• Molecules and Cells
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• 제23권3호
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• pp.272-279
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• 2007

The maintenance of normal blood glucose levels at rest and during exercise is critical. The maintenance of blood glucose homeostasis depends on the coordination and integration of several physiological systems, including the sympathetic nervous system and the endocrine system. During prolonged exercise increased demand for glucose by contracting muscle causes to increase glucose uptake to working skeletal muscle. Increase in glucose uptake by working skeletal muscle during prolonged exercise is due to an increase in the translocation of insulin and contraction sensitive glucose transporter-4 (GLUT4) proteins to the plasma membrane. However, normal blood glucose level can be maintained by the augmentation of glucose production and release through the stimulation of liver glycogen breakdown, and the stimulation of the synthesis of glucose from other substances, and by the mobilization of other fuels that may serve as alternatives. Both feedback and feedforward mechanisms allow glycemia to be controlled during exercise. This review focuses on factors that control blood glucose homeostasis during prolonged exercise.

• Journal of Ginseng Research
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• 제45권2호
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• pp.228-235
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• 2021

Backgroud: Ginsenoside compound K (GK) is a major metabolite of protopanaxadiol-type ginsenosides and has remarkable anticancer activities in vitro and in vivo. This work used an ionic cross-linking method to entrap GK within O-carboxymethyl chitosan (OCMC) nanoparticles (Nps) to form GK-loaded OCMC Nps (GK-OCMC Nps), which enhance the aqueous solubility and stability of GK. Methods: The GK-OCMC Nps were characterized using several physicochemical techniques, including x-ray diffraction, transmission electron microscopy, zeta potential analysis, and particle size analysis via dynamic light scattering. GK was released from GK-OCMC Nps and was conducted using the dialysis bag diffusion method. The effects of GK and GK-OCMC Nps on PC3 cell viability were measured by using the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay. Fluorescent technology based on Cy5.5-labeled probes was used to explore the cellular uptake of GK-OCMC Nps. Results: The GK-OCMC NPs had a suitable particle size and zeta potential; they were spherical with good dispersion. In vitro drug release from GK-OCMC NPs was pH dependent. Moreover, the in vitro cytotoxicity study and cellular uptake assays indicated that the GK-OCMC Nps significantly enhanced the cytotoxicity and cellular uptake of GK toward the PC3 cells. GK-OCMC Nps also significantly promoted the activities of both caspase-3 and caspase-9. Conclusion: GK-OCMC Nps are potential nanocarriers for delivering hydrophobic drugs, thereby enhancing water solubility and permeability and improving the antiproliferative effects of GK.

• 약학회지
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• 제40권6호
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• pp.705-712
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• 1996

We have previously shown that determination of glucose uptake using ${\alpha}$-methylglucose(${\alpha}$-MG) is very sensitive and rapid parameter for the assessment of loss of cellular fu nction in renal cell line($LLC-PK_1$). The present study was designed to elucidate the mechanism of inhibition of ${\alpha}$-MG uptake and the intracellular site of toxic action of cisplatin(CIS). $LLC-PK_1$ cells were exposed to various concentrations(5 ${\mu}$M-l00 ${\mu}$M) of CIS for 5 hrs or 24 hrs and ${\alpha}$-MG uptake was determined. Mitochondrial function was evaluated by measuring intracellular ATP content and MTT reduction. The activities of marker enzymes for the basolateral membrane(Na$^+$-K$^+$ ATPase) and brush border membrane (alkaline phosphatase: ALP) were also measured. CIS treatment significantly inhibited the ${\alpha}$-MG uptake in a time- and dose-dependent manner above 25 ${\mu}$M for 5 hrs. Intracellular ATP content and MTT reduction were affected by 24 hr-treatment of 50 ${\mu}$M CIS. The activities of Na$^+$-K$^+$ ATPase and ALP were significantly decreased at 10 ${\mu}$M and 5 ${\mu}$M of CIS for 24 hrs, respectively. The incubation with CIS for 5 hrs had no effects on the intracellular ATP content, MTT reduction and the activities of marker enzymes up to 100 ${\mu}$M. These results partly indicate that inhibition of ${\alpha}$-MG uptake by CIS may not be attributed to the disturbance of mitochondrial function or inhibition of the activity of Na$^+$-K$^+$ ATPase and can be resulted from direct effect of CIS on the Na$^+$/glucose cotransporter in brush border membrane. This study shows that additional mechanistic information, indicating the intracellular site of nephrotoxic action, can be gained by coupling the ${\alpha}$-MG uptake and ATP content or the activity of Na$^+$-K$^+$ ATPase.

• Natural Product Sciences
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• 제19권1호
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• pp.1-7
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• 2013

AMP-activated protein kinase (AMPK) is a major cellular energy sensor and master regulator of metabolic homeostasis. On activation, this cellular fuel sensing enzyme induces a series of metabolic changes to balance energy consumption via multiple downstream signaling pathways controlling nutrient uptake and energy metabolism. This pivotal role of AMPK has led to the development of numerous AMPK activators which might be used as novel drug candidates in the treatment of AMPK related disorders, diabetes, obesity, and other metabolic diseases. Consequently, a number of patents have been published on AMPK activators from natural products and other sources. This review covers the patented AMPK activators from natural products and their therapeutic potential in treatment or prevention of metabolic diseases including diabetes and obesity.

• Mycobiology
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• 제43권3호
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• pp.179-183
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• 2015

Zinc is an essential micronutrient required for many enzymes that play essential roles in a cell. It was estimated that approximately 3% of the total cellular proteins are required for zinc for their functions. Zinc has long been considered as one of the key players in host-pathogen interactions. The host sequesters intracellular zinc by utilizing multiple cellular zinc importers and exporters as a means of nutritional immunity. To overcome extreme zinc limitation within the host environment, pathogenic microbes have successfully evolved a number of mechanisms to secure sufficient concentrations of zinc for their survival and pathogenesis. In this review, we briefly discuss the zinc uptake systems and their regulation in the model fungus Saccharomyces cerevisiae and in major human pathogenic fungi such as Aspergillus fumigatus, Candida albicans, and Cryptococcus gattii.

• Journal of Microbiology and Biotechnology
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• 제23권1호
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• pp.131-135
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• 2013

A DOTAP analog labeled by NBD on the head group (DTNBD) was designed and synthesized to label DOTAP liposome. The structure was confirmed by $^1H$ NMR and FAB-MS, and the fluorescence of the newly synthesized DT-NBD was observed by fluorescent microscopy. The transfection efficiency of DOTAP liposome containing DT-NBD was comparable to commonly used NBD PE in COS7 and MCF7 cells. Furthermore, the level of cellular uptake and fluorescent intensity of fluorescent liposome containing DT-NBD was higher than NBD PE. Therefore, the novel NBD-labeled DOTAP analog seems to be effectively used for investigation of the cellular interaction and transfection mechanism of DOTAP liposome.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 2001년도 학술 발표회 진행표 및 논문초록
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• pp.39-39
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• 2001

Many physiological processes of plant cells, such as nutrient uptake, salt tolerance, and cell enlargement, are mediated by ion transports across the plasma membrane. H$^{＋}$-ATPases on both plasma and vacuolar membranes play major roles on active transports and ion channels mediate passive transports of various ions. It has been known that these proteins involved in cellular osmotic regulation and salt tolerance in the salt-accumulated soils.(omitted)

• Toxicological Research
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• 제7권2호
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• pp.183-189
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• 1991

Since streptozotocin has been known to be chemically stable only under acidic condition(pH 4), the spontaneous degradation and cellular uptake of streprozotocin in neutral incubation medium was determined by chemical assay. Streptozotocin levels in both phosphate buffered saline (pH 7.4) and Krebs-Henseleit buffer (pH 7.4) decreased with a half life of about 2 hours. The presence of erythrocytes or pepatocytes under the same buffers did not affect the streptozotocin degradation rate at all. However, streptozotocin levels in plasma isolated from rats decreased rapidly compared to those in neutral buffers.

• 미생물학회지
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• 제5권2호
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• pp.69-78
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• 1967

Kim, Jong Hyup, (Div. of Biology, Atomic Energy Research Institute.) Studies on the Cellular Metabolism in Microorganisms as influenced by Gamma-irradiation(II). On respiration rate and dehydrogenase activity of yeast cells irradiated by gamma ray from cobalt-60. 1. Oxygen uptake rate of the gamma irraiated yeast cells had been measured with Warburg's manometer, and the $O_{2}$-uptake was compared with those of normal cells. The rate of endogetious respiration increases in its $O_2$-uptake at 150, 000 rentgen dose, and at higher rentoen doses it was decreased. Exogenous respiration begin to decrease in its O_2$-uptake at 5, 000r. doses of irradiation, further decrease with increasing of doses unproportionally. 2. It appears that plasma-membrane and nuclear membrane of yeast cells have changed and denatured by gamma-irradiation, as exogenous respiration of glucose had been decreased at a dose of 200, 000r's irradiation. 3. The activity of glucose, alcoholic, lactic, succinic and glutamic deliydrogenase (G.D.H., A.D.H., L.D.H., S.D.11., and GL.D.H.) in the gamma irradaited cells had been assayed by T.T.C.(Triphenyl tetrazolium chloride) method and spectrophotometry, the obtained results were compared with those of normal cells. 4. At a dose of and 10, 000 rentgens' irradiation of gamma ray, the activty of each debydrogenase (G.D.H., A.D.H., L.D.H., ) shows a sharp and highest peak in optical absorbalicy, but each abtivity of S.D.H and Gl.D.H shows its' maximum peak at a dose of 30, 000r. 5. The curve of each dehydrogenase activity was found to be rhythmical according to dose-rate of gamma irradiation. 6. Comparing with activity of debydrogenase each other, the maximum peak in optical absorbency can be arranged according to order as follows; glucose > alcoholoic > lactic > glutamic > succinic, this order is identical to the order of breakdown utility in respiration of normal yeast cells. 7. The activity of dehydrogenase experimented exhibit a resistance against gamma irradiation at lethal dose of cells, and the activity of dehydrogenase are found to be much resistant than those of respiratory system. We may assume that the membrane substrate of mitochondria or cytoplasm had been destructed by gamma-irradiation much more than that of dehydronase system.

• Molecules and Cells
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• 제43권1호
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• pp.66-75
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• 2020

Saturated fatty acids contribute to β-cell dysfunction in the onset of type 2 diabetes mellitus. Cellular responses to lipotoxicity include oxidative stress, endoplasmic reticulum (ER) stress, and blockage of autophagy. Palmitate induces ER Ca²⁺ depletion followed by notable store-operated Ca²⁺ entry. Subsequent elevation of cytosolic Ca²⁺ can activate undesirable signaling pathways culminating in cell death. Mitochondrial Ca²⁺ uniporter (MCU) is the major route for Ca²⁺ uptake into the matrix and couples metabolism with insulin secretion. However, it has been unclear whether mitochondrial Ca²⁺ uptake plays a protective role or contributes to lipotoxicity. Here, we observed palmitate upregulated MCU protein expression in a mouse clonal β-cell, MIN6, under normal glucose, but not high glucose medium. Palmitate elevated baseline cytosolic Ca²⁺ concentration ([Ca²⁺]_i) and reduced depolarization-triggered Ca²⁺ influx likely due to the inactivation of voltage-gated Ca²⁺ channels (VGCCs). Targeted reduction of MCU expression using RNA interference abolished mitochondrial superoxide production but exacerbated palmitate-induced [Ca²⁺]_i overload. Consequently, MCU knockdown aggravated blockage of autophagic degradation. In contrast, co-treatment with verapamil, a VGCC inhibitor, prevented palmitate-induced basal [Ca²⁺]_i elevation and defective [Ca²⁺]_i transients. Extracellular Ca²⁺ chelation as well as VGCC inhibitors effectively rescued autophagy defects and cytotoxicity. These observations suggest enhanced mitochondrial Ca²⁺ uptake via MCU upregulation is a mechanism by which pancreatic β-cells are able to alleviate cytosolic Ca²⁺ overload and its detrimental consequences.