• Journal of Ginseng Research
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• 제24권2호
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• pp.83-88
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• 2000

6년생 고려인삼근(Panax ginseng C.A. Meyer) 중의 Sucrose synthase, UDP-glucose pyrophosphorylase 및 ADP-glucose pyrophosphorylase의 활성을 생육 시기별로 조사한 결과, Sucrose synthase 와 ADP-glucose pyrophosphorylase는 뿌리저장활성 지표로서 adaptive enzyme의 특성을 나타내는 반면, UDP-glucose pyrophosphorylase는 maintenance enzyme으로서 존재하였다. 평균기온이 24。C 이상일 때 전분합성이 저하되고 중심부의 산소소비량이 급격히 증가되었다.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2002년도 Molecular and Cellular Response to Toxic Substances
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• pp.147-147
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• 2002

In this study, a mechanism by which glucose level modulates glucose transport in Jurkat cells was investigated. Glucose uptake was more efficient in the cells cultivated in low glucose (2.5 mM) medium than that grown in high glucose (20 $\mu$M) medium. Vmax (0.74 n㏖/10$^6$ cells$\cdot$min) of glucose uptake measured with the cells grown in the low glucose medium was higher than the one (1.06 n㏖/10$^6$ cells$\cdot$min) in the high glucose medium while Km was almost consistent through the change of glucose levels, indicating the increase of glucose transporter number.

• 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.

• Reproductive and Developmental Biology
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• 제39권4호
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• pp.97-104
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• 2015

Glucose is universal and essential fuel of energy metabolism and in the synthesis pathways of all mammalian cells. Glucose is the one of the major precursors of lactose synthesis using glycolysis result in producing milk fat and protein. During the milk fat synthesis, lipoprotein lipase (LPL) and CD36 are required for glucose uptake. Various morecules such as acyl-CoA synthetase 1 (ACSL1) activity of acetyl-CoA synthetase 2 (ACSS2), ACACA, FASN AGPAT6, GPAM, LPIN1 are closely related with milk fat synthesis. Additionally, glucose plays a major role for synthesizing lactose. Activations of lactose synthesize enzymes such as membranebound enzyme, beta-1,4-galactosyl transferase (B4GALT), glucose-6-phosphate dehydrogenase (G6PD) are changed by concentration of glucose in blood resulting change of amount of lactose production. Glucose transporters are a wide group of membrane proteins that facilitate the transport of glucose over a plasma membrane. There are 2 types of glucose transporters which consisted facilitative glucose transporters (GLUT); and sodium-dependent transport, mediated by the Na+/glucose cotransporters (SGLT). Among them, GLUT1, GLUT8, GLUT12, SGLT1, SGLT2 are main glucose transporters which involved in mammary gland development and milk synthesis. However, more studies are required for revealing clear mechanism and function of other unknown genes and transporters. Therefore, understanding of the mechanisms of glucose usage and its regulation in mammary gland is very essential for enhancing the glucose utilization in the mammary gland and improving dairy productivity and efficiency.

• 대한수의학회지
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• 제43권4호
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• pp.563-571
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• 2003

Dysfunction of mesangial cells has been contributed to the onset of diabetic nephropathy. Insulin like growth factors (IGFs) are also implicated in the pathogenesis of diabetic nephropathy. However, it is not yet known about the effect of high glucose on IGF-I and IGF-II secretion in the mesangial cells. Furthermore, the relationship between cAMP and high glucose on the secretion of IGFs was not elucidated. Thus, we examined the mechanisms by which high glucose regulates secretion of IGFs in mesangial cells. Glucose increased IGF-I secretion in a time- (>8 hr) and dose- (>15 mM) dependent manner (p<0.05). Stimulatory effect of high glucose on IGF-I secretion is predominantly observed in 25 mM glucose (high glucose), while 25 mM glucose did not affect cell viability and lactate dehydrogenase release. High glucose also increased IGF-II secretion. The increase of IGF-I and IGF-II secretion is not mediated by osmotic effect, since mannitol and L-glucose did not affect IGF-I and IGF-II secretion. 8-Br-cAMP mimicked high glucose-induced secretion of IGF-I and IGF-II. High glucose-induced stimulation of IGF-I and IGF-II secretion was blocked not by pertussis toxin but by SQ 22536 (adenylate cyclase inhibitor). Rp-cAMP (cAMP antagonist), and myristoylated protein kinase A (PKA) inhibitor amide 14-22 (protein kinase A inhibitor). These results suggest that cAMP/PKA pathways independent of Gi protein may mediate high glucose-induced increase of IGF-I and IGF-II secretion in mesangial cells. Indeed, glucose (>15 mM glucose) increased cAMP formation. In conclusion, high glucose stimulates IGF-I and IGF-II secretion via cAMP/PKA pathway in mesangial cells.

• 공업화학
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• 제1권2호
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• pp.107-115
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• 1990

Glucose의 redox 반응에 의한 새로운 인슐린 방출계를 5, 5'-dithiobis(2-nitrobcnzoic acid)의 disulfide 결합을 이용해 인슐린을 pmma 막과 glucose oxidase에 고정화시켜 합성하였다. glucose와 glucose dehydrogenase 및 glucose oxidise와의 산화반응에 의해 disulfide 결합이 파괴되어 막과 효소로부터 인슐린이 방출된다. enzyme cofact들(nicotinamide adenin dinucleotide와 flavin adenin dinucleotide)을 coimmobilization 시켜 membrane device에 대해 electron mediator로 작용하도록 하여 glucose의 농도 민감성을 향상시켰고 protein device에 대해서는 glucose oxidase에 인슐린을 직접 고정화시켜 민감성을 더욱 향상시켰다. 이 두 가지 계들은 glucose 특이성을 나타내며 방출된 인슐린은 생체인슐린과 구분되지 않았다. 방출인슐린의 생리활성은 생체인슐린의 81%였다.

• 중환자간호학회지
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• 제8권2호
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• pp.1-12
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• 2015

Purpose: The study sought to determine the state of blood glucose control, and the consequent clinical effects and variation in blood glucose level, of adult patients admitted to intensive care units following cardiothoracic surgery by comparing the blood glucose levels before and after the application of a blood glucose control protocol. Methods: The protocol was developed by modifying and supplementing the Yale protocol, and was first used in 2012. The resulting blood glucose data of an experimental group (n = 314), to which the blood glucose control protocol had been applied, and a control group (n = 347), whose blood glucose levels had been controlled according to physicians'prescriptions without the protocol, were collected through the medical records. Results: The target blood glucose ratio increased significantly in the experimental group, and the low blood glucose ratio decreased significantly in the experimental group. The two groups exhibited a significant difference (p < .001) in the degree of variation in the blood glucose levels. The duration of the use of a ventilator was significantly reduced in the experimental group (p < .001). Conclusion: It is expected that the protocol can be used for the safe and effective control of critically ill cardiothoracic surgery patients' blood glucose levels.

• Nutritional Sciences
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• 제9권4호
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• pp.280-287
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• 2006

The aims of this study were to describe the effects of glucose-sweetened drinks on blood glucose, energy, and water intake at a meal 3 hours later. The effect of blood glucose on prandial energy intake and the relationship between water and energy intake during a meal were also determined. Twenty healthy normal-weight men were fed pizza test meals 3h after consuming four drinks of 0, 50g, 65g, and 75g glucose in random order, within-subjects design. Blood samples were measured at baseline and every 30 min after ingestion of drinks and 30min after the end of the test meal and the appetite was also assessed by visual analog test at the same interval. The results of this study showed that various glucose drinks altered blood glucose responses compared with that of water control(p<0.0001). Blood glucose areas under the curve(AUC) for glucose-sweetened drinks were significantly(p<0.05) higher than that for the control over 3 hours after a drink and 30 min after the test meal. Consumption of the glucose-sweetened drinks significantly increased(p<0.05) energy and water intake at a test meal compared with the water control, except the drink containing 75g glucose. For all drinks combined, the energy intake was negatively correlated with the blood glucose and positively correlated with the volume of water consumed at a test meal at 3 hours later.

• 센서학회지
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• 제24권2호
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• pp.83-87
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• 2015

In this paper, we fabricated a low-cost glucose sensor with a simpler structure and fabrication process than the existing glucose sensor. The currently used glucose sensor has a three-layer structure with upper, middle, and bottom plates; here, we fabricated a single-layer glucose sensor using only a printing and dispensing process. We successfully fabricated the glucose sensor using a simple method involving the formation of an electrode and insulator layer through a 2- or 3-step printing process on plastic or paper film, followed by the dispensing of glucose oxidase solution on the electrode. Cyclic voltammetry (CV) and cyclic amperometry (CA) measurements were used to evaluate the characteristics of the fabricated single-layer glucose sensor. Also, its sensitivity was analyzed through glucose-controlled blood measurements. Hence, a low-cost single-layer glucose sensor was fabricated with evaluation of its characteristics demonstrating that it has useful application in medicine.

• Diabetes and Metabolism Journal
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• 제42권6호
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• pp.465-471
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• 2018

My professional journey to understand the glucose homeostasis began in the 1990s, starting from cloning of the promoter region of glucose transporter type 2 (GLUT2) gene that led us to establish research foundation of my group. When I was a graduate student, I simply thought that hyperglycemia, a typical clinical manifestation of type 2 diabetes mellitus (T2DM), could be caused by a defect in the glucose transport system in the body. Thus, if a molecular mechanism controlling glucose transport system could be understood, treatment of T2DM could be possible. In the early 70s, hyperglycemia was thought to develop primarily due to a defect in the muscle and adipose tissue; thus, muscle/adipose tissue type glucose transporter (GLUT4) became a major research interest in the diabetology. However, glucose utilization occurs not only in muscle/adipose tissue but also in liver and brain. Thus, I was interested in the hepatic glucose transport system, where glucose storage and release are the most actively occurring.