scholarly journals Low-Energy Extracorporeal Shock Wave Ameliorates Streptozotocin Induced Diabetes and Promotes Pancreatic Beta Cells Regeneration in a Rat Model

2019 ◽  
Vol 20 (19) ◽  
pp. 4934 ◽  
Author(s):  
Chang-Chun Hsiao ◽  
Cheng-Chan Lin ◽  
You-Syuan Hou ◽  
Jih-Yang Ko ◽  
Ching-Jen Wang
Keyword(s):  
Pancreatic Islets ◽  
Beta Cells ◽  
Rat Model ◽  
Pancreatic Beta Cells ◽  
Urine Volume ◽  
Pancreatic Tissue ◽  
Low Energy ◽  
Insulin Production ◽  
Extracorporeal Shock Wave ◽  
Streptozotocin Induced Diabetes

Traditional therapy for diabetes mellitus has focused on supportive treatment, and is not significant in the promotion of pancreatic beta cells regeneration. We investigated the effect of low- energy extracorporeal shock wave (SW) on a streptozotocin induced diabetes (DM) rat model. Methods: The DM rats were treated with ten sessions of low-energy SW therapy (weekly for ten consecutive weeks) or left untreated. We assessed blood glucose, hemoglobin A1c (HbA1c), urine volume, pancreatic islets area, c-peptide, glucagon-like peptide 1 (GLP-1) and insulin production, beta cells number, pancreatic tissue inflammation, oxidative stress, apoptosis, angiogenesis, and stromal cell derived factor 1 (SDF-1) ten weeks after the completion of treatment. Results: The ten- week low-energy SW therapy regimen significantly reduced blood glucose, HbA1c, and urine volume as well as significantly enhancing pancreatic islets area, c-peptide, GLP-1, and insulin production in the rat model of DM. Moreover, low-energy SW therapy increased the beta cells number in DM rats. This was likely primarily attributed to the fact that low-energy SW therapy reduced pancreatic tissue inflammation, apoptosis, and oxidative stress as well as increasing angiogenesis, cell proliferation, and tissue repair potency. Conclusions: Low-energy SW therapy preserved pancreatic islets function in streptozotocin-induced DM. Low-energy SW therapy may serve as a novel noninvasive and effective treatment of DM.

DsAAV8-Mediated Expression of GLP-1 in Pancreatic Beta-Cells Prevents Streptozotocin-Induced Diabetes.

2008 ◽  
Vol 32 (4) ◽  
pp. 335
Author(s):  
Michael J. Riedel ◽  
Daniel F. Gaddy ◽  
Robert K. Baker ◽  
Paul D. Robbins ◽  
Timothy J. Kieffer
Keyword(s):  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Streptozotocin Induced Diabetes

scholarly journals Hedgehog signaling regulation of insulin production by pancreatic beta-cells

Diabetes ◽  
2000 ◽  
Vol 49 (12) ◽  
pp. 2039-2047 ◽  
Author(s):  
M. K. Thomas ◽  
N. Rastalsky ◽  
J. H. Lee ◽  
J. F. Habener
Keyword(s):  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Hedgehog Signaling ◽  
Insulin Production ◽  
Signaling Regulation

Polyclonal origin of pancreatic islets in aggregation mouse chimaeras

Development ◽  
1991 ◽  
Vol 112 (4) ◽  
pp. 1115-1121 ◽  
Author(s):  
L. Deltour ◽  
P. Leduque ◽  
A. Paldi ◽  
M.A. Ripoche ◽  
P. Dubois ◽  
...  
Keyword(s):  
Cell Division ◽  
Pancreatic Islets ◽  
Progenitor Cells ◽  
Beta Cells ◽  
Growth Pattern ◽  
Pancreatic Beta Cells ◽  
Progenitor Cell ◽  
Histological Sections ◽  
Small Clusters

In the present study, we have examined the origin and growth pattern of the beta cells in pancreatic islets, to determine whether a single progenitor cell gave rise to all the precursors of the islets, or if each of a few progenitor cells is the founder of a different islet, or if each islet is a mixture of cells originating from a pool of progenitor cells. Aggregation mouse chimaeras where the pancreatic beta cells derived from each embryo can be identified in the islets on histological sections were analyzed. In two chimaeras, all the islets contained cells from both the aggregated embryo. This clearly demonstrates that each islet resulted from several independent cells. In addition, the beta cells derived from either embryo component were in very small clusters in the islets, suggesting that in situ cell division did not account significantly for islet growth.

scholarly journals Low-Energy Extracorporeal Shock Wave Therapy Ameliorates Kidney Function in Diabetic Nephropathy

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Chang-Chun Hsiao ◽  
Wei-Han Huang ◽  
Kuang-Hung Cheng ◽  
Chien-Te Lee
Keyword(s):  
Oxidative Stress ◽  
Shock Wave ◽  
Diabetic Nephropathy ◽  
Rat Model ◽  
Renal Fibrosis ◽  
Tissue Repair ◽  
Extracorporeal Shock Wave Therapy ◽  
Low Energy ◽  
Shock Wave Therapy ◽  
Extracorporeal Shock Wave

Background. Diabetic nephropathy is the most common cause of end-stage renal disease. Traditional therapy for diabetic nephropathy has focused on supportive treatment, and there is no significant effective therapy. We investigated the effect of low-energy extracorporeal shock wave therapy on a diabetic nephropathy rat model. Methods. Streptozotocin-induced diabetic nephropathy rats were treated with six sessions of low-energy extracorporeal shock wave therapy (weekly for six consecutive weeks) or left untreated. We assessed urinary creatinine and albumin, glomerular volume, renal fibrosis, podocyte number, renal inflammation, oxidative stress, and tissue repair markers (SDF-1 and VEGF) six weeks after the completion of treatment. Results. The six-week low-energy extracorporeal shock wave therapy regimen decreased urinary albumin excretion as well as reduced glomerular hypertrophy and renal fibrosis in the rat model of diabetic nephropathy. Moreover, low-energy extracorporeal shock wave therapy increased podocyte number in diabetic nephropathy rats. This was likely primarily attributed to the fact that low-energy extracorporeal shock wave therapy reduced renal inflammation and oxidative stress as well as increased tissue repair potency and cell proliferation. Conclusions. Low-energy extracorporeal shock wave therapy preserved kidney function in diabetic nephropathy. Low-energy extracorporeal shock wave therapy may serve as a novel noninvasive and effective treatment of diabetic nephropathy.

Comparative toxicity of alloxan, N-alkylalloxans and ninhydrin to isolated pancreatic islets in vitro

1997 ◽  
Vol 155 (2) ◽  
pp. 283-293 ◽  
Author(s):  
A Jorns ◽  
R Munday ◽  
M Tiedge ◽  
S Lenzen
Keyword(s):  
Beta Cell ◽  
Pancreatic Islets ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Ultrastructural Changes ◽  
Cell Necrosis ◽  
High Concentrations ◽  
Beta Cell Necrosis

The in vitro toxicity of the diabetogenic agent alloxan as documented by the induction of beta cell necrosis was studied in isolated ob/ob mouse pancreatic islets. The effect of alloxan has been compared with that of a number of N-alkyl alloxan derivatives and with that of the structurally related compound, ninhydrin. Alloxan and its derivatives were selectively toxic to pancreatic beta cells, with other endocrine cells and exocrine parenchymal cells being well preserved, even at high concentration. In contrast, ninhydrin was selectively toxic to pancreatic beta cells only at comparatively low concentration, destroying all islet cell types at high concentrations. The ultrastructural changes induced by all the test compounds in pancreatic beta cells in vitro were very similar to those observed during the development of alloxan diabetes in vivo. The relative toxicity of the various compounds to pancreatic beta cells in vitro was not, however, related to their ability to cause diabetes in vivo. Indeed, the non-diabetogenic substances ninhydrin, N-butylalloxan and N-isobutylalloxan were very much more toxic to isolated islets than the diabetogenic compounds alloxan and N-methylalloxan. These results suggest that the differences in diabetogenicity among alloxan derivatives are not due to intrinsic differences in the susceptibility of the pancreatic beta cells to their toxicity, but may reflect differences in distribution or metabolism. High concentrations of glucose protected islets against the harmful effects of alloxan and its derivatives, but not those of ninhydrin. Low levels of glucose, and non-carbohydrate nutrients, afforded little protection, indicating that the effect of glucose is not due to the production of reducing equivalents within the cell, 3-O-Methylglucose, which protects against alloan diabetes in vivo, did not protect against alloxan toxicity in vitro. Since 3-O-methylglucose is known to prevent uptake of alloxan by pancreatic beta cells, it appears that uptake of alloxan by the cell is not a prerequisite for the induction of beta cell necrosis.

Transplantation of pancreatic beta-cells prevents development of hypothalamic obesity in rats.

1978 ◽  
Vol 235 (3) ◽  
pp. E266 ◽  
Author(s):  
S Inoue ◽  
G A Bray ◽  
Y S Mullen
Keyword(s):  
Insulin Secretion ◽  
Food Intake ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Pancreatic Tissue ◽  
Diabetic Rats ◽  
Significant Rise ◽  
Neural Mechanisms ◽  
Renal Capsule ◽  
Hypothalamic Obesity

The present experiments have tested the hypothesis that ventromedial hypothalamic (VMH) lesions enhance insulin secretion by neural mechanisms. Rats were made diabetic by injecting streptozotocin to destroy their own pancreatic beta-cells. Subsequently, transplants of fetal pancreatic tissue were placed under the renal capsule. VMH lesions were placed in rats whose diabetes was cured with transplants as well as sham-transplanted animals. The animals were followed for 4 wk. The lesioned rats with pancreatic transplants gained no more weight than the sham-operated controls. There was no significant rise in insulin in the transplanted rats after VMH lesioning, but the VMH lesioned rats with intact pancreatic tissue showed the expected rise in insulin. Food intake rose 71% in the VMH lesioned rats with intact beta-cells, but only 23% in the VMH lesioned rats with transplants. Hypertrophy of the pancreatic islets was also observed in the VMH lesioned rats with an intact pancreas, but was not found in the VMH lesioned rats with a transplanted pancreas. Thus, transplantation of pancreatic tissue beneath the renal capsule of diabetic rats prevented the characteristic hyperphagia, hyperinsulinemia, and obesity in VMH lesioned rats whose pancreas was free from intact innervation. The results support the hypothesis that neural mediation of the rise in insulin is the primary factor in the development of hypothalamic obesity.

scholarly journals The Effect of Melissa officinalis Extract on Streptozotocin-Induced Diabetes in Rats: A Stereological Study on Pancreatic Islets and Beta-cells

2021 ◽  
Vol 29 (132) ◽  
pp. 34-40
Author(s):  
Soheil Ashkani-Esfahani ◽  
Alireza Ebrahimi ◽  
Maryam Bahmani-Jahromi ◽  
Elham Nadimi ◽  
Hossein Arabzadeh ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Beta Cells ◽  
Melissa Officinalis ◽  
Streptozotocin Induced Diabetes

scholarly journals PCSK9 affects expression of key surface proteins in human pancreatic beta cells through intra- and extracellular regulatory circuits

2021 ◽  
Author(s):  
kevin Saitoski ◽  
Maria Ryaboshapkina ◽  
Ghaith Hamza ◽  
Andrew F Jarnuczak ◽  
claire berthault ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Beta Cell ◽  
Pancreatic Islets ◽  
Cell Line ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Pancreatic Beta Cell ◽  
Loss Of Function ◽  
Beta Cell Line ◽  
Gain And Loss

Aims/hypothesis: Proprotein convertase subtilisin/kexin 9 (PCSK9) is involved in the degradation of LDLR. However, PCSK9 can target other proteins in a cell-type specific manner. While PCSK9 has been detected in pancreatic islets, its expression in insulin-producing pancreatic beta cells is debated. Herein, we studied PCSK9 expression, regulation and function in the human pancreatic beta cell line EndoC-βH1. Methods: We assessed PCSK9 expression in mouse and human pancreatic islets, and in the pancreatic beta cell line EndoC-βH1. We also studied PCSK9 regulation by cholesterol, lipoproteins, Mevastatin, and by SREBPs transcription factors. To evaluate PCSK9 function in pancreatic beta cells, we performed PCSK9 gain-and loss-of-function experiments in EndoC-βH1 using siPCSK9 or recombinant PCSK9 treatments, respectively. Results: We demonstrate that PCSK9 is expressed and secreted by pancreatic beta cells. In EndoC-βH1 cells, PCSK9 expression is regulated by cholesterol and by SREBPs transcription factors. Importantly, PCSK9 knockdown results in multiple transcriptome, proteome and secretome deregulations and impaired insulin secretion. By gain- and loss-of- function experiments, we observed that PCSK9 regulates the expression levels of LDLR and VLDLR through an extracellular mechanism while CD36, PD-L1 and HLA-ABC are regulated through an intracellular mechanism. Conclusions/interpretation: Collectively, these results highlight PCSK9 as an important regulator of CD36, PD-L1 and HLA-ABC cell surface expression in pancreatic beta cells. Data availability: RNA-seq data have been deposited to GEO database with accession number GSE182016. Mass spectrometry proteomics data have been deposited to the ProteomeXchange Consortium via the PRIDE partner repository with the following identifiers: PXD027921, PXD027911 and PXD027913.

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