE 0.1% and 0.5% effectively lowered levels of glucose, insulin, oral glucose tolerance test, and Homa-insulin resistance, suggesting reduced insulin resistance. Blood levels of HbA1c and AGEs were significantly reduced in a dose-dependent manner. As oxidative stress plays a key role in accelerating production of HbA1c and AGEs, which worsen symptoms of type 2 diabetes, levels of malonaldehyde and pro-inflammatory cytokines were measured. Lipid peroxidation in both blood and liver tissues was significantly reduced, and induction of pro-inflammatory cytokines interleukin-${\beta}$ and tumor necrosis factor-${\alpha}$, which elevate production of HbA1c and AGEs, was inhibited (P<0.05). To evaluate the possible cellular events after AGEs receptor activation, genetic expression of protein kinase C (PKC)-${\delta}$ and transforming growth factor (TGF)-${\beta}$ was measured by real-time polymerase chain reaction. Supplementation with both ASE 0.1% and 0.5% significantly inhibited mRNA expression of PKC-${\delta}$ and TGF-${\beta}$, indicating that ASE may have beneficial effects on preventing insulin-resistant cells or tissues from progressing to diabetic complications. Taken together, ASE has potential to improve type 2 diabetes by inhibiting insulin resistance and protein glycosylation, including production of HbA1c and AGEs. Anti-oxidative activities of ASE are a main requisite for reducing production of HbA1c and AGEs and are also related to regulation of the PKC signaling pathway, resulting in suppression of TGF-${\beta}$, which increases synthesis of collagen, prostaglandin, and disease-related proteins.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.20 no.9
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• pp.306-314
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• 2019

As dipeptidyl peptidase-4(DPP-4) inhibitors are used widely as a secondary treatment for type 2 diabetes because they tend to be well tolerated with minimal side effects, the human DPP-4(hDPP-4) gene was injected into a pig zygote through micro-injection, and 1-cell stage fertilized embryos were then transplanted surgically into the oviduct. Three pigs were fertilized with hDPP-4 genes and produced sixteen piglets, in which one male piglet was identified to be transgenic. Finally, transgenic pigs showing hDPP-4 gene expression in the tail were produced. Western blot and RT-PCR analysis confirmed that the hDPP-4 is expressed strongly in the membrane cells of the transgenic pig, and that the hDPP-4 gene appears in various tissues and tails. This suggests that the expression vector is normally expressed in transgenic pigs. These results are anticipated to be a model animal to check the endocrine function for insulin resistance that occurs in a hDPP-4 transgenic pig and to increase its value for use as a material in newly developed medicines.