• Journal of Physiology & Pathology in Korean Medicine
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• v.22 no.6
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• pp.1462-1469
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• 2008

The purpose of the study was to confirm what effect HRHDT treatment had on cell extinction by damage of endoplasmic reticulum induced to PC-12 cell damage by glucose deprivation. The study confirmed what effect it had on forming the condition of glucose deprivation within a culture fluid of PC-12 cell and on a nerve cell's survival rates and tested whether HRHDT could prevent extinction of PC-12 cell by glucose deprivation. Also, the study confirmed what effect HRHDT treatment had on the emitted quantity of LDH by glucose deprivation. To examine PC-12 cell's behavioral change under the condition of glucose deprivation and a protective effect of HRHDT on the change, the study observed PC-12 cell's behavioral change with a microscope. Also, the study confirmed density of calcium ion within cells followed by a culture time in the condition of glucose deprivation with FACS and confirmed what effect HRHDT treatment had on the above density of calcium ion within cells. Finally, the study carried out the western blot and confirmed what effect HRHDT treatment had on revelation of GRP 78 and CHOP protein and a segmental type of aspase 12. In this study, HRHDT rescued PC-12 cells from glucose deprivation-induced cell death. HRHDT also prevents the LDH release, Ca++ accumulation, and morphological change, which was associated with the ER stress. Furthermore, HRHDT reduced the expression of ER chaperone (Grp78 and CHOP) proteins by glucose deprivation in PC-12 cells. These results suggest that HRHDT might provide a useful therapeutic strategy in treatment of the neurodegenerative diseases caused by glucose deprivation injuries.

• Biomolecules & Therapeutics
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• v.5 no.4
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• pp.364-368
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• 1997

Onion (Allium cepa Linn) has been reported to have hypoglycemic activity in human and several animal models. In the present study, we performed intraperitoneal glucose tolerance test (IPGTT) in young (1.5mo) and aged (5 mo) rats treated with onion in order to determine whether aging can influence on the anti-hy-perglycemic effect of onion. In addition, we investigated the hypoglycemic effect of onion in streptozotocin- induced diabetic rats treated with aqueous extracts of onion (500 mg/kg, i.p., daily) for 4 weeks. Blood glucose level was determined in fasted and fed rats by using a glucometer (Johnson & Johnson). In glucose tolerance test, blood glucose level was maximally increased 15 min after glucose load (2 g/kg, i.p.), and recovered to the basal level 3 hr after glucose challenge in young and old rats. The maximum blood glucose levels of young and aged rat were 184$\pm$7.49 and 225.2$\pm$ 12.55 mg/dl, respectively. A single i.p. injection of aqueous extract of onion (1 g/kg) 30 min before glucose challenge significantly decreased blood glucose levels at 15, 30, 60, 90 min after glucose load in aged rats, while the administration of onion did not show any significant effect in young rats. In onion-treated diabetic rats, significant hypoglycemic effect (p<0.05) was observed, and the effect was greater in fasted rats than in fed. In conclusion, these results suggest that anti-hyperlycemic effect of onion can be changed by age and fasting.

• Journal of the Semiconductor & Display Technology
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• v.21 no.4
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• pp.116-120
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• 2022

In this paper, we developed a paper blood glucose sensor that can minimize the effect of hematocrit. The paper blood glucose sensor has the advantage of being very simple in its production process as it is manufactured with only three printing processes on the top of the paper substrate. This glucose sensor consists of a total of six electrodes, including blood glucose measurement electrodes, hematocrit measurement electrodes, strip detection electrodes, and blood detection electrodes. A paper blood glucose sensor measures hematocrit with electrodes formed on the same sensor substrate when measuring blood glucose concentration, and compensates for the effect of hematocrit in real time to enable accurate blood glucose measurement.

• YAKHAK HOEJI
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• v.41 no.6
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• pp.782-788
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• 1997

This study was designed to characterize glucose-enhancing effects on endotoxin-induced prostaglandin production in primary cultured rat vascular smooth muscle cells (VSMC). High glucose treatment significantly augmented prostaglandin (PG) synthesis in lipopolysaccharide (LPS)-stimulated VSMC and this effect was maximal at the concentration of 4mg/ml. It has been reported that increases in glucose metabolism through sorbitol pathway could alter the cytosolic $NADH/NAD^+$ ratio and this change favors de novo synthesis of diacylglycerol (DAG) and, in turn. Results in the activation of protein kinase C (PKC) in vascular tissues. Protein kinase C (PKC) inhibitors, staurosporin and H7, blocked the glucose enhancing effect, and DAG, a PKC activator, significantly increased the PG production stimuated by LPS. Sodium pyruvate, which can reverse the alteration in cytosolic NADH/NAD+ ratio, reduced the high glucose effect on PG production. And also, zopolrestat, a strong aldose reductase inhibitor, almost completely blocked the augmentation effect of glucose on PG synthesis. Arachidonic acid release was significantly increased in high glucose treated group, which implied the increase in $PLA_2$ activity was associated with glucose enhancing effect. Metabloic, labeling study clearly showed that de novo synthesis of prostaglandin H synthase-2 (PGHS-2) is greatly increased in high glucose treated group and this was mitigated by the treatment of zopolrestat. Taken together, the activation of PKC through sorbitol pathway increased the activities of $PLA_2$ and PGHS which resulted in the augmentation in LPS-induced PG production in high glucose treated VSMC.

• YAKHAK HOEJI
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• v.35 no.6
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• pp.509-514
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• 1991

The effect of diacylglycerol on glucose release was studied by using 1,2-dioctanoyl-sn-glycerol ($diC_8$), a cell permeable diacylglycerol, in perfused rat liver. The glucose release was increased by $diC_8(50\;{\mu}M$), and the effect was depended on calcium ions. The increment of glucose release by $diC_8(50\;{\mu}M$) was inhibited by indomethacin ($50\;{\mu}M$); the amount of glucose release was almost the same with that of control group. Arachidonic acid($200\;{\mu}M$) also increased glucose release and the release was inhibited by indomethacin. There was no synergistic effect on glucose release by the combination of $diC_8(50\;{\mu}M$) and phenylephrine($10\;{\mu}M$).

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.4
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• pp.447-454
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• 1999

The production of nitric oxide (NO) and the expression of inducible nitric oxide synthase (iNOS) are known to be modulated by a variety of factors. Recent study showed that endotoxin-induced NO synthesis and iNOS expression were greatly enhanced by elevation of extracellular glucose concentration in murine macrophages. Although this was suggested to be due to the activation of protein kinase C (PKC) via sorbitol pathway, there was lack of evidence for this speculation. This study was performed to delineate the underlying intracellular mechanisms of glucose-enhancing effect on endotoxin-induced NO production in Raw264.7 macrophages. The levels of NO release induced by lipopolysaccharide (LPS) significantly increased by the treatment of glucose in a concentration dependent manner and also, this effect was observed in LPS-preprimed cells. Concurrent incubation of cells with PKC inhibitors, H-7 or chelerythrine, and LPS resulted in the diminution of NO production regardless of glucose concentration but this was not in the case of LPS-prepriming, that is, chelerythrine showed a minimal effect on the glucose- enhancing effect. PMA, a PKC activator, did not show any significant effect on glucose-associated NO production. Modulation of sorbitol pathway with zopolrestat, an aldose reductase inhibitor, did not affect LPS-induced NO production and iNOS expression under high glucose condition. And also, sodium pyruvate, which is expected to normalize cytosolic $NADH/NAD^+$ ratio, did not show any significant effect at concentrations of up to 10 mM. Glucosamine marginally increased the endotoxin-induced nitrite release in both control and high glucose treated group. 6-diazo-5-oxonorleucine (L-DON) and azaserine, glutamine: fructose- 6-phosphate amidotransferase (GFAT) inhibitors, significantly diminished the augmentation effect of high glucose on endotoxin-induced NO production. On the other hand, negative modulation of GFAT inhibitors was not reversed by the treatment of glucosamine, suggesting the minimal involvement, if any, of glucosamine pathway in glucose-enhancing effect. In summary, these results strongly suggest that the hexosamine biosynthesis pathway and the activation of PKC via sorbitol pathway do not contribute to the augmenting effect of high glucose on endotoxin induced NO production in macrophage-like Raw264.7 cells.

• Korean Journal of Veterinary Research
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• v.43 no.4
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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.

• Archives of Pharmacal Research
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• v.9 no.4
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• pp.219-222
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• 1986

Dose-dependent increasesin blood glucose were produced by epinephrine and clonidine in fasted male mice. Isoproterenol was ineffective in increasing blood glucose at lower doses ($10^{-8}M$/kg-$10^{-7}M$/kg); with higher dose ($10^{-6}M$/kg) the glucose level was increased. The hyperglycemia induced by epinephrine was inhibited by yobimbine, prazosin and propranolol, indicating that the hyperglycemic effect of epinephrine is mediated by alpha-1, alpha-2 and beta adrenoceptor. When clonidine (10$^{-6}$ M/kg) was administered simultaneously with sioproterenol ($10^{-6}M$/kg), an enhenced hyperglycemic effect was observed. The increment produced by clonidine plus isoproterenol was higher than that by clonidine alone. These increment produced by clonidine plus isoproterenol was higher than that by clonidine alone. These results suggest that stimulation of alpha-2 adrenoceptor may be reponsible for the exertion of the hyperglycemic effect by beta agonists in fasted mice.

• Archives of Pharmacal Research
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• v.29 no.9
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• pp.786-794
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• 2006

We observed the suppressive effect of a powder formulation of African black tea extract prepared from the leaves of Camellia sinensis on type 2 non-insulin dependent diabetic mice, $KK-A^y/TaJcl$. Black tea extract significantly showed suppressive effect of the elevation of blood glucose on oral glucose tolerance test of 8 week-old $KK-A^y/TaJcl$ mice (p<0.05). Long-term treatment with black tea extract showed significant suppression of post-prandial blood glucose and obesity (p<0.05). The weight of the intestine of mice treated with black tea extract was significantly reduced (p<0.05). From these results, African black tea used in this study showed a suppressive effect on the elevation of blood glucose during food intake and the body weight.

• Microbiology and Biotechnology Letters
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• v.24 no.2
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• pp.149-154
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• 1996

Effect of glucose addition to xylose medium on xylitol production was investigated by using Candida parapsilosis ATCC 21019 mutant. With increasing the ratio of glucose to xylose in total amount of 50 g/l as glucose and/or xylose, xylitol production was decreased but ethanol and glycerol production were increased. Ethanol and glycerol concentration were maxmum in 10 g/l of xylose and 40 g/l of glucose medium as 21.5 g/l and 3.6 g/l, respecti- vely. No xylitol was formed in glucose medium without xylose because xylitol could be not produced from glucose. With increasing the ratio of glucose to xylose, the activity of xylose reductase which converted xylose to xylitol were decreased. The activities of xylitol dehydrogeiiase which converted xylitol to xylulose and then cell materials were found to be constant regardless of the ratio of glucose to xylose. This results indicated that glucose addition to xylose medium on cell growth was not affected. In order to prevent the inhibitory effect of glucose on xylitol production, glucose in a fermentor was fed with low concentration and then ethanol and glycerol was critically decreased and the xylitol yield from xylose of the culture with glucose feeding was recovered the almost same as that with only 50 g/l of xylose. However, the xylitol yield from total sugars (xylose and glucose) was decreased and glucose was not contributed to xylitol production. Therefore, the fermentation at high concentration of xylose without glucose was carried out. A final xylitol concentration of 242 g/l which corresponding 80.7% of xylitol yield was obtained from 300 g/l of xylose for 273 hours.