• Proceedings of the Plant Resources Society of Korea Conference
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• 2019.04a
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• pp.121-121
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• 2019

In Islamic dietary guidelines, Halal foods are allowed as edible blessed food. Most foods were categorized within halal for Muslims. The main point of Halal food is that foods are clean in every process and based on Halal standard which might be different in each country. Most pancreatic ${\beta}$ cells synthetize, store, and release insulin. Specific molecular, functional as well as ultrastructural traits of pancreatic ${\beta}$ cells could control their insulin secretion properties and survival phentoype. Insulin-secreting pancreatic ${\beta}$-cells are essential regulators of mammalian metabolism. In addition, the pancreatic ${\beta}$ cell plays an important role in the pathogenesis of type 1 and type 2 diabetes as improving glucose homeostasis by preserving, expanding and improving the function of this key cell type. However, the pharmacological effect of halal food has not been unclear yet, especially food habit-dependent diabetes. The aim of the this study was to determine the preventive effect of Iran plants extract (Almond, Garlic, Cumin, Ginkgo biloba, Holy basil, Psyllium, Satureja khuzistanica, Fenugreek, Green tea, Ipomoea betatas, Blueberry) on RINm5F cells and MIN6 cells as pancreatic ${\beta}$ cell line. The cytotoxicity of the extracts of Iran plants on RINm5F cells and MIN6 cells were measured by using MTT assays. The preventive effects of Iran plant extracts were measured by WST-8 cell proliferation assay on streptozotocin (STZ)-induced cell death in MIN6 cells. In presented result showed that all extract of Iran plants (0.01-10mg/ml) did not show cytotoxicity in RINm5F cells and MIN6 cells. Among non-cytotoxic extract, the protective effects could be detect in high dose concentration. These results suggest that the extract of Iran plants may serve as a potential therapy for diabetes.

• The Korean Journal of Physiology and Pharmacology
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• v.16 no.6
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• pp.463-468
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• 2012

Type 1 diabetes (T1D) is caused by dysregulation of the immune system in the pancreatic islets, which eventually leads to insulin-producing pancreatic ${\beta}$-cell death and destabilization of glucose homeostasis. One of the major characteristics of T1D pathogenesis is the production of inflammatory mediators by macrophages that result in destruction or damage of pancreatic ${\beta}$-cells. In this study the inflammatory microenvironment of T1D was simulated with RAW264.7 cells and MIN6 cells, acting as macrophages and pancreatic ${\beta}$-cells respectably. In this setting, peroxiredoxin-1, an anti-oxidant enzyme was knocked down to observe its functions in the pathogenesis of T1D. RAW264.7 cells were primed with lipopolysaccharide and co-cultured with MIN6 cells while PRX-1 was knocked down in one or both cell types. Our results suggest that hindrance of PRX-1 activity or the deficiency of this enzyme in inflammatory conditions negatively affects pancreatic ${\beta}$-cell survival. The observed decrease in viability of MIN6 cells seems to be caused by nitric oxide production. Additionally, it seems that PRX-1 affects previously reported protective activity of IL-6 in pancreatic ${\beta}$ cells as well. These results signify new, undiscovered roles for PRX-1 in inflammatory conditions and may contribute toward our understanding of autoimmunity.

• 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.

• YAKHAK HOEJI
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• v.42 no.4
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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.

• Nutrition Research and Practice
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• v.12 no.3
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• pp.183-190
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• 2018

BACKGROUND/OBJECTIVE: This study was designed to investigate how a Portulaca oleracea L. extract (POE) stimulates insulin secretion in INS-1 pancreatic ${\beta}-cells$. MATERIALS/METHOD: INS-1 pancreatic ${\beta}-cells$ were incubated in the presence of various glucose concentrations: 1.1 or 5.6, 16.7 mM glucose. The cells were treated with insulin secretagogues or insulin secretion inhibitor for insulin secretion assay using an insulin ELISA kit. In order to quantify intracellular influx of $Ca^{2+}$ caused by POE treatment, the effect of POE on intracellular $Ca^{2+}$ in INS-1 pancreatic ${\beta}-cells$ was examined using Fluo-2 AM dye. RESULTS: POE at 10 to $200{\mu}g/mL$ significantly increased insulin secretion dose-dependently as compared to the control. Experiments at three glucose concentrations (1.1, 5.6, and 16.7 mM) confirmed that POE significantly stimulated insulin secretion on its own as well as in a glucose-dependent manner. POE also exerted synergistic effects on insulin secretion with secretagogues, such as L-alanine, 3-isobutyl-1-methylxanthine, and especially tolbutamide, and at a depolarizing concentration of KCl. The insulin secretion caused by POE was significantly attenuated by treatment with diazoxide, an opener of the $K{^+}_{ATP}$ channel (blocking insulin secretion) and by verapamil (a $Ca^{2+}$ channel blocker). The insulinotropic effect of POE was not observed under $Ca^{2+}$-free conditions in INS-1 pancreatic ${\beta}-cells$. When the cells were preincubated with a $Ca^{2+}$ fluorescent dye, Fluo-2 (acetoxymethyl ester), the cells treated with POE showed changes in fluorescence in red, green, and blue tones, indicating a significant increase in intracellular $Ca^{2+}$, which closely correlated with increases in the levels of insulin secretion. CONCLUSIONS: These findings indicate that POE stimulates insulin secretion via a $K{^+}_{ATP}$ channel-dependent pathway in INS-1 pancreatic ${\beta}-cells$.

• 대한약리학회:학술대회논문집
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• 2006.11a
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• pp.63-63
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• 2006

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.5
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• pp.261-266
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• 2003

Type 1 diabetes is an organ-specific autoimmune disease caused by the cytotoxic T cells-mediated destruction of the insulin-producing beta cells in the Langerhans pancreatic islets. Hepatocyte growth factor (HGF) is a potent mitogen and a promoter of proliferation of insulin producing beta cells of pancreatic islets. To study the role of HGF via viral vector in the development of streptozotocin (STZ)-induced diabetes in mice, we have developed an adenoviral vector genetically engineered to carry the gene for human HGF (hHGF) and evaluate the change of blood glucose, insulin level, and insulin-secreting beta cells of pancreatic islets. We demonstrate that the treatment with hHGF gene prevented the development of STZ-induced diabetes and increased serum insulin level to above normal range. Furthermore, it preserved pancreatic beta cells from destruction. These in vivo results may support previous findings that HGF is insulinotropic agent for beta cells and HGF treatment renders the cells to be resistant to the development of diabetes from STZ administration. We suggest that an adenoviral mediated hHGF gene therapy is a good candidate for the prevention and treatment of type 1 diabetes.

• Biomolecules & Therapeutics
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• v.22 no.1
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• pp.47-54
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• 2014

The present study was aimed to evaluate the antioxidant defense system of cinnamaldehyde in normal, diabetic rats and its possible protection of pancreatic ${\beta}$-cells against its gradual loss under diabetic conditions. In vitro free radical scavenging effect of cinnamaldehyde was determined using DPPH (1,1-diphenyl-2-dipicrylhydrazyl), superoxide radical, and nitric oxide radical. Streptozotocin (STZ) diabetic rats were orally administered with cinnamaldehyde at concentrations of 5, 10 and 20 mg/kg body weight for 45 days. At the end of the experiment, the levels of plasma lipid peroxides and antioxidants such as vitamin C, vitamin E, ceruloplasmin, catalase, superoxide dismutase, reduced glutathione and glutathione peroxidase were determined. A significant increase in the levels of plasma glucose, vitamin E, ceruloplasmin, and lipid peroxides and significant decrease in the levels of plasma insulin and reduced glutathione were observed in the diabetic rats. Also the activities of pancreatic antioxidant enzymes were altered in the STZ-induced diabetic rats. The altered enzyme activities were reverted to near-normal levels after treatment with cinnamaldehyde and glibenclamide. Histopathological studies also revealed a protective effect of cinnamaldehyde on pancreatic ${\beta}$-cells. Cinnamaldehyde enhances the antioxidant defense against reactive oxygen species produced under hyperglycemic conditions and thus protects pancreatic ${\beta}$-cells against their loss and exhibits antidiabetic properties.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.416.3-417
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• 2002

Among the promising cancer therapy is targeting of the drug to tumor cells via receptor specific ligands. CR2945, $\beta$-2-( ［2-(8-azaspiro ［4.5］ dec-8-ylcarbony!)-4.6-dimethylphenyl］amino-2-oxoethyl］ -(R)-1-naphthalenepropanoic acid. is known to have an inhibitory effect on a gastrin receptor of colorectal cancer cells. As the human pancreatic cancer cells (BxPC-3) express gastrin receptors. interruption of binding of gastrin with gastrin receptor of human pancreatic cancer cells by CR2945 inhibits the growth of human pancreatic cancer cells. (omitted)

• Asian-Australasian Journal of Animal Sciences
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• v.16 no.7
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• pp.1060-1065
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• 2003

To determine whether dietary fatty acids affect pancreatic $\beta$-cell function, the INS-1 $\beta$-cells and the pancreatic islets isolated from Zucker obese (fa/fa) rats were cultured with stearic acid and conjugated linoleic acid (CLA). As a result, DNA fragmentation laddering was substantially decreased in the INS-1 $\beta$-cells and the isolated pancreatic islets cultured with 2 mM CLA compared to those cultured with stearic acid. To investigate the mechanism by which CLA alleviates cell apoptosis under DNA fragmentation assay, we examined mRNA expressions of apoptosis-related proteins including Bax and Bcl-2 associated with cell death agonist and antagonist, respectively, in both INS-1 cells and islets cultured with 2 mM fatty acids. Bax mRNA expression was not altered by either stearic acid or CLA, whereas Bcl-2 mRNA expression was enhanced by CLA when compared to the stearic acid cultures. However, there were no changes in cell apoptosis and apoptotic-regulating gene products in either INS-1 cells or isolated islets treated with or without 2 mM CLA. It is concluded that CLA maintains $\beta$-cell viability via increased Bcl-2 expression compared to the stearic acid cultures, which may help to alleviate, at least somewhat, the onset of NIDDM in the physiological status. More detailed study is still needed to elucidate the effect of CLA on the prevention of fatty acid-induced $\beta$-cell apoptosis.