scholarly journals The Investigation of Antidiabetic Effects of Leontice leontopetalum Extract on Human Pancreatic β Cell Lines (1.1B4) Treated with Streptozotocin

2018 ◽  
Vol 6 (6) ◽  
pp. 792
Author(s):  
Celal Güven ◽  
Eylem Taşkın ◽  
Önder Yumrutaş ◽  
Leyla Türker Şener ◽  
Fulya Dal ◽  
...  
Keyword(s):  
Beta Cell ◽  
Cell Survival ◽  
Pancreatic Beta Cell ◽  
Insulin Content ◽  
Dependent Manner ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Glucose Levels ◽  
Dose Dependent ◽  
Antidiabetic Effects

One of the alternative therapeutic methods is herbal medicine. Leontice leontopetalum belongs to Berberidaceae family. The aim of study was investigated the extract of LL on human pancreatic beta cell-treated with STZ. Materials and methods: The human pancreatic beta cell (1.1B4) line was used the current study. LL’s extracts (1, 10, 100, and 1000 ug/ml) were supplemented in media for twenty-four hours and/or after STZ treatment (10 and 20 mM). Cells survivals (MTT), cells proliferation were shown by using xCelligence. Insulin content and releasing were measured at 1.1, 8.4 and 16.7 mM glucose concentrations. Results: The result of MTT was shown that cell survival was decreased, based on dose-dependent. When looked at xCelligence results, cell proliferation in STZ groups and the lowest and highest concentrations of LL were attenuated in a dose-dependent manner. Also, cotreatments of LL and STZ were decreased as well. The result of insulin-releasing on glucose induction was shown that STZ concentration gave rise to reduce insulin content at low and high glucose levels. Also, co-treatment of LL and STZ attenuated insulin content based on dose. Conclusion: It was considered that LL treatment led to increased insulin realizing, resulting from decreasing insulin content in diabetic beta cells, but decrease cell survival.

Vitamin D supplementation induces CatG-mediated CD4+ T cell inactivation and restores pancreatic beta-cell function in mice with type 1 diabetes

2021 ◽  
Author(s):  
Xiaoyang Lai ◽  
Xuyang Liu ◽  
Xia Cai ◽  
Fang Zou
Keyword(s):  
Vitamin D ◽  
Type 1 Diabetes ◽  
Beta Cell ◽  
Cell Function ◽  
Pancreatic Beta Cell ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Β Cell Function

Type 1 diabetes (T1D) is a chronic autoimmune disease accompanied by the immune-mediated destruction of pancreatic β-cells. In this study, we aimed to explore the regulatory effects of Vitamin D (VD) supplementation on pancreatic β-cell function by altering the expression of bioinformatically identified cathepsin G (CatG) in T1D model mice. A T1D mouse model was established in non-obese diabetic (NOD) mice, and their islets were isolated and purified. Pancreatic mononuclear cells (MNCs) were collected, from which CD4+ T cells were isolated. The levels of interleukin (IL)-2, IL-10, tumor necrosis factor-α (TNF-α) and interferon-gamma (IFN-γ) in the supernatant of mouse pancreatic tissue homogenate were assessed using ELISA. Immunohistochemistry and TUNEL staining were conducted to evaluate the effects of VD supplementation on pancreatic tissues of T1D mice. The pancreatic beta-cell line MIN6 was used for in vitro substantiation of findings in vivo. VD supplementation reduced glucose levels and improved glucose tolerance in T1D mice. Further, VD supplementation improved pancreatic β-cell function and suppressed immunological and inflammatory reactions in the T1D mice. We documented overexpression of CatG in diabetes tissue samples, and then showed that VD supplementation normalized the islet immune microenvironment through down-regulating CatG expression in T1D mice. Experiments in vitro subsequently demonstrated that VD supplementation impeded CD4+ T activation by down-regulating CatG expression, and thereby enhanced pancreatic β-cell function. Results of the present study elucidated that VD supplementation can down-regulate the expression of CatG and inhibit CD4+ T cell activation, thereby improving β-cell function in T1D.

scholarly journals Protective Effects of Astragaloside IV on Uric Acid-Induced Pancreatic β-Cell Injury through PI3K/AKT Pathway Activation

2022 ◽  
Vol 2022 ◽  
pp. 1-8
Author(s):  
Zhenhuan Jiang ◽  
Gang Wang ◽  
Lingling Meng ◽  
Yunzhao Tang ◽  
Min Yang ◽  
...  
Keyword(s):  
Uric Acid ◽  
Insulin Secretion ◽  
Akt Pathway ◽  
Dependent Manner ◽  
Protective Effects ◽  
Pancreatic Β Cell ◽  
Astragaloside Iv ◽  
Β Cell ◽  
Min6 Cells ◽  
Dose Dependent

Background. Elevated uric acid (UA) has been found to damage pancreatic β-cell, promote oxidative stress, and cause insulin resistance in type 2 diabetes (T2D). Astragaloside IV (AS-IV), a major active monomer extracted from Astragalus membranaceus (Fisch.) Bunge. which belongs to TRIB. Galegeae (Br.) Torrey et Gray, Papilionaceae, exhibits various activities in a pathophysiological environment and has been widely employed to treat diseases. However, the effects of AS-IV on UA-induced pancreatic β-cell damage need to be investigated and the associating mechanism needs to be elucidated. This study was designed to determine the protective effects and underlying mechanism of AS-IV on UA-induced pancreatic β-cell dysfunction in T2D. Methods. UA-treated Min6 cells were exposed to AS-IV or wortmannin. Thereafter, the 3-(45)-dimethylthiahiazo(-z-y1)-35-di-phenytetrazoliumromide (MTT) assay and flow cytometry were employed to determine the effect of AS-IV on cell proliferation and apoptosis, respectively. Insulin secretion was evaluated using the glucose-stimulated insulin secretion (GSIS) assay. Finally, western blot and quantitative real-time polymerase chain reaction (qRT-PCR) were performed to determine the effect of AS-IV on the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway in UA-treated cells. Results. AS-IV had no cytotoxic effects on Min6 cells. UA significantly suppressed Min6 cell growth, promoted cell apoptosis, and enhanced caspase-3 activity; however, AS-IV abolished these effects in a dose-dependent manner. Further, decreased insulin secretion was found in UA-treated Min6 cells compared to control cells, and the production of insulin was enhanced by AS-IV in a dose-dependent manner. AS-IV significantly increased phosphorylated (p)-AKT expression and the ratio of p-AKT/AKT in Min6 cells exposed to UA. No evident change in AKT mRNA level was found in the different groups. However, the effects of AS-IV on UA-stimulated Min6 cells were reversed by 100 nM wortmannin. Conclusion. Collectively, our data suggest that AS-IV protected pancreatic β-cells from UA-treated dysfunction by activating the PI3K/AKT pathway. Such findings suggest that AS-IV may be an efficient natural agent against T2D.

scholarly journals Effect of linagliptin on glucose metabolism and pancreatic beta cell function in patients with persistent prediabetes after metformin and lifestyle

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mildred Fátima de la Luz Alvarez-Canales ◽  
Sara Stephania Salazar-López ◽  
Diana Farfán-Vázquez ◽  
Yosceline Estrella Martínez-López ◽  
Jessica Noemí González-Mena ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Cell Function ◽  
Pancreatic Beta Cell ◽  
Disposition Index ◽  
Oral Glucose ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Double Blind ◽  
Glucose Levels ◽  
Β Cell Function

AbstractThe goal of the study was to evaluate the effect of adding linagliptin to metformin and lifestyle on glucose levels and pancreatic β-cell function in patients with persistent impaired glucose tolerance (IGT) after 12 months of metformin and lifestyle. A single center parallel double-blind randomized clinical trial with 6 months of follow-up was performed in patients with persistent IGT after 12 months of treatment with metformin and lifestyle; patients were randomized to continue with metformin 850 mg twice daily (M group, n = 12) or linagliptin/metformin 2.5/850 mg twice daily (LM group, n = 19). Anthropometric measurements were obtained by standard methods and by bioelectrical impedance; glucose was measured by dry chemistry, insulin by chemiluminescence, and pancreatic β-cell function was calculated with the disposition index using glucose and insulin values during oral glucose tolerance test (OGTT) and adjusting by insulin sensitivity. The main outcomes were glucose levels during OGTT and pancreatic β-cell function. Patients in the LM group had a reduction in weight (−1.7 ± 0.6, p < 0.05) and body mass index (BMI, −0.67 ± 0.2, p < 0.05). Glucose levels significantly improved in LM group with a greater reduction in the area under the glucose curve during OGTT (AUCGluc0_120min) as compared to the M group (−4425 ± 871 vs −1116 ± 1104 mg/dl/120 min, p < 0.001). Pancreatic β-cell function measured with the disposition index, improved only in LM group (2.3 ± 0.23 vs 1.7 ± 0.27, p 0.001); these improvements persisted after controlling for OGTT glucose levels. The differences in pancreatic β-cell function persisted also after pairing groups for basal AUCGluc0_120min. The addition of linagliptin to patients with persistent IGT after 12 months of treatment with metformin and lifestyle, improved glucose levels during OGTT and pancreatic β-cell function after 6 months of treatment.Trial registration: Clinicaltrials.gov with the ID number NCT04088461

scholarly journals Cholecystokinin Suppresses β-Cell Apoptosis, Including in Human Islets in a Transplant Model

2021 ◽  
Author(s):  
Hung Tae Kim ◽  
Arnaldo H. de Souza ◽  
Heidi Umhoefer ◽  
JeeYoung Han ◽  
Lucille Anzia ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Cell Survival ◽  
Cell Apoptosis ◽  
Cell Mass ◽  
Human Islets ◽  
Dependent Manner ◽  
Pancreatic Β Cell ◽  
Β Cell

AbstractLoss of functional pancreatic β-cell mass and increased β-cell apoptosis are fundamental to the pathophysiology of both type 1 and type 2 diabetes. Pancreatic islet transplantation has the potential to cure type 1 diabetes but is often ineffective due to the death of the islet graft within the first few years after transplant. Therapeutic strategies to directly target pancreatic β-cell survival are needed to prevent and treat diabetes and to improve islet transplant outcomes. Reducing β-cell apoptosis is also a therapeutic strategy for type 2 diabetes. Cholecystokinin (CCK) is a peptide hormone typically produced in the gut after food intake, with positive effects on obesity and glucose metabolism in mouse models and human subjects. We have previously shown that pancreatic islets also produce CCK. The production of CCK within the islet promotes β-cell survival in rodent models of diabetes and aging. Now, we demonstrate a direct effect of CCK to reduce cytokine-mediated apoptosis in a β-cell line and in isolated mouse islets in a receptor-dependent manner. However, whether CCK can protect human β-cells was previously unknown. Here, we report that CCK can also reduce cytokine-mediated apoptosis in isolated human islets and CCK treatment in vivo decreases β-cell apoptosis in human islets transplanted into the kidney capsule of diabetic NOD/SCID mice. Collectively, these data identify CCK as a novel therapy that can directly promote β-cell survival in human islets and has therapeutic potential to preserve β-cell mass in diabetes and as an adjunct therapy after transplant.One Sentence SummaryCholecystokinin ameliorates pancreatic β-cell death under models of stress and after transplant of human islets.

2123-P: Peroxiredoxin6 Is a Novel Promoter of Pancreatic Beta-Cell Survival

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 2123-P
Author(s):  
FRANCESCA PACIFICI ◽  
DAVID DELLA-MORTE ◽  
BARBARA CAPUANI ◽  
DONATELLA PASTORE ◽  
ROBERTO ARRIGA ◽  
...  
Keyword(s):  
Beta Cell ◽  
Cell Survival ◽  
Pancreatic Beta Cell

Ameliorating activity of polyphenolic-rich extracts of Basella rubra L. leaves on pancreatic β-cell dysfunction in streptozotocin-induced diabetic rats

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Basiru Olaitan Ajiboye ◽  
Amaka Diayi ◽  
Shedrach Oludare Agunbiade ◽  
Ayodele Jacob Akinyemi ◽  
Olusola Bolaji Adewale ◽  
...  
Keyword(s):  
Bioactive Compounds ◽  
Serum Lipid ◽  
Serum Insulin ◽  
Pancreatic Beta Cell ◽  
Total Phenolic ◽  
Gamma Glutamyl Transferase ◽  
Dependent Manner ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Glutamyl Transferase

Abstract Objectives To assess the ameliorative activity of polyphenolic-rich extracts of Basella rubra leaves on β-cell dysfunction in type-II diabetes (T2DM). Methods Total phenolic and flavonoid contents; α-amylase and α-glucosidase inhibitory actions and qualitative analysis of the bioactive compounds of the polyphenolic-rich extract of B. rubra leaves were investigated using gas chromatography-mass spectroscopy (GC-MS). Diabetes mellitus (DM) was induced by single intraperitoneal injection of streptozotocin (60 mg/kg body weight) and the rats were orally given bound phenolic (BPE) and free phenolic extracts (FPE) of B. rubra (B.R) leaves at 200 and 400 mg/kg b.w once daily for 14 days. Biochemical analyses were executed for evaluation of serum insulin, serum lipid profile concentrations, liver enzymes activities. Results The extracts demonstrated antioxidant potentials and enzymes inhibitory activities in dose dependent manner; and several bioactive compounds as revealed by GC-MS. BPE and FPE considerably (p<0.05) reduced hyperglycemia, improved serum insulin levels, ameliorated the concentration of serum lipid profiles and improved liver antioxidant activities. Additionally, BPE and FPE expressively decreased alanine aminotransferases (ALT), aspartate aminotransferases (AST), gamma-glutamyl transferase (GGT) activities along with levels of bilirubin and urea when compare to diabetic control rats. Conclusions Data acquired exhibited the ability of BPE and FPE to improve pancreatic beta-cell in streptozotocin-induced rats.

W46 ROLE OF LIPOPROTEINS IN PANCREATIC BETA-CELL SURVIVAL, PROLIFERATION AND FUNCTION

2010 ◽  
Vol 11 (2) ◽  
pp. 10
Author(s):  
R.A. Sibler ◽  
S. Rütti ◽  
J.A. Ehses ◽  
R. Prazak ◽  
D.T. Meier ◽  
...  
Keyword(s):  
Beta Cell ◽  
Cell Survival ◽  
Pancreatic Beta Cell ◽  
And Function

scholarly journals A Pilot Study on Antimalarial Effects of Moringa oleifera Leaf Extract in Plasmodium berghei Infection in Mice

2017 ◽  
Vol 15 (2) ◽  
pp. 151-156
Author(s):  
Somrudee NAKINCHAT ◽  
Voravuth SOMSAK
Keyword(s):  
Plasma Glucose ◽  
Crude Extract ◽  
Plasmodium Berghei ◽  
Leaf Extract ◽  
Moringa Oleifera ◽  
Dependent Manner ◽  
Glucose Levels ◽  
New Compounds ◽  
Dose Dependent

The emergence and spread of antimalarial drug resistance of Plasmodium parasites, as well as hypoglycemia, during malaria infection, and subsequent death, are critical problems in malaria-endemic areas. Hence, finding new compounds, especially plant extracts having antimalarial and anti-hypoglycemic activities, are urgently needed. The present study aimed to investigate the antimalarial and anti-hypoglycemic effects of Moringa oleifera leaf extract in Plasmodium berghei infection in mice. Aqueous crude extract of M. oleifera leaves was freshly prepared and used for an efficacy test in vivo. Groups of ICR mice (5 mice in each) were infected with 1´107 infected red blood cells of P. berghei ANKA by intraperitoneal injection and given the extract orally with doses of 100, 500, and 1000 mg/kg for 4 consecutive days. Parasitemia and plasma glucose levels were subsequently measured. The results showed that M. oleifera leaf extract presented significant (p < 0.001) inhibition of parasitemia in a dose-dependent manner. Moreover, this extract exerted anti-hypoglycemia effects in infected mice in a dose-dependent manner. The highest degrees of activity were found at a dose of 1000 mg/kg of the extract. Additionally, no effect on plasma glucose was found in normal mice treated with this extract. It can be concluded that aqueous crude extract of M. oleifera leaves exerted antimalarial and anti-hypoglycemic effects in P. berghei infection in mice.

scholarly journals AGEs and Glucose Levels Modulate Type I and III Procollagen mRNA Synthesis in Dermal Fibroblasts Cells Culture

2008 ◽  
Vol 2008 ◽  
pp. 1-7 ◽  
Author(s):  
Serban Iren Andreea ◽  
Costache Marieta ◽  
Dinischiotu Anca
Keyword(s):  
Extracellular Matrix ◽  
High Glucose ◽  
Dermal Fibroblasts ◽  
Type I ◽  
Dependent Manner ◽  
Human Dermal Fibroblasts ◽  
Mrna Synthesis ◽  
Quantitative Real Time Pcr ◽  
Glucose Levels ◽  
Dose Dependent

In the dermis, fibroblasts play an important role in the turnover of the dermal extracellular matrix. Collagen I and III, the most important dermal proteins of the extracellular matrix, are progressively altered during ageing and diabetes. For mimicking diabetic conditions, the cultured human dermal fibroblasts were incubated with increasing amounts of AGE-modified BSA andD-glucose for 24 hours. The expression of procollagenα2(I) and procollagenα1(III) mRNA was analyzed by quantitative real-time PCR. Our data revealed that the treatment of fibroblasts with AGE-modified BSA upregulated the expression of procollagenα2(I) and procollagenα1(III) mRNA in a dose-dependent manner. High glucose levels mildly induced a profibrogenic pattern, increasing the procollagenα2(I) mRNA expression whereas there was a downregulation tendency of procollagenα1(III) mRNA.

Adenosine inhibition of neutrophil damage during reperfusion does not involve KATP-channel activation

1997 ◽  
Vol 273 (4) ◽  
pp. H1677-H1687 ◽  
Author(s):  
Zhi-Qing Zhao ◽  
James C. Todd ◽  
Hiroki Sato ◽  
Xin-Liang Ma ◽  
J. Vinten-Johansen
Keyword(s):  
Infarct Size ◽  
Superoxide Radical ◽  
Receptor Activation ◽  
Polymorphonuclear Neutrophils ◽  
Vehicle Group ◽  
Myeloperoxidase Activity ◽  
Dependent Manner ◽  
Glucose Levels ◽  
Radical Generation ◽  
Dose Dependent

This study tests the hypothesis that cardioprotection exerted by adenosine A2-receptor activation and neutrophil-related events involves stimulation of ATP-sensitive potassium (KATP) channels on neutrophils during reperfusion. The adenosine A2 agonist CGS-21680 (CGS) inhibited superoxide radical generation from isolated rabbit polymorphonuclear neutrophils (PMNs) in a dose-dependent manner from 17.7 ± 2.1 to 7.4 ± 1.3 nmol/5 × 106 PMNs ( P < 0.05). Pinacidil, a KATP-channel opener, partially inhibited superoxide radical production, which was completely reversed by glibenclamide (Glib). Incremental doses of Glib in combination with CGS (1 μM) did not alter CGS-induced inhibition of superoxide radical generation. CGS significantly reduced PMN adherence to the endothelial surface of aortic segments in a dose-dependent manner from 189 ± 8 to 50 ± 6 PMNs/mm2( P < 0.05), which was also not altered by incremental doses of Glib. Infusion of CGS (0.025 mg/kg) before reperfusion reduced infarct size from 29 ± 2% in the Vehicle group to 15 ± 1% in rabbits undergoing 30 min of ischemia and 120 min of reperfusion ( P< 0.05). Glib (0.3 mg/kg) did not change the infarct size (28 ± 2%) vs. the Vehicle group and did not attenuate infarct size reduction by CGS (16 ± 1%). Glib did not change blood glucose levels. Cardiac myeloperoxidase activity was decreased in the ischemic tissue of the CGS group (0.15 ± 0.03 U/100 mg tissue) compared with the Vehicle group (0.37 ± 0.05 U/100 mg tissue; P < 0.05). We conclude that adenosine A2 activation before reperfusion partially reduces infarct size by inhibiting neutrophil activity and that this effect does not involve KATP-channel stimulation.

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