• Biomolecules & Therapeutics
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• v.7 no.4
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• pp.342-346
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• 1999

This study was performed to investigate the effect of cyclosporine (CsA) on glucose tolerance and peripheral insulin sensitivity in normal Sprague-Dawley rats. After daily treament of CsA (10 mg/kg, i.p.) for two weeks, glucose tolerance tests were carried out by the treatment of glucose (Glu, 2 g/kg, i.p.) alone or in conjunction with exogenous insulin (Ins; human regular insulin, 5 U/kg, s.c.) and measured the decrement of area under the time-plasma glucose concentration curve ($AUC_{o\longrightarrow120}$; g.min/ml) by the trapezoidal rule. The rats were divided into three groups (Glu- (Control), Ins+Glu- and CsA+Ins+Glu-, n=7 in each group). The $AUC_{o\longrightarrow120}$ of the CsA+Ins+Glu-group was significantly (p<0.01) lower than that of Glu-group (61.0% of control) and significantly (p<0.05) higher than that of Ins+Glu-group (197.4% of Ins+Glu-). The CsA+Ins+Glu- grou showed higher levels of maximal blood glucose concentration and higher $AUC_{o\longrightarrow120}$ than those of Ins+Glu-group in normal rats. Besides direct pancreatic toxicity of CsA previously reported (Hahn et al., 1972), these results suggest that CsA also make the possibility to induce peripheral insulin insensitivity and glucose intolerance in normal rats.

• The Korean Journal of Physiology
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• v.24 no.2
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• pp.331-344
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• 1990

What makes glucose transport function sensitive to insulin in one cell type such as adipocyte, and insensitive in another such as liver cells is unresolved question at this time. Recently it is known that insulin stimulates glucose transport in adipocytes largely by redistributing transporter from the storage pool that is included in a low density microsomal fraction to plasma membrane. Therefore, insulin sensitivity may depend upon the relative distribution of gluscose transporters between the plasma membrane and in an intracellular storage compartment. In hepatocytes, the subcellular distribution of glucose transporter is less well documented. It is thus possible that the apparent insensitivity of the hepatocyte system could be either due to lack of the constitutively maintained, intracellular storage pool of glucose transporter or lack of insulin-mediated transporter translocation mechanism in this cell. In this study, I examined if any intracellular glucose transporter pool exists in hepatocytes and this pool is affected by insulin. The results obtained summarized as followings: 1) Distribution of subcellular fractions of hepatocyte showed that there are $24.9{\pm}1.3%$ of plasma membrane, $36.9{\pm}1.7%$ of nucleus-mitochondria enriched fraction, $23.5{\pm}1.2%$ of lysosomal fraction, $9.6{\pm}1.0%$ of high density microsomal fraction and $4.9{\pm}0.5%$ of low density microsomal fraction. 2) In adipocyte, there were $29.9{\pm}2.6%$ of plasma membrane, $19.4{\pm}1.9%$ of nucleus-mitochondria enriched fraction, $26.7{\pm}1.8%$ of high density microsomal fraction and $23.9{\pm}2.1%$ of low density microsomal fraction. 3) Surface labelling of sodium borohydride revealed that plasma membrane contaminated to lysosomal fraction by $26.8{\pm}2.8%$, high density microsomal fraction by $8.3{\pm}1.3%$ and low density microsomal fraction by $1.7{\pm}0.4%$ respectively. 4) Cytochalasin B bound to all of subcellular fractions with a Kd of $1.0{\times}10^{-6}M$. 5) Photolabelling of cytochalasin B to subcellular fractions occurred on 45 K dalton protein band, a putative glucose transporter and D-glucose inhibited the photolabelling. 6) Insulin didn't affect on the distribution of subcellular fractions and translocation of intracellular glucose transporters of hepatocytes. 7) HEGT reconstituted into hepatocytes was largely associated with plasma membrane and very little was found in low density microsomal fraction which equals to the native glucose transporter distribution. Insulin didn't affect on the distribution of exogeneous glucose transporter in hepatocytes. From the above results it is concluded that insulin insensitivity of hepatocyte may due to lack of intracellular storage pool of glucose transporter and thus intracellular storage pool of glucose transporter is an essential feature of the insulin action.

• Journal of Life Science
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• v.17 no.5 s.85
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• pp.641-645
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• 2007

We conducted a seed germination screening under saline conditions to identify salt tolerance(sto) mutants with ethyl methane sulfonate(EMS) mutagenesis seed pool. During the screening, we identified three mutant lines that seemed to confer elevated salt tolerance in high concentrations of NaCl. At 175 mM NaCl, germination rate of sto42-14 mutant(one of the EMS salt tolerance mutants) was 7-fold higher than that of wild-type plants. Interestingly, sto42-14 mutant exhibited insensitivity to high glucose concentration and growth inhibition to gibberellin. Our results suggest that sto42-14 is involved in salt stress tolerance as well as in glucose and gibberellin response in Arabidopsis.

• Journal of Yeungnam Medical Science
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• v.7 no.1
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• pp.29-37
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• 1990

The effects of insulin and exercise on glucose uptake of skeletal muscle were investigated in soleus muscle isolated from low dose streptozotocin induced diabetic rats in vitro. Glucose uptake was assessed by measuring $^3H$-methylglucose uptake in vitro. Basal glucose uptake in diabetes was reduced by approximately one-third of the control value($5.6{\pm}0.73{\mu}Mol$/g/20min. in diabetes versus $8.4{\pm}0.77$ in control, P<0.01). There was also a significant decrease(P<0.01) in glucose uptake of diabetes at physiologic insulin concentration ($200{\mu}IU$/ml) by 40% ($6.1{\pm}1.20$ versus $10.0{\pm}0.81$). Furthermore, maximal insulin($20000{\mu}IU$/ml)-stimulated glucose uptake was 36% lower in diabetes as compared with control($7.3{\pm}1.29$ versus $11.4{\pm}1.29$, P<0.01). In contrast, exercise(1.0km/hr, treadmill running for 45min.) effect on glucose uptake was so dramatic in diabetes that glucose uptake at basal state was 8.4+1.09 and insulin stimulated-glucose uptake were $10.2{\pm}1.47$ and $11.9{\pm}1.64$, in 200 and $20000{\mu}IU$/ml added insulin, respectively. These results suggest that insulin insensitivity develops in skeletal muscle after 2 weeks of streptozotocin-induced diabetes, but these insensitivity was recovered significantly by single session of running exercise.

• Journal of Life Science
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• v.21 no.9
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• pp.1295-1300
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• 2011

The AtPGR gene is induced by pathogen infection, jasmonic acid and salicylic acid treatment and may therefore play a role in plant defense responses. Arabidopsis thaliana Plasma membrane Glucose-responsive Regulator (AtPGR) was previously isolated from Arabidopsis, which confers glucose insensitivity on plants. To study its biological functions directly, we have characterized both loss-of-function RNAi mutant and gain-of-function transgenic overexpression plants for AtPGR in Arabidopsis. The AtPGR-overexpressing plants displayed enhanced resistance to a virulent strain of the bacterial pathogen Pseudomonas syringae as measured by a significant decrease in both bacterial growth and symptom development as compared to those in wild-type and RNAi plants. The enhanced resistance in the gain-of-function transgenic plants was associated with increased induction of SA-regulated PDF1.2 and JA-regulated PR1 by the bacterial pathogen. Thus, pathogen-induced AtPGR plays a positive role in defense responses to P. syringae.