• 제목/요약/키워드: glucose regulation

검색결과 354건 처리시간 0.026초

OP9 세포에서 포도당 흡수능에 대한 대계 추출물의 효과 (Effects of Herba Cirsii Extracts on Glucose Uptake in OP9 Cells)

  • 김미성;송제호
    • 동의생리병리학회지
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    • 제28권2호
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    • pp.195-199
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    • 2014
  • Although the Herba Cirsii is known to posses beneficial health effects, the anti-diabetic effects and the mechanism of action have not been elucidated. In the present study we have shown that Herba Cirsii Extract (HCE) can stimulate glucose uptake in OP9 adipocytes. Unlike insulin, HCE did not stimulate the Ser473 phosphorylation and activation of Akt. The increasing effects of HCE on glucose uptake were inhibited by PD680509 and compound C pretreatment, which means that the glucose uptake effects by HCE were carried out by extracelluar signal-regulated kinase1/2(ERK1/2) and AMP-activated protein kinase (AMPK) activation. Further studies revealed that HCE stimulated glucose transport occurs through a mechanism involving ERK1/2 activation and AMPK activation.

갈락토스-글루코스 혼합당 수소 발효 (Hydrogen Fermentation of the Galactose-Glucose Mixture)

  • 천효창;김상현
    • 한국수소및신에너지학회논문집
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    • 제23권4호
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    • pp.397-403
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    • 2012
  • Galactose, an isomer of glucose with an opposite hydroxyl group at the 4-carbon, is a major fermentable sugar in various promising feedstock for hydrogen production including red algal biomass. In this study, hydrogen production characteristics of galactose-glucose mixture were investigated using batch fermentation experiments with heat-treated digester sludge as inoclua. Galactose showed a hydogen yield compatible with glucose. However, more complicated metabolic steps for galactose utilization caused a slower hydrogen production rate. The existence of glucose aggravated the hydrogen production rate, which would result from the regulation of galactose-utilizing enzymes by glucose. Hydrogen produciton rate at galactose to glucose ratio of 8:2 or 6:4 was 67% of the production rate for galactose and 33% for glucose, which could need approximately 1.5 and 3 times longer hydraulic retention time than galacgtose only condition and glucose only condition, respectively, in continuous fermentation. Hydrogen production rate, Hydrogen yield, and organic acid production at galactose to glucose ratio of 8:2 or 6:4 were 0.14 mL H2/mL/hr, 0.78 mol $H_2$/mol sugar, and 11.89 g COD/L, respectively. Galactose-rich biomass could be usable for hydogen fermenation, however, the fermentation time should be allowed enough.

Association Analysis between Genes' Variants for Regulating Mitochondrial Dynamics and Fasting Blood Glucose Level

  • Jung, Dongju;Jin, Hyun-Seok
    • 대한의생명과학회지
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    • 제22권3호
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    • pp.107-114
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    • 2016
  • Maintenance of fasting blood glucose levels is important for glucose homeostasis. Disruption of feedback mechanisms are a major reason for elevations of glucose level in blood, which is a risk factor for type 2 diabetes mellitus that is mainly caused by malfunction of pancreatic beta-cell and insulin. The fasting blood glucose level has been known to be influenced by genetic and environmental factors. Mitochondria have many functions for cell survival and death: glucose metabolism, fatty acid oxidation, ATP generation, reactive oxygen species (ROS) metabolism, calcium handling, and apoptosis regulation. In addition to these functions, mitochondria change their morphology dynamically in response to multiple signals resulting in fusion and fission. In this study, we aimed to examine association between fasting blood glucose levels and variants of the genes that are reported to have functions in mitochondrial dynamics, fusion and fission, using a cohort study. A total 416 SNPs from 36 mitochondrial dynamics genes were selected to analyze the quantitative association with fasting glucose level. Among the 416 SNPs, 4 SNPs of PRKACB, 13 SNPs of PPP3CA, 6 SNPs of PARK2, and 3 SNPs of GDAP1 were significantly associated. In this study, we were able to confirm an association of mitochondrial dynamics genes with glucose levels. To our knowledge our study is the first to identify specific SNPs related to fasting blood glucose level.

Effect of White, Taegeuk, and Red Ginseng Root Extracts on Insulin-Stimulated Glucose Uptake in Muscle Cells and Proliferation of β-cells

  • Cha, Ji-Young;Park, Eun-Young;Kim, Ha-Jung;Park, Sang-Un;Nam, Ki-Yeul;Choi, Jae-Eul;Jun, Hee-Sook
    • Journal of Ginseng Research
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    • 제34권3호
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    • pp.192-197
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    • 2010
  • Recent studies have indicated that $\beta$-cell dysfunction and insulin resistance are important factors in the development of type 2 diabetes. The present study investigated the effect of extracts from different parts of white, Taegeuk, and red ginseng root on insulin-stimulated glucose uptake in muscle cells and proliferation of $\beta$-cells. Extracts of the fine roots of Taegeuk ginseng significantly enhanced glucose uptake compared with the control. White ginseng lateral root extracts enhanced insulin-induced glucose uptake. Proliferation of $\beta$-cells was significantly increased by Taegeuk ginseng main and lateral root extracts and by red ginseng lateral and fine root extracts. In conclusion, different root parts of white, Taegeuk, and red ginseng differentially affect glucose uptake and pancreatic $\beta$-cell proliferation.

The Regulation of Insulin-Like Growth (IGF) Factors and IGF Binding Proteins by High Glucose in Mesangial Cells

  • Park Soo-hyun
    • 대한의생명과학회지
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    • 제10권3호
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    • pp.203-210
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    • 2004
  • It has been reported that glomerulosclerosis mediated by the dysfunction of mesangial cells and insulin-like growth factors (IGFs) are associated with the development of diabetic nephropathy. However, it is not yet known the effect of high glucose on IGF-I, -II secretion, IGF-I receptor, and IGFBPs expression in the mesangial cells. Thus, this study was conducted to examine the effect of high glucose on IGF system and its involvement of protein kinase C (PKC) and oxidative stress in mesangial cells. In this study, high glucose (25 mM) increased IGF-I and IGF-II secretion and mRNA expression (P<0.05), which was blocked by PKC inhibitor (staurosporine, 10/sup -8/ M) and antioxidant (N-acetyl cystein, 10/sup -5/ M). High glucose decreased IGFBP-1 and -2 expression but increased IGFBP-5 expression. These alteration of IGFBPs by high glucose was also prevented by staurosporine and NAC, suggesting the role of PKC and oxidative stress. Indeed, high glucose increased PKC activity. Furthermore, high glucose-induced increase of lipid peroxide (LPO) formation was blocked by PKC inhibitors. In conclusion, high glucose alters IGF system via PKC-oxidative pathways in mesangial cells.

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Pancastatin A and B Have Selective Cytotoxicity on Glucose-Deprived PANC-1 Human Pancreatic Cancer Cells

  • Park, Hae-Ryong
    • Journal of Microbiology and Biotechnology
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    • 제30권5호
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    • pp.733-738
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    • 2020
  • Glucose deprivation and hypoxia frequently occur in solid tumor cells, including pancreatic cancer cells. Glucose deprivation activates the unfolded protein response (UPR) and causes the up-regulation of glucose-regulated protein 78 (GRP78). Induction of GRP78 has been shown to protect cancer cells. Therefore, shutting down of GRP78 expression may be a novel strategy in anticancer drug development. Based on this understanding, a screening system established for anticancer agents that exhibit selective cytotoxicity on pancreatic cancer cells under glucose-deprived conditions. To test this hypothesis, the new compounds isolated, pancastatin A (PST-A) and B (PST-B), from Ponciri Fructus. PST-A and B were identified as glabretal triterpenoid moieties by electrospray ionization mass spectrometry and nuclear magnetic resonance spectroscopic methods. PST-A and B suppressed the accumulation of the UPR hallmark gene, GRP78, during glucose deprivation. Furthermore, PST-A and B showed selective cytotoxicity on PANC-1 pancreatic cancer cells under glucose deprivation. Interestingly, PST-A and B had no effect on these cells under normal growth conditions. Our results suggest that PST-A and B act as novel therapeutic agents to induce selective cell death in glucose-deprived pancreatic cancer cells.

Aloe-Emodin Protects RIN-5F (Pancreatic β-cell) Cell from Glucotoxicity via Regulation of Pro-Inflammatory Cytokine and Downregulation of Bax and Caspase 3

  • Alshatwi, Ali A;Subash-Babu, P.
    • Biomolecules & Therapeutics
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    • 제24권1호
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    • pp.49-56
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    • 2016
  • To determine the protective effect of aloe-emodin (AE) from high glucose induced toxicity in RIN-5F (pancreatic ${\beta}$-cell) cell and restoration of its function was analyzed. RIN-5F cells have been cultured in high glucose (25 mM glucose) condition, with and without AE treatment. RIN-5F cells cultured in high glucose decreased cell viability and increased ROS levels after 48 hr compared with standard medium (5.5 mM glucose). Glucotoxicity was confirmed by significantly increased ROS production, increased pro-inflammatory (IFN-${\gamma}$, IL-$1{\beta}$,) & decreased anti-inflammatory (IL-6&IL-10) cytokine levels, increased DNA fragmentation. In addition, we found increased Bax, caspase 3, Fadd, and Fas and significantly reduced Bcl-2 expression after 48 hr. RIN-5F treated with both high glucose and AE ($20{\mu}M$) decreased ROS generation and prevent RIN-5F cell from glucotoxicity. In addition, AE treated cells cultured in high glucose were transferred to standard medium, normal responsiveness to glucose was restored within 8hr and normal basal insulin release within 24 hr was achieved when compared to high glucose.

당뇨병 환자의 혈당 변동에 대한 시스템다이내믹스 모델 개발 (Development of System Dynamics Model for the Variation of Plasma Glucose Levels in Patients with Type 2 Diabetes)

  • 최은옥;곽찬영
    • 한국시스템다이내믹스연구
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    • 제9권1호
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    • pp.155-170
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    • 2008
  • The purpose of this study was to develop a system dynamics model for management of glucose metabolism disorders that demonstrated dynamic relationships between insulin and plasma glucose levels over the time. The model was developed to 1) represent the physiology of glucose metabolism for an normal adult subject, 2) to draw causal loop diagram that demonstrate feedback systems of glucose regulation in normal condition and pathologic condition of the type 2 diabetes, 3) to develop an interactive computer simulation model for management of glucose metabolism disorders. The simulation results showed the plasma glucose level for normal persons varied from 75 to 140 which was consistent with clinical findings. As an example for patients we selected a case which varied from 110 to 310. Two types of interventions were chosen to review the model; meal control and insulin administration. The simulation results for those cases also matched well with clinical findings. The developed model can be used as an effective educational tool for patients to develop healthy lifestyle choices. The results also provide a blueprint for health providers to maintain normal blood glucose levels in diabetes patients.

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Regulation of Electrochemical Oxidation of Glucose by lonic Strength-Controlled Virtual Area of Nanoporous Platinum Electrode

  • Kim, Jong-Won;Park, Se-Jin
    • 전기화학회지
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    • 제10권3호
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    • pp.203-206
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    • 2007
  • Electrochemical reaction of glucose was regulated by the electrochemically active area of nanoporous platinum, which is controlled by ionic strength. The profile of the oxidation current of glucose vs. ionic strength was identical with that of the electrochemically active area. This result confirms that the nanopores are virtually opened for the electrochemical reaction of glucose when the ionic strength climbs over a specific concentration and implies that the electrochemical reactions on nanoporous electrode surfaces can be controlled by concentration of electrolyte.

항정신병 약물과 혈당조절이상 (Antipsychotics and Abnormality in Glucose Regulation)

  • 황재승;김현;권영준;정희연
    • 생물정신의학
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    • 제10권2호
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    • pp.107-115
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    • 2003
  • Objective:The purpose of this study was to know about the mechanism of pathogenesis of type 2 diabetes mellitus by using of blood glucose, glucoregulatory factor, insulin resistance in schizophrenic patients receiving antipsychotics. Method:Modified oral glucose tolerance tests were performed in 20 schizophrenic patients receiving haloperidol, risperidone and olanzapine. Insulin, glucagon, C-peptide and cortisol were measured in 0, 15, 45, 75 minutes after glucose loading, and insulin resistance was calculated by HOMA(homeostasis model assessment) method. Result:Olanzapine-treated patients had significant glucose elevation 45 minutes after glucose challenge. Also modest increases in HOMA IR values were detected in patients treated with olanzapine. Conclusion:Olanzapine treatment of non-diabetic patients with schizophrenia can be associated with type 2 diabetes mellitus through the elevation of glucose and insulin resistance. Elevated insulin resistance may be a causative mechanism of type 2 diabetes mellitus in patients receiving olanzapine.

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