• Proceedings of the PSK Conference
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• 2003.04a
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• pp.125.1-125.1
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• 2003

Diabetes is complex in nature but it gets further complicated in associating with number of other diseases like hypertension, ratinal disintegration, renal failure and many others. The latest addition to diabetic-complication is its association with bone degeneration disease:osteoporosis, which is a form of bone loss. In both the types of primary diabetes, the insulin dependent diabetes militus (IDDM) as well in insulin independent diabetes millitus (IIDM) the glucose metabolism is altered. (omitted)

• KSBB Journal
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• v.18 no.2
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• pp.94-99
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• 2003

The effect of medium composition on the production of bacterial cellulose (BC) by Gluconacetobacter hansenii PJK was investigated. The addition of yeast extract and peptone in the medium increased the production yield (Y/sub p/s/) of BC. The amount of BC produced by G. hansenii PJK was constant if the initial pH of the medium was in the range 4.5 to 6.0. Strains from the supernatant of the culture medium produced more BC than those from inside the BC. BC production was dependent on glucose metabolism, and the addition of fructose or lactate as a carbon source converted cells to Cel/sup -/ mutants. Cel/sup -/ mutants produced by the addition of fructose or lactate to the medium caused 73% or 30% decreases in BC production, respectively. The addition of succinate, which is one of the constituents of the TCA cycle, did not affect the production of BC.

• Korean Journal of Food Science and Technology
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• v.11 no.4
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• pp.217-223
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• 1979

The present study was to investigate the effect of sugars on the psychrophillic spoilage in ground meat. The obtained results were summarized as follows: 1. The minimum pH values for the ground beef containing 2, 5 and 10 % glucose were 5.25, 5.15 and 4.5, respectively. For the ground pork, the respective values were 5.1, 4.45 and 4.1. 2. Total aerobes, coliform, lactic acid bacteria and lactobacillus counts per gram for the control and 2% glucose-contained ground beef after 9 days for storage at $5^{\circ}C$ were $8.3{\times}10^9vs\;6.0{\times}10^7,\;3.5{\times}10^5vs\;2.4{\times}10^3,\;5.8{\times}10^7vs\;4.7{\times}10^6$ and $3.6{\times}10^5vs\;4.2{\times}10^6$ respectively. For the ground pork, the respective values were $1.2{\times}10^{10}vs\;7.8{\times}10^8,\;3.4{\times}10^5vs\;3.1{\times}10^4,\;5.5{\times}10^7vs\;4.5{\times}10^6$ and $3.3{\times}10^5vs\;3.7{\times}10^5$. The glucose-added ground meat showed higher counts than those of the controls only in the case of lactobacillus without any apparent adverse effects. 3. The length of storage time until the depletion of added glucose was 12, 16 and 28 days for the 2, 5 and 10 % glucose contained ground beef and 9, 16 and 30 days for the ground pork, respectively. pH did not start to increase until the added glucose was depleted completely. 4. The addition of glucose extended significantly the average shelf-life of ground beef at refrigeration condition $(5^{\circ}C)$. The extended shelf-life over the control was 7, 9 and 12days for the 2, 5 and 10 % glucose contained ground beef and 8, 10 and 12 days for the respective ground porks. 5. Although the addition of disaccharides (maltose, lactose, saccharose) lowered the pH of ground meat, the extension of shelf-life as seen in glucose treatment was not affected. In fact, the higher the concentration of added disaccharides was, the greater the degree of putrefaction occurred.

• Microbiology and Biotechnology Letters
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• v.26 no.3
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• pp.264-268
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• 1998

Many enzymes catalyze a primary reaction and/or secondary reaction. Dextransucrase usually synthesizes dextran from sucrose as a primary reaction. The secondary reaction of dextransucrase is the transfer of glucose from sucrose to carbohydrate accepters. We have reacted dextransucrase from Leuconostoc mesenteroides B-742CB with sucrose and pullulan as an acceptor under different reaction conditions; various concentrations of pullulan, enzyme, sucrose and different pHs and temperatures of reaction digests. The yield of modified pullulan was 57%(<${\pm}$5%) of theoretical under the reaction condition of pH 5.2, temperature 28$^{\circ}C$, 0.37% of pullulan, and 0.l U/$m\ell$ of dextransucrase. Modified products were more resistant against the hydrolysis of pullulanase and endo-dextranase than those of native pullulan. The positions of glucose substitution in the modified products were determined by methylation followed by acid hydrolysis and analyzed by TLC. The products were modified by the addition of glucose to the position of C3, C4, C6 free hydroxyl group of glucose residues in the pullulan.

• Journal of Ginseng Research
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• v.35 no.3
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• pp.308-314
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• 2011

In the present study, we investigate anti-diabetic effect of pectinase-processed ginseng radix (GINST) in high fat diet-fed ICR mice. The ICR mice were divided into three groups: regular diet group, high fat diet control group (HFD), and GINSTtreated group. To induce hyperglycemia, mice were fed a high fat diet for 10 weeks, and mice were administered with 300 mg/kg of GINST once a day for 5 weeks. Oral glucose tolerance test revealed that GINST improved glucose tolerance after glucose challenge. Compared to the HFD control group, fasting blood glucose and insulin levels were decreased by 57.8% (p<0.05) and 30.9% (p<0.01) in GINST-treated group, respectively. With decreased plasma glucose and insulin levels, the insulin resistance index of the GINST-treated group was reduced by 68.1% (p<0.01) compared to the HFD control group. Pancreas of GINST-treated mice preserved a morphological integrity of islets and consequently having more insulin contents. In addition, GINST up-regulated the levels of phosphorylated AMP-activated protein kinase (AMPK) and its target molecule, glucose transporter 4 (GLUT4) protein expression in the skeletal muscle. Our results suggest that GINST ameliorates a hyperglycemia through activation of AMPK/GLUT4 signaling pathway, and has a therapeutic potential for type 2 diabetes.

• Nutrition Research and Practice
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• v.7 no.1
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• pp.34-42
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• 2013

This study investigated the effects of magnetized water supplementation on blood glucose, DNA damage, antioxidant status, and lipid profiles in streptozotocin (STZ)-induced diabetic rats. There were three groups of 4-week-old male Sprague-Dawley rats used in the study: control group (normal control group without diabetes); diabetes group (STZ-induced diabetes control); and magnetized water group (magnetized water supplemented after the induction of diabetes using STZ). Before initiating the study, diabetes was confirmed by measuring fasting blood glucose (FBS > 200 dl), and the magnetized water group received magnetized water for 8 weeks instead of general water. After 8 weeks, rats were sacrificed to measure the fasting blood glucose, insulin concentration, glycated hemoglobin level, degree of DNA damage, antioxidant status, and lipid profiles. From the fourth week of magnetized water supplementation, blood glucose was decreased in the magnetized water group compared to the diabetes group, and such effect continued to the 8th week. The glycated hemoglobin content in the blood was increased in the diabetes group compared to the control group, but decreased significantly in the magnetized water group. However, decreased plasma insulin level due to induced diabetes was not increased by magnetized water supplementation. Increased blood and liver DNA damages in diabetes rats did significantly decrease after the administration of magnetized water. In addition, antioxidant enzyme activities and plasma lipid profiles were not different among the three groups. In conclusion, the supplementation of magnetized water not only decreased the blood glucose and glycated hemoglobin levels but also reduced blood and liver DNA damages in STZ-induced diabetic rats. From the above results, it is suggested that the long-term intake of the magnetized water over 8 weeks may be beneficial in both prevention and treatment of complications in diabetic patients.

• Journal of the Korea Concrete Institute
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• v.27 no.3
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• pp.265-272
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• 2015

In this study, a method to reduce temperature rise due to hydration in mass concrete is investigated. It is to use retarder (glucose) for reducing heat of hydration and to use calcium silicate hydrate (C-S-H) for compensating the retardation effect due to its role as a nucleation seed. For this purpose, the temperature rise of cement paste due to hydration was measured and the effect of using both C-S-H and glucose on setting and 28-day compressive strength of mortar specimens was investigated. According to the experimental results, using C-S-H and glucose caused the reduction in the maximum temperature but accelerated the time to reach the maximum temperature compared to that of retarded cement paste using glucose. In addition, using C-S-H and glucose did not show significant effect on 28-day compressive strength of mortar specimens, indicating that the method shown in this study can be a successful alternative to control maximum temperature rise in mass concrete.

• Biomedical Science Letters
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• v.11 no.3
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• pp.327-332
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• 2005

Sf21 cells become popular as the host permissive cell line to support the baculovirus AcNPV replication and protein synthesis. The cells grow well on TC-100 medium that contains $0.1\%$ D-glucose as the major carbon source, strongly suggesting the presence of endogenous glucose transporters. However, unlike human glucose transporters, very little is known about the characteristics of the endogenoussugar transporter(s) in Sf21 cells. Thus, some kinetic properties of the sugar transport system were investigated, involving the uptake of 2-deoxy-D-glucose (2dG1c). In order to obtain a true measure of the initial rate of uptake, the uptake of $[^3H]2dGlc$ from both low $(100{\mu}M)$ and high (10 mM) extracellular concentrations was measured over periods ranging from 30 sec to30 min. The data obtained indicated that the uptake was linear for at least 2 min at both concentrations, suggesting that measurements made over a 1min time course would reflect initial rates of the jexpse uptake. To determine $K_m\;and\;V_{max}$ of the endogenous glucose transporter(s) in Sf21 cells, the uptake of 2dG1c was measured over a range of substrate concentrations $(50{\mu}M\~10mM)$ 2dG1c uptake by the Sf21 cells appeared to involve both saturable and non-saturable (or very low affinity) components. A saturable transport system for 2dG1c was relatively high, the $K_m$ value for uptake being < 0.45 mM. The $V_{max}$ value obtained for 2dG1c transport in the Sf21 cells was about 9.7-folds higher than that reported for Chinese hamster ovary cells, which contain a GLUT1 homologue. Thus, it appeared that the transport activity of the Sf21 cells was very high. In addition, the Sf21 glucose transporter was found to have very low affinity for cytochalasin B, a potent inhibitor of human erythrocyte glucose transporter

• Biomedical Science Letters
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• v.8 no.4
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• pp.211-215
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• 2002

The baculovirus/Sf9 cell expression can be employed as a powerful system for producing large amounts of the human erythrocyte glucose transporter, GLUT1 heterologously In order to exploit the system further, it is necessary to develop a convenient method for demonstrating that the transporter expressed in insect cells is biologically active. To achieve this, we have expressed the human CLUT1 in insect cells and photolabelled the expressed protein with [$^3$H] cytochalasin B, a potent inhibitor of the human erythrocyte glucose transporter. Subsequently, the labelled proteins were analysed by SDS-polyacrylamide gel electrophoresis (SDS-PAGE). Membranes labelled with [$^3$H] cytochalasln B in the presence of L-Glucose yielded a single sharp peak of labelling of apparent $M_r$ 45,000 on SDS/polyacrylamide gels. The mobility of this peak corresponded exactly to that of the band detected by anti-glucose transporter antibodies on Western blots of membranes prepared from insect cells infected with recombinant virus. In addition, the sharpness of the radioactive peak provides further evidence for the conclusion that the expressed protein is much less heavily and heterogeneously glycosylated than its erythrocyte counterpart. No peak of labelling was seen with the membranes prepared from non-infected Sf9 cells. Furthermore, the incorporation of label into this peak was completely inhibited by the presence of 500 mM-D-Glucose during tile photolabelling procedure, showing the stereoselectivity of the labelling. These evidences clearly show that human glucose transporter expressed in insect cells exhibits native-like biological activity, and that photolabelling with [$^3$H] cytochalasin B can be a convenient means for analysing the biological activity of the transport protein expressed in insect cells.

• Molecules and Cells
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• v.41 no.10
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• pp.909-916
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• 2018

In pancreatic ${\beta}$ cells, glucose stimulates the biosynthesis of insulin at transcriptional and post-transcriptional levels. The RNA-binding protein, polypyrimidine tract-binding protein 1 (PTBP1), also named hnRNP I, acts as a critical mediator of insulin biosynthesis through binding to the pyrimidine-rich region in the 3'-untranslated region (UTR) of insulin mRNA. However, the underlying mechanism that regulates its expression in ${\beta}$ cells is unclear. Here, we report that glucose induces the expression of PTBP1 via the insulin receptor (IR) signaling pathway in ${\beta}$ cells. PTBP1 is present in ${\beta}$ cells of both mouse and monkey, where its levels are increased by glucose and insulin, but not by insulin-like growth factor 1. PTBP1 levels in immortalized ${\beta}$ cells established from wild-type (${\beta}IRWT$) mice are higher than levels in ${\beta}$ cells established from IR-null (${\beta}IRKO$) mice, and ectopic re-expression of IR-WT in ${\beta}IRKO$ cells restored PTBP1 levels. However, PTBP1 levels were not altered in ${\beta}IRKO$ cells transfected with IR-3YA, in which the Tyr1158/1162/1163 residues are substituted with Ala. Consistently, treatment with glucose or insulin elevated PTBP1 levels in ${\beta}IRWT$ cells, but not in ${\beta}IRKO$ cells. In addition, silencing Akt significantly lowered PTBP1 levels. Thus, our results identify insulin as a pivotal mediator of glucose-induced PTBP1 expression in pancreatic ${\beta}$ cells.