GLP-1 could improve the similarity of IPCs and pancreatic beta cells in cellular ultrastructure and function

2013 ◽  
Vol 114 (10) ◽  
pp. 2221-2230
Author(s):  
Qiping Shi ◽  
Simin Luo ◽  
Haiying Jia ◽  
Lie Feng ◽  
Xiaohua Lu ◽  
...  
Keyword(s):  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Cellular Ultrastructure ◽  
Ultrastructure And Function ◽  
And Function

scholarly journals Regulation and function of the cytosolic viral RNA sensor RIG-I in pancreatic beta cells

2009 ◽  
Vol 1793 (11) ◽  
pp. 1768-1775 ◽  
Author(s):  
Mónica García ◽  
Zeynep Dogusan ◽  
Fabrice Moore ◽  
Shintaro Sato ◽  
Gunther Hartmann ◽  
...  
Keyword(s):  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Viral Rna ◽  
And Function

scholarly journals Human Pluripotent Stem Cells to Model Islet Defects in Diabetes

2021 ◽  
Vol 12 ◽  
Author(s):  
Diego Balboa ◽  
Diepiriye G. Iworima ◽  
Timothy J. Kieffer
Keyword(s):  
Stem Cells ◽  
Beta Cells ◽  
Pluripotent Stem Cells ◽  
Pancreatic Beta Cells ◽  
Molecular Mechanisms ◽  
Disease Modeling ◽  
Human Pluripotent Stem Cells ◽  
Pancreatic Endocrine Cells ◽  
Onset Of Diabetes ◽  
And Function

Diabetes mellitus is characterized by elevated levels of blood glucose and is ultimately caused by insufficient insulin production from pancreatic beta cells. Different research models have been utilized to unravel the molecular mechanisms leading to the onset of diabetes. The generation of pancreatic endocrine cells from human pluripotent stem cells constitutes an approach to study genetic defects leading to impaired beta cell development and function. Here, we review the recent progress in generating and characterizing functional stem cell-derived beta cells. We summarize the diabetes disease modeling possibilities that stem cells offer and the challenges that lie ahead to further improve these models.

Effects of ORP150 on appearance and function of pancreatic beta cells following acute necrotizing pancreatitis

2011 ◽  
Vol 207 (6) ◽  
pp. 370-376 ◽  
Author(s):  
Wen-Hong Deng ◽  
Chen Chen ◽  
Wei-Xing Wang ◽  
Jia Yu ◽  
Jin-You Li ◽  
...  
Keyword(s):  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Necrotizing Pancreatitis ◽  
Acute Necrotizing Pancreatitis ◽  
Acute Necrotizing ◽  
And Function

scholarly journals The expression and function of histamine H3receptors in pancreatic beta cells

2013 ◽  
Vol 171 (1) ◽  
pp. 171-185 ◽  
Author(s):  
T Nakamura ◽  
T Yoshikawa ◽  
N Noguchi ◽  
A Sugawara ◽  
A Kasajima ◽  
...  
Keyword(s):  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
And Function

LDL receptor (LDLR) expression and function in human pancreatic beta cells

2016 ◽  
Vol 252 ◽  
pp. e115-e116 ◽  
Author(s):  
A. Thedrez ◽  
R. Scharfmann ◽  
P. Parnet ◽  
E. Nobécourt ◽  
G. Lambert
Keyword(s):  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Ldl Receptor ◽  
And Function

scholarly journals MicroRNAs Regulate the Wnt/Ca2+ Signaling Pathway to Promote the Secretion of Insulin in Pancreatic Nestin-Positive Progenitor Cells

2014 ◽  
Author(s):  
Chunyu Bai ◽  
Xiangchen Li ◽  
Yuhua Gao ◽  
Taofeng Lu ◽  
Kunfu Wang ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Progenitor Cells ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Target Genes ◽  
Cell Function ◽  
Expression Profiles ◽  
Control Cell ◽  
Small Noncoding Rnas ◽  
And Function

MicroRNAs (miRNAs) are small noncoding RNAs that bind to the 3?-UTR of mRNAs and function mainly in post-transcriptional regulation. MiRNAs have been implicated to play roles in organ development, including that of the pancreas. Many miRNAs, such as miR-375, miR-124, miR-7, miR-21 and miR-221, have been shown to regulate insulin production as well as insulin secretion. However, it is not known whether miRNAs can regulate insulin secretion via the control of intracellular Ca2+ in pancreatic beta cells. In this research, expression profiles of miRNAs and mRNAs were investigated using RNA-sequencing and microarray analysis in chicken pancreatic nestin-positive progenitor cells and differentiated pancreatic beta cells. A number of miRNAs were up-regulated after differentiation of progenitors into beta cells, which regulate cell signaling pathways to control cell function. miR-223 and miR146a were shown to promote insulin secretion from pancreatic beta cells by regulating the concentration of intracellular Ca2+ via the down-regulation of their target genes.

scholarly journals Fatty Aldehyde Dehydrogenase (ALDH3A2)-Dependent Neutralization of Advanced Lipid Peroxidation End Products (ALEs) at the Bifurcation of Hormetic and Degenerative Pathways in Pancreatic Beta Cells

Proceedings ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 10
Author(s):  
Sasson
Keyword(s):  
Lipid Peroxidation ◽  
Insulin Secretion ◽  
Palmitic Acid ◽  
Beta Cells ◽  
Aldehyde Dehydrogenase ◽  
Adaptive Response ◽  
Pancreatic Beta Cells ◽  
Fatty Aldehyde ◽  
End Products ◽  
And Function

Hyperglycemia and hyperlipidemia synergistically and adversely impair insulin secretion and ultimately lead to pancreatic beta cell decomposition. We found that both nutrient overload conditions displace arachidonic and linoleic acids from membrane phospholipids and subject them to free radical-mediated peroxidation and generation of advanced lipid peroxidation end products (ALEs), of which the aldehyde 4-hydroxy-2-nonenal (4-HNE) is prominent. When present at high levels this electrophilic molecule binds covalently to nucleophilic moieties in proteins, phospholipids and nucleic acid, modifies their structure and function and leads to severe cellular dysfunction and apoptosis. However, when present at low and unharmful levels this same molecule activates the nuclear receptor PPARδ and augments insulin secretion. The level of endogenous 4-HNE is determined by the extent of lipid peroxidation on one hand, and by enzymatic neutralization of the aldehyde, on the other. The latter step is mediated by enzymatic processes of which the transformation of the aldehyde to the corresponding inactive carboxylic derivative 4-hydroxy-2-nonenoic acid (4-HNA) is significant. The enzyme responsible for this transformation, which belongs to the large family of aldehyde dehydrogenases and selectively neutralizes fatty acid-derived aldehydes, is ALDH3A2, which is also known as fatty aldehyde dehydrogenase (FALDH). Consequently, we hypothesized that the expression level and function of ALDH3A2 may determine the fate of beta cells under nutrient overload conditions: insufficient neutralization of 4-HNE by the enzyme will lead to cell demise, whereas increased expression and function will extend the adaptive response of beta cells. This adaptive response that is characterized with increased insulin secretion enables effective storage of the nutrient surplus in peripheral tissues and organs while minimizing the dire consequences of the nutrient overload. We aimed at investigating the expression pattern of ALDH3A2 in pancreatic beta cells (the INS-1E cell line) under hyperglycemic condition without or with supplementation with saturated fatty acids (e.g., palmitic acid). Our results show significant glucose- and palmitic acid-dependent induction of ALDH3A2 expression in the cells. We also found that the transformation of palmitic acid (16:1) to mono-unsaturated palmitoleic acid (16:1, cis 9) by the enzyme Stearoyl-CoA desaturase-1 (SCD1) decreased the burden of the lipid stress on the cells and abrogated the stimulus for the induction of ALDH3A2. Preliminary experiments indicated that the upregulation of the induction of ALDH3A2 was partly induced by PPARδ. These findings correlate to our previous discovery that the hormetic effects of 4HNE were mediated via activation of this nuclear receptor. In summary, this study assigns a central role to the enzyme ALDH3A2 in the protective mechanism beta cells employ to mitigate detrimental effects of ALEs, and divert them into hormetic agents, that by feedback mechanism through PPARδ increase ALDH3A2 expression.

scholarly journals Transcriptional Mechanisms Controlling miR-375 Gene Expression in the Pancreas

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Tali Avnit-Sagi ◽  
Tal Vana ◽  
Michael D. Walker
Keyword(s):  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Transcriptional Control ◽  
Endocrine Pancreas ◽  
Biological Activities ◽  
Regulatory Element ◽  
Cell Mass ◽  
Luciferase Reporter ◽  
And Function

MicroRNAs (miRNAs) are a class of small non-coding RNAs that play an important role in mediating a broad and expanding range of biological activities. miR-375 is expressed selectively in the pancreas. We have previously shown that selective expression of miR-375 in pancreatic beta cells is controlled by transcriptional mechanisms operating through a TATA box-containing promoter. Expression of miR-375 has been reported in non-beta cells within the endocrine pancreas, and indeed inactivation of miR-375 leads to perturbation in cell mass and number of both alpha and beta cells. Consistent with its expression throughout the endocrine pancreas, we now show that the promoter of the miR-375 gene shows selective activity in pancreatic endocrine alpha cells, comparable to that observed in beta cells. We previously identified a novel negative regulatory element located downstream of the miR-375 gene transcription start site. By generating luciferase reporter genes, we now show that the sequence is functional also when positioned upstream of a heterologous promoter, thus proving that the repressor effect is mediated at least in part at the level of transcription. Further characterization of the transcriptional control mechanism regulating expression of miR-375 and other pancreatic miRNAs will contribute to a better understanding of pancreas development and function.

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