• 식품산업과 영양
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• 제4권3호
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• pp.83-87
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• 1999

Non-insulin-dependent diabetes mellitus (NIDDM) is characterized by insulin resistance and impaired insulim secretion. The transgenic technology, in which a specific gene can be introduced or deleted to study its function, has been established. A number of transgenic mice, altered the expression of genes potentially involved in insulin action or pancreatic ${\beta}$-cell function, have recently been developed to address questions concerning NIDDM. Thransgenic mice model may help understanding the molecular basis of complex patho-physiologies of NIDDM. This review outlines the new insights obtained from the studies of transgenic mice that overxpress or show decreased expression of putative key genes involved in the regulation of insulin resistance and pancreatic ${\beta}$-cell function, therefore in the control of glucose homeostasis.

• BMB Reports
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• 제51권7호
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• pp.362-367
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• 2018

A major feature of type 1 diabetes mellitus (T1DM) is hyperglycemia and dysfunction of pancreatic ${\beta}$-cells. In a previous study, we have shown that Tat-DJ-1 protein inhibits pancreatic RINm5F ${\beta}$-cell death caused by oxidative stress. In this study, we examined effects of Tat-DJ-1 protein on streptozotocin (STZ)-induced diabetic mice. Wild type (WT) Tat-DJ-1 protein transduced into pancreas where it markedly inhibited pancreatic ${\beta}$-cell destruction and regulated levels of serum parameters including insulin, alkaline phosphatase (ALP), and free fatty acid (FFA) secretion. In addition, transduced WT Tat-DJ-1 protein significantly inhibited the activation of $NF-{\kappa}B$ and MAPK (ERK and p38) expression as well as expression of COX-2 and iNOS in STZ exposed pancreas. In contrast, treatment with C106A mutant Tat-DJ-1 protein showed no protective effects. Collectively, our results indicate that WT Tat-DJ-1 protein can significantly ameliorate pancreatic tissues in STZ-induced diabetes in mice.

• 한국축산식품학회지
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• 제43권1호
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• pp.170-183
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• 2023

This study evaluated the effects of milk fermented with Pediococcus acidilactici strain BE and Pediococcus pentosaceus strain M103 on diabetes in rats (Rattus norvegicus). The bacteria were separately used as starter cultures for milk fermentation, and the products were then fed to diabetic rats for 15 days. Blood glucose levels, immunohistochemical and histological indicators, lipid profiles, and total lactic acid bacterium counts were evaluated before and after treatment. The administration of milk fermented with P. acidilactici strain BE reduced blood glucose levels from 410.27±51.60 to 304.07±9.88 mg/dL (p<0.05), similar to the effects of metformin (from 382.30±13.39 mg/dL to 253.33±40.66 mg/dL, p<0.05). Increased insulin production was observed in diabetic rats fed milk fermented with P. acidilactici strain BE concomitant with an increased number and percentage area of immunoreactive beta-cells. The structure of insulin-producing beta-cells was improved in diabetic rats fed milk fermented with P. acidilactici strain BE or metformin (insulin receptor substrate scores of 5.33±0.94 and 3.5±0.5, respectively). This suggests that the administration of milk fermented with P. acidilactici BE potentially reduces blood glucose levels and improves pancreatic beta-cell function in diabetic rats.

• 대한한의학회지
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• 제15권2호
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• pp.429-444
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• 1994

The present study was undertaken in order to elucidate the effect of pretreatment with Saengchinyanghyoltang(SYT) on changes in serum glucose level, body weight. water consumption. serum insulin concentration and activities of pancreatic enzymes in rats treated with streptozocin(STZ)-induced diabetic state. Histological studies were also carried out to elevate the effects on pancreatic tissues and Langelhans islet cells. SYT pretreatment in STZ diabetic rats inhibited the rise of fasting serum glucose concentration and water consumption. Pretreatment with SYT significantly increased the concentration of blood insulin and body weight changes compared to the STZ-treated group. Pancreatic lipase and trypsin activities were increased. but amylase activity was decreased and pancreatic ${\beta}-cell$ was destroyed by STZ but. pretreatment with SYT prevented these STZ-induced changes.

• 한국동물학회:학술대회논문집
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• 한국동물학회 1997년도 공동 춘계학술대회
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• pp.56.2-56
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• 1997

No Abstract, See Full Text

• 대한약학회:학술대회논문집
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• 대한약학회 2000년도 NEW STRATEGY FOR DRUG DEVELOPMENT IN POST-GENOMIC ERA(대한약학회)
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• pp.108-108
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• 2000

• 대한방사선기술학회지:방사선기술과학
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• 제37권1호
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• pp.21-28
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• 2014

배양된 췌장베타세포와 신경세포를 10% FBS (fetal bovine serum), 11.1 mM glucose의 normal 조건과 1% FBS, 30 mM glucose의 hyperglycemia 조건으로 배양하고, 저 LET X-선을 0.5 Gy/hr의 선량률로 총 선량이 0.5, 1, 1.5, 2, 2.5, 3, 3.5, 4, 4.5, 5 Gy가 되도록 저 LET 방사선을 조사한 후 MTT assay로 생존율을 측정하고 비교하였다. 분화된 췌장베타세포에 방사선을 조사하지 않았을 때는 normal 조건에 비해 hyperglycemia 조건의 생존율이 경미한 감소를 보였다. 그러나 X선의 총 선량이 점차 누적됨에 따라 normal 조건에서 생존율이 조금씩 감소하는 것에 비해 hyperglycemia 조건에서는 급격히 감소하여 시너지 효과를 나타냈다. 미분화된 신경세포에서는 방사선을 조사하지 않은 때도 normal 조건에 비해 hyperglycemia 조건의 생존율이 뚜렷하게 감소하였다. X선의 총 선량이 점차 누적됨에 따라 normal 과 hyperglycemia 조건 모두에서 비교적 급격한 세포사멸이 나타났지만 그 생존율의 감소비율이 거의 평행하게 진행되어 시너지 효과를 보이지 않았다.

• BMB Reports
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• 제48권3호
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• pp.172-177
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• 2015

Upregulation of pro-inflammatory mediators contributes to ${\beta}$-cell destruction and enhanced infiltration of immune cells into pancreatic islets during development of type 1 diabetes mellitus. In this study, we examined the regulatory effects and the mechanisms of action of celastrol against cytotoxicity and pro-inflammatory immune responses in the RINm5F rat pancreatic ${\beta}$-cell line stimulated with a combination of interleukin-1 beta, tumor necrosis factor-alpha, and interferon-${\gamma}$. Celastrol significantly restored cytokine-induced cell death and significantly inhibited cytokine-induced nitric oxide production. In addition, the protective effect of celastrol was correlated with a reduction in pro-inflammatory mediators, such as inducible nitric oxide synthase, cyclooxygenase-2, and CC chemokine ligand 2. Furthermore, celastrol significantly suppressed cytokine-induced signaling cascades leading to nuclear factor kappa B (NF-${\kappa}B$) activation, including $I{\kappa}B$-kinase (IKK) activation, $I{\kappa}B$ degradation, p65 phosphorylation, and p65 DNA binding activity. These results suggest that celastrol may exert its cytoprotective activity by suppressing cytokine-induced expression of pro-inflammatory mediators by inhibiting activation of NF-${\kappa}B$ in RINm5F cells.

• Applied Microscopy
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• 제31권3호
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• pp.267-274
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• 2001

Streptozotocin(STZ)을 투여하여 고혈당을 유발시킨 생쥐의 이자섬에 생진양혈탕가미방이 미치는 영향을 규명하고자, 전방액 (0.4ml/day)을 21일간 투여하여 혈당 및 BUN의 변화와 인슐린 면역조직화학적 검색 및 전자 현미경을 이용한 $\beta$세포의 미세구조 변화를 관찰하였다. STZ을 투여한 대조군 이자섬의 면역조직화학적 검사 결과 insulin에 양성반응을 보이는 세포가 거의 관찰되지 않았으나, 생진양혈탕가미방을 투여한 실험군의 $\beta$세포들은 대조군에 비하여 강한 양성반응을 보였다. 전자현미경 관찰에서, 대조군 생쥐의 $\beta$세포는 핵의 핵막이 정상군에 비하여 뚜렷하지 않았으며 세포질소기관의 발달도 미약하였다. 세포질내에 함유되어 있는 분비과립의 수가 현저히 감소하였으며 전자밀도가 높은 중심부분의 크기도 정상군에 비하여 현저히 작았다. 실험군의 $\beta$세포에서는 insulin분비소포의 수는 정상군에 비하여 다소 적게 관찰되었으나 대조준에 비해서는 증가하였으며, 전자밀도가 높은 중심부분의 크기도 대조군에 비하여 다소 증가하였다. 혈당은 대조군($365.33{\pm}91.01$, mg/dl)에비하여 실험군($179.56{\pm}73.36$, mg/dl)에서 유의성있게 감소하였다. 위와 같은 결과로 보아 생진양혈탕가미방이 STZ로 유발된 당뇨 생쥐의 치료에 효능이 있음을 확인할 수 있었다.

• Fisheries and Aquatic Sciences
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• 제27권1호
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• pp.17-22
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• 2024

Diabetes Mellitus (DM) is a major health issue increasing worldwide. Currently, nearby half a billion people have diabetes. Two major types of DM that type 1 and type 2-DM have different etiologies but feature a crucial common pathological transition into dysfunction of pancreatic β-cells and consequently leading hyperglycemia and finally go into DM. Therefore, maintaining of β-cells such as preventing β-cells degeneration, and promoting β-cells regeneration and proliferation will be essential approaches in prevention and/or treatment of DM. There are many reports that various types of seaweed control metabolic diseases such as obesity, high blood pressure, and blood sugar control. However, no new drug candidates have been developed yet. Additionally, although seaweed has excellent blood sugar control effects, there is no evidence that it directly proliferates or regenerates beta cells. Therefore, we studied on the promotion of β-cell regeneration by a seaweed, Polysiponia morrowii extract (PME) which preserves β-cells and maintains its function. As a result, it was confirmed that PME directly promotes the proliferation of pancreatic islet β-cells with insulin secretion function in in vivo. Therefore, PME shows potential as a candidate for β-cell regeneration that may play a fundamental role in the treatment of diabetes.