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Dissertations / Theses on the topic 'Pancreatic β-islet cell'

Author: Grafiati
Published: 6 September 2023

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1

Mokhtari, Dariush. "MEKK-1 and NF-κB Signaling in Pancreatic Islet Cell Death". Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8896.

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Type 1 diabetes is an autoimmune disease resulting in the selective destruction of the insulin producing β-cells in the pancreas. Pro-inflammatory cytokines and the free radical nitric oxide (NO) have been implicated in mediating the destruction of β-cells, possibly through activation of the mitogen activated protein kinases (MAPKs) JNK, ERK and p38. In addition to MAPKs, cytokine signaling also results in activation of the transcription factor nuclear factor-kappaB (NF-κB). The upstream signaling events leading to MAPK and NF-κB activation in β-cells are not well known. The work presented in
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2

Tian, Geng. "On the Generation of cAMP Oscillations and Regulation of the Ca2+ Store-operated Pathway in Pancreatic Islet α- and β-cells". Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-191852.

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Insulin and glucagon are released in pulses from pancreatic β- and α-cells, respectively. Both cell types are electrically excitable, and elevation of the cytoplasmic Ca2+ concentration ([Ca2+]i) due to depolarization with voltage-dependent entry of the cation is the main trigger of hormone secretion. Store-operated Ca2+ entry  (SOCE) also contributes to the [Ca2+]i elevation and this process has been suggested to be particularly important for glucagon secretion. cAMP is another important messenger that amplifies Ca2+-triggered secretion of both hormones, but little is known about cAMP dynamic
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3

Cadavez, Trigo Lisa. "Islet amylold in type 2 diabetes: The role of chaperones in endoplasmic reticulum stress and amyloid formation in pancreatic β-cell". Doctoral thesis, Universitat de Barcelona, 2014. http://hdl.handle.net/10803/290734.

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La disminución de la masa de célula ß pancreática y la función en la diabetes tipo 2 (T2D) se puede atribuir a una serie de factores estresantes experimentados por el islote durante el desarrollo y la progresión de la enfermedad, incluyendo el amiloide de los islotes. El amiloide de los islotes pancreáticos se compone predominantemente del péptido humano amilina, también conocido como polipeptido amiloide del islote humano (hIAPP). Estos depósitos están implicados en el proceso de deterioro de las células ß y en la reducción de la masa celular ß e implica la agregación de monómeros solubles no
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4

Ngamjariyawat, Anongnad. "The beneficial Effects of Neural Crest Stem Cells on Pancreatic β–cells". Doctoral thesis, Uppsala universitet, Institutionen för neurovetenskap, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-233157.

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Patients with type-1 diabetes lose their β-cells after autoimmune attack. Islet transplantation is a co-option for curing this disease, but survival of transplanted islets is poor. Thus, methods to enhance β-cell viability and function as well as methods to expand β-cell mass are required. The work presented in this thesis aimed to study the roles of neural crest stem cells or their derivatives in supporting β-cell proliferation, function, and survival. In co-culture when mouse boundary cap neural crest stem cells (bNCSCs) and pancreatic islets were in direct contact, differentiating bNCSCs st
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5

Kanase, Nilesh. "The impact of oxidative stress and potential antioxidant therapy on function and survival of cultured pancreatic β-islet cells". Thesis, University of the Highlands and Islands, 2011. https://pure.uhi.ac.uk/portal/en/studentthesis/the-impact-of-oxidative-stress-and-potential-antioxidant-therapy-on-function-and-survival-of-cultured-pancreatic-islet-cells(ec0cd703-3902-4410-8c58-e7c7e49f33e7).html.

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Dietary antioxidant curcumin derived from turmeric has been suggested to decrease the risk of many chronic diseases. Much of the existing data for curcumin stem from experiments performed at supra-physiological concentrations (μM-mM) that are impossible to attain through oral ingestion. It was therefore hypothesized that curcumin at low plasma achievable concentration, though itself not acting as a direct antioxidant might up-regulate the intracellular antioxidants and thus helping combat oxidative stress and protect β-islet cells. The results indicated that Curcumin, DMC and BDMC were able to
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6

Elshebani, Asma Basheir. "Studies of the Effect of Enterovirus Infection on Pancreatic Islet Cells." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7208.

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7

Zallocco, Lorenzo. "Protein post translational modifications and diabetes. Pro-inflammatory cytokines reshape lysin acetylome of rat clonal β cells and human pancreatic islets". Doctoral thesis, Università di Siena, 2022. http://hdl.handle.net/11365/1203952.

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Type I diabetes mellitus (T1DM) is characterized by insulin deficiency due to β cells death caused by inflammation and immune reaction. Pro-inflammatory cytokines play a key role in T1DM pathogenesis by activating the pro-apoptotic pathway. Cytokine-activated NF-κB and STAT1 signalling also leads to oxidative stress and triggers the antigen presentation pathway. Stressful stimuli and self-defence responses combined cause mitochondrial dysfunction and endoplasmic reticulum (ER) stress, which progress to β cell functional impairments and death. Some molecular mechanisms involved in the progressi
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8

Berg, Anna-Karin. "Enterovirus Infections of β-Cells : A Mechanism of Induction of Type 1 Diabetes?" Doctoral thesis, Uppsala University, Department of Women's and Children's Health, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6019.

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<p>The process of β-cell destruction that leads to type 1 diabetes (T1D) is incompletely understood and it is believed to be a result of both genetic and environmental factors. Enterovirus (EV) infections of the β-cells have been proposed to be involved, however, the effects of EV infections on human β-cells have been little investigated. This thesis summarises studies of three different Coxsackie B4 virus strains that have previously been shown to infect human islets. The effects of infections with these EV were studied <i>in vitro</i> in human islets and in a rat insulin-producing cell line.
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9

Brusco, Noemi. "Phenotyping of single pancreatic islets reveals a crosstalk between proinsulin intracellular alteration, ER stress and loss of β cell identity in impaired glucose tolerant and type 2 diabetic patients". Doctoral thesis, Università di Siena, 2021. http://hdl.handle.net/11365/1127686.

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Type 2 diabetes mellitus is a heterogeneous group of metabolic diseases characterized by increased levels of blood glucose due to insulin resistance and alteration of insulin secretion by pancreatic β cells. Recent studies suggest that β cell loss in T2D results from endoplasmic reticulum stress which can cause an alteration in the processing of PI to INS. In particular, it has been reported that the increased circulating levels of PI and elevated PI/INS ratio are well-known abnormalities in type 2 diabetes. Several studies have hypothesized that an elevated PI/INS ratio was caused by increase
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10

Ahmed, Meftun. "Oscillatory Ca2+ signaling in glucose-stimulated murine pancreatic β-cells : Modulation by amino acids, glucagon, caffeine and ryanodine". Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2001. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1408.

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Oscillations in cytoplasmic Ca2+ concentration ([Ca2+]i) is the key signal in glucose-stimulated β-cells governing pulsatile insulin release. The glucose response of mouse β-cells is often manifested as slow oscillations and rapid transients of [Ca2+] i. In the present study, microfluorometric technique was used to evaluate the role of amino acids, glucagon, ryanodine and caffeine on the generation and maintenance of [Ca2+] i oscillations and transients in individual murine β-cells and isolated mouse pancreatic islets. The amino acids glycine, alanine and arginine, at around their physiologica
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11

Jaffredo, Manon. "Communications intercellulaires dynamiques au sein des îlots pancréatiques analysées par multi-electrode arrays : rôles physiologiques et applications biotechnologiques en diabétologie." Thesis, Bordeaux, 2021. http://www.theses.fr/2021BORD0120.

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Les îlots pancréatiques sont le principal capteur de glycémie et intègrent toutes les informations métaboliques et hormonales pour adapter en temps réel la sécrétion des hormones, telles que l'insuline par les cellules β majoritaires et le glucagon par les cellules α. Dans le diabète de type 1 (DT1) les cellules β sont détruites par réaction auto-immune et dans le DT2 la masse de cellules β, la fonction et le réseau intra-îlot sont altérés. La réactivité de ces micro-organes est due à leurs propriétés électriques, encodant rapidement l’information, et aux communications entre cellules β/β et β
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12

Andersson, Annika K. "Role of Inducible Nitric Oxide Synthase and Melatonin in Regulation of β-cell Sensitivity to Cytokines". Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3537.

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<p>The mechanisms of β-cell destruction leading to type 1 diabetes are complex and not yet fully understood, but infiltration of the islets of Langerhans by autoreactive immune cells is believed to be important. Activated macrophages and T-cells may then secrete cytokines and free radicals, which could selectively damage the β-cells. Among the cytokines, IL-1β, IFN-γ and TNF-α can induce expression of inducible nitric synthase (iNOS) and cyclooxygenase-2. Subsequent nitric oxide (NO) and prostaglandin E<sub>2</sub> (PGE<sub>2</sub>) formation may impair islet function.</p><p>In the present stu
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13

Ahmed, Meftun. "Oscillatory Ca2+ signaling in glucose-stimulated murine pancreatic β-cells : Modulation by amino acids, glucagon, caffeine and ryanodine". Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2001. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1408.

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<p>Oscillations in cytoplasmic Ca<sup>2+</sup> concentration ([Ca<sup>2+</sup>]<sub>i</sub>) is the key signal in glucose-stimulated β-cells governing pulsatile insulin release. The glucose response of mouse β-cells is often manifested as slow oscillations and rapid transients of [Ca<sup>2+</sup>]<sub> i</sub>. In the present study, microfluorometric technique was used to evaluate the role of amino acids, glucagon, ryanodine and caffeine on the generation and maintenance of [Ca<sup>2+</sup>]<sub> i</sub> oscillations and transients in individual murine β-cells and isolated mouse pancreatic isl
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14

Khand, Bishnu. "Studies on differentiation of mouse GS-2 ES-cells to pancreatic β-islet-like cells and their functional maturation status". Thesis, 2018. https://etd.iisc.ac.in/handle/2005/5392.

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Embryonic stem cells (ES-cells) are an excellent source for generating insulin-producing β-islet cells for potential use in the management of diabetes mellitus. Although many protocols have been developed to promote the differentiation of ESCs into β-islet cells, they are limited in terms of (i) low efficiency of differentiation and (ii) generation of functionally immature β-islet cells with inefficient glucose stimulated insulin secretion (GSIS). The present study is aimed at understanding the differentiation and functional maturity of pancreatic β-islet cell. Earlier in our lab EGFP-expressi
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15

Johnson, Justin Sean. "Pdx-1 modulates endoplasmic reticulum calcium homeostasis in the islet β cell via transcriptional enhancement of SERCA2b". Thesis, 2014. http://hdl.handle.net/1805/6455.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>Diabetes mellitus affects an estimated 285 million people worldwide, and a central component of diabetes pathophysiology is diminished pancreatic islet beta cell function resulting in the inability to manage blood glucose effectively. The beta cell is a highly specialized metabolic factory that possesses a number of specialized characteristics, chief among these a highly developed endoplasmic reticulum (ER). The sarco endoplasmic reticulum Ca2+ ATPase 2b (SERCA2b) pump maintains a steep Ca2+ gradient between the cytosol and ER lumen,
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16

"The role of cystic fibrosis transmembrane conductance regulator in insulin secretion in pancreatic islet β-cells". 2013. http://library.cuhk.edu.hk/record=b5549850.

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囊性纖維化（CF）是由囊性纖維化跨膜電導調節器（CFTR）的突變引起的一種隱性遺傳病。CF病人的肺、肝、胰腺、腸道與生殖道受到嚴重影響，其中有50%的成年病人患有糖尿病。由CF引起的糖尿病被稱為CF相關糖尿病（CFRD）, 关于它的病因至今仍然存有爭議。2007年，人們發現CFTR在分泌胰島素的胰島β細胞上有表達。儘管如此，β細胞上的CFTR与糖尿病发病的关系却一直被忽略。我們的研究目標是闡述β細胞上的CFTR在胰島素分泌中的作用。<br>在β細胞上，葡萄糖刺激的胰島素分泌伴隨著複雜的電活動，這種電活動被描述為細胞膜電位去极化疊加的動作電位的爆發。葡萄糖引起的ATP敏感的鉀離子通道（K[subscript Asubscript Tsubscript P]）的關閉被普遍認為是β細胞去極化的初始事件，初始的去極化啟動了電壓依賴的鈣離子通道，由此產生的鈣離子內流成為構成動作電位的去極化電流，引起了細胞內鈣離子的震盪，從而引起胰島素的釋放。雖然氯離子電流被認為參與了β細胞去極化電流，但是，人們仍然不能確定是哪一種氯離子通道介導了這個去極化電流。在我們研究的第一部分，CFTR被證明功能性的表達在β細胞上，並且可以被葡萄糖激活。CFTR可以被葡萄糖激活这一性质，在CFTR超表達的CHO 细胞上被進一步驗證。在原代培養的β細胞與β細胞株RIN-5F细胞中的葡萄糖引起的全細胞電流、膜電位的去極化、
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17

Bansal, Pritpal. "Insulin-induced Suppression of A-type GABA Receptor Signaling in the INS-1 Pancreatic β-cell Line". Thesis, 2010. http://hdl.handle.net/1807/25419.

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GABA and GABA type A receptor (GABAAR) are expressed in pancreatic β-cells and comprise an autocrine signaling system. How the GABA-GABAAR system is regulated is unknown. In this study, I investigated insulin’s effect on this system in the INS-1 β-cell line. I found that GABA evoked current (IGABA) in INS-1 cells, resulting in membrane depolarization. Perforated-patch recordings showed that pre-treatment of insulin or zinc-free insulin suppressed IGABA in INS-1 cells (p < 0.01). Radioimmunossay showed that GABA (30 μM) increased C-peptide secretion from INS-1 cells, which was blocked by GAB
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18

"Protective mechanism(s) of anti-oxidants in pancreatic-islet β-cells against glucose toxicity and oxidative stress". 2011. http://library.cuhk.edu.hk/record=b5896936.

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Poon, Chui Wa Christina.<br>"August 2011."<br>Thesis (M.Phil.)--Chinese University of Hong Kong, 2011.<br>Includes bibliographical references (leaves 123-131).<br>Abstracts in English and Chinese.<br>ABSTRACT --- p.i<br>論文摘要 --- p.vi<br>ACKNOWLEDGEMENTS --- p.ix<br>PUBLICATIONS --- p.x<br>Abstracts --- p.x<br>ABBREVIATIONS --- p.xii<br>Chapter 1. --- GENERAL INTRODUCTION --- p.1<br>Chapter 1.1. --- Diabetes --- p.1<br>Chapter 1.1.1. --- Overview --- p.1<br>Chapter 1.1.2. --- Diagnostic Criteria of Type-2 Diabetes --- p.2<br>Chapter 1.1.3. --- Type-2 Diabetes (T2DM) --- p.3<br>Chapte
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19

Templin, Andrew Thomas. "Mechanisms of translational regulation in the pancreatic β cell stress response". Thesis, 2014. http://hdl.handle.net/1805/6162.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>The islet beta cell is unique in its ability to synthesize and secrete insulin for use in the body. A number of factors including proinflammatory cytokines, free fatty acids, and islet amyloid are known to cause beta cell stress. These factors lead to lipotoxic, inflammatory, and ER stress in the beta cell, contributing to beta cell dysfunction and death, and diabetes. While transcriptional responses to beta cell stress are well appreciated, relatively little is known regarding translational responses in the stressed beta cell. To st
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20

Maganti, Vijaykumar Aarthi. "Mechanisms of transcriptional regulation in the maintenance of β cell function". Thesis, 2015. http://hdl.handle.net/1805/7944.

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Indiana University-Purdue University Indianapolis (IUPUI) Indiana University School of Medicine<br>The islet β cell is central to the maintenance of glucose homeostasis as the β cell is solely responsible for the synthesis of Insulin. Therefore, better understanding of the molecular mechanisms governing β cell function is crucial to designing therapies for diabetes. Pdx1, the master transcription factor of the β cell, is required for the synthesis of proteins that maintain optimal β cell function such as Insulin and glucose transporter type 2. Previous studies showed that Pdx1 interacts with
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21

Benterki, Isma. "Rôles des facteurs de croissance dans la prolifération de la cellule β-pancréatique en réponse à un excès de nutriments : étude du facteur de croissance HB-EGF et du récepteur à l’EGF". Thèse, 2015. http://hdl.handle.net/1866/13131.

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Le diabète de type 2 (DT2) résulte d’une résistance à l’insuline par les tissus périphériques et par un défaut de sécrétion de l’insuline par les cellules β-pancréatiques. Au fil du temps, la compensation des îlots de cellules β pour la résistance à l’insuline échoue et entraine par conséquent une baisse progressive de la fonction des cellules β. Plusieurs facteurs peuvent contribuer à la compensation de la cellule β. Toutefois, la compréhension des mécanismes cellulaires et moléculaires sous-jacents à la compensation de la masse de la cellule β reste à ce jour inconnue. Le but de ce mémoire é
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22

Amyot, Julie. "Rôles du stress du réticulum endoplasmique et de l'immunité innée dans l'inhibition de la transcription du gène de l'insuline : étude du facteur de transcription ATF6 et du récepteur TLR4." Thèse, 2011. http://hdl.handle.net/1866/6961.

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Le diabète de type 2 (DT2) est caractérisé par une résistance des tissus périphériques à l’action de l’insuline et par une insuffisance de la sécrétion d’insuline par les cellules β du pancréas. Différents facteurs tels que le stress du réticulum endoplasmique (RE) et l’immunité innée affectent la fonction de la cellule β-pancréatique. Toutefois, leur implication dans la régulation de la transcription du gène de l’insuline demeure imprécise. Le but de cette thèse était d’identifier et de caractériser le rôle du stress du RE et de l’immunité innée dans la régulation de la transcription du gène
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