• 고려인삼학회:학술대회논문집
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• 고려인삼학회 1984년도 학술대회지
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• pp.191-197
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• 1984

인삼의 저혈당성 분획 (DPG-3-2)이 적출한 랑겔한스섬에서 인슐린 분비를 증가시킨다고 일전에 본 저자들이 발표하였다. 근래에 이와 같은 DPG-3-2 분획으로부터 사포닌, 뉴크레오사이드, 뉴크레오타이드, 아미노산, 당 등을 완전히 제거시켜 더욱 정제한 D-O-ANa 성분을 추출하였다. D-O-ANa 유발성 인슐린 분비효과를 DPG 3-2 분획과 그외 잔여성분과 비교 검토하였다. D-O-ANa는 글루코우즈 농도의 고저에 무관하게 인슐린 분비를 가장 강하게 촉진하였다. 특히 D-O-ANa는 제 2 차증 글루코운즈 유발성 인슐린 분비를 촉진하였다. DPG 3-2 분획은 당뇨병 쥐로부터 떼어낸 랑겔한스섬에서 세포외 체액의 칼슘이온이 증가됨에 따라($0.16{\~}6.25$mM) 글루코우즈 유발성 인슐린 분비를 더욱 현저히 증가시켰다. 칼슘이온 흡수와 인슐린분비의 상호관계가 뚜렷이 밝혀졌다. 이 관계는 single sucrose gap 방법에 의해 주의 적출 간 문맥에서 칼슘주파수가 증가되는 실험을 통해 증명되었다.

• Asian-Australasian Journal of Animal Sciences
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• 제2권3호
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• pp.187-188
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• 1989

• Asian-Australasian Journal of Animal Sciences
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• 제9권1호
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• pp.57-61
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• 1996

Four castrated Corriedale sheep were used in an experiment to observe the changes in insulin, growth hormone and cortisol in blood plasma following a prolonged infusion of a high rate of somatostatin (SRIF). The animals wee infused with either saline, 25 or $50{\mu}g/kg/h$ of SRIF for 3 hours. Blood samples wee taken every 20 minutes until 1 hour following the end of the SRIF infusion. Both SRIF infusion levels suppressed the release of insulin into plasma to approximately 3.5 mU/l. The SRIF infusions reduced the concentration of growth hormone to barely detectable levels. Following the withdrawal of SRIF there was a massive release of growth hormone. The plasma concentration of growth hormone reached 60 ng/ml within 20 minutes, the length of the growth hormone discharge was in excess of 1 hour. The extent of the discharge of growth hormone following the SRIF infusions was greater than that suppressed by the infusion. The SRIF apparently caused an increase in the plasma concentration of cortisol at the end of the infusion and following is withdrawal. This is possibly associated with some change in the metabolic rate associated with the suppression of insulin or glucagons release. The present experiment demonstrates that a high rate of SRIF infusion can not completely inhibit the release of insulin into the plasma.

• Biomolecules & Therapeutics
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• 제6권4호
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• pp.371-377
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• 1998

The aim of the present study was to investigate the effect of Palmiwon on the type 1-prediabetic models induced by streptozotocin (STZ) in RINm5F cells and HIT-T15 cells. Palmiwon increased the cell proliferation and insulin release when pre- and post-treated for the STZ-exposed pancreatic beta cells. The cell proliferation and insulin release of these beta cells were measured by $^3$H-thymidine uptake and RIA, respectively. We also analyzed nutrients such as sugars, fatty acid and amino acids and minerals containing in Palmiwon using by gas chromatography, amino acid analyzer and AA spectrometer, respectively. Palmiwon seems to have protective and recovery properties on the prediabetic model in cellular level, which were ascribe to various nutrients and minerals containing in Palmiwon. From these results, it could be suggested that Palmiwon may be available as preventive and therapeutic prescription of type 1 diabetes mellitus.

• 공업화학
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• 제20권6호
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• pp.581-585
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• 2009

당뇨병은 인슐린 분비가 부족하거나 그 인식 기능이 감소하여 발생하는 만성질환으로, 현재까지도 완전한 치료법은 개발되지 못하고 있다. 그 중 제I형 당뇨병에 가장 많이 쓰이는 치료법은 인슐린 주사로 알려져 있다. 하지만 인슐린 주사는 때로 치명적인 위험과 불편함을 수반하므로, 이를 개선하기 위한 많은 연구들이 수행되고 있다. 이러한 방법의 일환으로, 자가 조절 인슐린 전달 시스템이 제안되었다. 본 총설에서는 현재까지 연구되고 있는 대표적인 자가 조절 인슐린 전달 시스템의 포도당 응답성 방출 원리에 대해 살펴보고자 한다.

• 약학회지
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• 제42권4호
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• pp.408-413
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• 1998

To establish prediabetes in vitro/ model concerning the etiology of Insulin Dependent Diabetes Mellitus (IDDM) in cellular level we have designed experimental prediabefic model in pancreatic beta cells. RINm5F, HIT-T15 and isolated rat islets were chosen as pancreatic beta cells. Since interleukin-$1{\beta}$-induced beta cell cytotoxicity has been implicated in the autoimmune cytotoxicity of IDDM, we used inteleukin-$1{\beta}$ as diabetogenic agent. For establishment of prediabetic in vitro model, the degree of beta cell deterioration was determined by cell proliferation, insulin release and morphological appearance. Cell proliferation, insulin release and morphology were changed dose-dependently in condition that inteleuldn-$1{\beta}$ was exposured to pancreatic beta cells. The concentration and exposure time of interleukin-$1{\beta}$ to set up prediabetic model in beta cell lines and isolated rat islets were 100${\sim}$1000U/ml, 48hr. And 25${\sim}$100U/ml, 48hr, respectively.

• The Korean Journal of Physiology and Pharmacology
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• 제2권6호
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• pp.725-732
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• 1998

In order to elucidate the molecular mechanism of the intracellular $Ca^{2+}$ overload frequently reported from diabetic heart, diabetic rats were induced by the administration of streptozotocin, the membrane vesicles of junctional SR (heavy SR, HSR) were isolated from the ventricular myocytes, and SR $Ca^{2+}$ uptake and SR $Ca^{2+}$ release were measured. The activity of SR $Ca^{2+}-ATPase$ was $562{\pm}14$ nmol/min/mg protein in control heart. The activity was decreased to $413{\pm}30$ nmol/min/mg protein in diabetic heart and it was partially recovered to $485{\pm}18$ nmol/min/mg protein in insulin-treated diabetic heart. A similar pattern was observed in SR $^{45}Ca^{2+}$ uptakes; the specific uptake was the highest in control heart and it was the lowest in diabetic heart. In SR $^{45}Ca^{2+}$ release experiment, the highest release, 45% of SR $^{45}Ca^{2+}$, was observed in control heart. The release of diabetic heart was 20% and it was 30% in insulin-treated diabetic heart. Our results showed that the activities of both SR $Ca^{2+}-ATPase$ and SR $Ca^{2+}$ release channel were decreased in diabetic heart. In order to evaluate how these two factors contribute to SR $Ca^{2+}$ storage, the activity of SR $Ca^{2+}-ATPase$ was measured in the uncoupled leaky vesicles. The uncoupling effect which is able to increase the activity of SR $Ca^{2+}-ATPase$ was observed in control heart; however, no significant increments of SR $Ca^{2+}-ATPase$ activities were measured in both diabetic and insulin-treated diabetic rats. These results represent that the $Ca^{2+}$ storage in SR is significantly depressed and, therefore, $Ca^{2+}-sequestering$ activity of SR may be also depressed in diabetic heart.

• Animal cells and systems
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• 제13권1호
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• pp.17-23
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• 2009

In previous studies, we found that Annexin I (Anx I) was co-secreted with insulin in response to glucose, and that extracellular Anx I stimulated the release of insulin via the Anx I binding site in rat pancreatic islets and the &-cell line. However, the role that Anx I plays in the insulin secretion was not established. Therefore, in this study, we evaluated the insulin secretion pattern in response to Anx I and the involvement of the cytoskeleton or PKC in Anx Istimulated insulin secretion in MIN6N8a cells. The peak time of insulin secretion in response to Anx I treatment corresponded with the second phase insulin secretion by glucose in the perifused pseudoislets. In addition, Anx I-stimulated insulin secretion was not affect by readily releasable pool depletion. Taken together, these findings indicate that Anx I treatment was associated with movement of the reserve pool of insulin. Furthermore, Anx I-stimulated insulin secretion was attenuated by treatment with a microfilament inhibitor, cytochalasin B, as well as by PKC down regulation. These results indicate that Anx I may be a regulator of second phase insulin secretion.

• BMB Reports
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• 제43권4호
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• pp.245-249
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• 2010

GDH has been known to be related with hyperinsulinism-hyperammonemia syndrome. We have screened new drugs with a view to developing effective drugs modulating GDH activity. In the present work, we investigated the effects of a new drug, KHG26377 on glutamate formation and GDH activity in cultured rat islets. When KHG26377 was added to the culture medium for 24 h prior to kinetic analysis, the $V_{max}$ of GDH was decreased by 59% whereas $K_m$ is not significantly changed. The concentration of glutamate decreased by 50% and perfusion of islets with KHG26377 reduced insulin release by up to 55%. Our results show that KHG26377 regulates insulin release by inhibiting GDH activity in primary cultured islets and support the previous studies for the connection between GDH activity and insulin release. Further studies are required to determine in vivo effects and pharmacokinetics of the drug.

• Journal of Pharmaceutical Investigation
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• 제27권3호
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• pp.189-198
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• 1997

The purpose of the present study was to investigate the effect of medium chain fatty acid salts, reported as enhancers in insulin nasal absorption, on the rectal absorption of insulin in rats. The serum glucose and remained insulin level in perfusate were measured after rectal recirculation of insulin with or without sod. laurate, sod. caprate and sod. caprylate in situ. The addition of sod. laurate or sod. caprate reduced serum glucose concentration considerably. Sod. caprate (1.0%) showed the greatest promoting effect on the decrement of serum glucose. Eudispert hv hydrogels containing insulin with medium chain fatty acid salts were, thereby, prepared and evaluated. The release rate of insulin from Eudispert hv hydrogels was reduced with an increase in the content of Eudispert hv, and was raised with increasing NaOH concentration. Ten percent Eudispert hv hydrogels were offered for the rectal administration of insulin. The addition of 1.0% sod. caprate reduced serum glucose concentration remarkably after rectal administration of 10% Eudispert hv hydrogels containing insulin. The level of glucose decrement was greater by 30% compared to subcutaneous administration of insulin solution. From the above findings, Eudispert hv hydrogels would be used as useful rectal delivery systems of insulin.