Bibliografie tematiche / Insulin signalling

Letteratura scientifica selezionata sul tema "Insulin signalling"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 10 marzo 2023

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Articoli di riviste sul tema "Insulin signalling"

Bevan, Paul. "Insulin signalling". Journal of Cell Science 114, n. 8 (1 gennaio 2001): 1429–30. http://dx.doi.org/10.1242/jcs.114.8.1429.

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Nystrom, Fredrik H., e Michael J. Quon. "Insulin Signalling". Cellular Signalling 11, n. 8 (agosto 1999): 563–74. http://dx.doi.org/10.1016/s0898-6568(99)00025-x.

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Persaud, Shanta J., Dany Muller e Peter M. Jones. "Insulin signalling in islets". Biochemical Society Transactions 36, n. 3 (21 maggio 2008): 290–93. http://dx.doi.org/10.1042/bst0360290.

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Studies in transgenic animals, rodent insulin-secreting cell lines and rodent islets suggest that insulin acts in an autocrine manner to regulate β-cell mass and gene expression. Very little is known about the in vitro roles played by insulin in human islets, and the regulatory role of insulin in protecting against β-cell apoptosis. We have identified mRNAs encoding IRs (insulin receptors) and downstream signalling elements in dissociated human islet β-cells by single-cell RT (reverse transcription)–PCR, and perifusion studies have indicated that insulin does not have an autocrine role to regulate insulin secretion from human islets, but activation of the closely related IGF-1 (insulin-like growth factor 1) receptors is linked to inhibition of insulin secretion. Knockdown of IR mRNA by siRNAs (small interfering RNAs) decreased IR protein expression without affecting IGF-1 receptor levels, and blocked glucose stimulation of preproinsulin gene expression. Similar results were obtained when human islet IRS (IR substrate)-2 was knocked down, whereas depletion of IRS-1 caused an increase in preproinsulin mRNA levels. Studies using the mouse MIN6 β-cell line indicated that glucose protected β-cells from undergoing apoptosis and that this was a consequence, at least in part, of insulin release in response to elevated glucose. IGF-1 also exerted anti-apoptotic effects. These data indicate that insulin can exert autocrine effects in human islets through receptors on β-cells. It protects β-cells against apoptosis and increases preproinsulin mRNA synthesis, but does not affect insulin secretion.

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Heinrichs, Arianne. "PTEN and insulin signalling". Trends in Molecular Medicine 7, n. 5 (maggio 2001): 200. http://dx.doi.org/10.1016/s1471-4914(01)02037-8.

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Lizcano, Jose M., e Dario R. Alessi. "The insulin signalling pathway". Current Biology 12, n. 7 (aprile 2002): R236—R238. http://dx.doi.org/10.1016/s0960-9822(02)00777-7.

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Jiang, G., e B. B. Zhang. "Modulation of insulin signalling by insulin sensitizers". Biochemical Society Transactions 33, n. 2 (1 aprile 2005): 358–61. http://dx.doi.org/10.1042/bst0330358.

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Insulin resistance is a hallmark of Type II diabetes. It is well documented that insulin sensitizers such as peroxisome-proliferator-activated receptor γ agonists and aspirin improve insulin action in vivo. The detailed mechanisms by which the insulin sensitizers promote insulin signalling, however, are not completely understood and remain somewhat controversial. In the present review, we summarize our studies attempting to explore the molecular mechanisms underlying the effects of insulin sensitizers in cells and in animal models of insulin resistance. In 3T3-L1 adipocytes and/or in HEK-293 cells stably expressing recombinant IRS1 protein (insulin receptor substrate protein 1), the peroxisome-proliferator-activated receptor γ agonist rosiglitazone and aspirin promote insulin signalling by decreasing inhibitory IRS1 serine phosphorylation. Increased IRS1 Ser-307 phosphorylation and concomitant decreased insulin signalling as measured by insulin-stimulated IRS1 tyrosine phosphorylation and Akt threonine phosphorylation were observed in adipose tissues of Zucker obese rats compared with lean control rats. Treatment with rosiglitazone for 24 and 48 h increased insulin signalling and decreased IRS1 Ser-307 phosphorylation concomitantly. Treatment of the Zucker obese rats with rosiglitazone for 24 h also reversed the high circulating levels of free fatty acids, which have been shown to correlate with increased IRS1 serine phosphorylation. Taken together, the results suggest that IRS1 inhibitory serine phosphorylation is a key component of insulin resistance and its reversal may be physiologically relevant to insulin sensitization in vivo.

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Pathak, Himani, e Jishy Varghese. "Edem1 activity in the fat body regulates insulin signalling and metabolic homeostasis in Drosophila". Life Science Alliance 4, n. 8 (17 giugno 2021): e202101079. http://dx.doi.org/10.26508/lsa.202101079.

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In Drosophila, nutrient status is sensed by the fat body, a functional homolog of mammalian liver and white adipocytes. The fat body conveys nutrient information to insulin-producing cells through humoral factors which regulate Drosophila insulin-like peptide levels and insulin signalling. Insulin signalling has pleiotropic functions, which include the management of growth and metabolic pathways. Here, we report that Edem1 (endoplasmic reticulum degradation–enhancing α-mannosidase–like protein 1), an endoplasmic reticulum–resident protein involved in protein quality control, acts in the fat body to regulate insulin signalling and thereby the metabolic status in Drosophila. Edem1 limits the fat body–derived Drosophila tumor necrosis factor-α Eiger activity on insulin-producing cells and maintains systemic insulin signalling in fed conditions. During food deprivation, edem1 gene expression levels drop, which aids in the reduction of systemic insulin signalling crucial for survival. Overall, we demonstrate that Edem1 plays a vital role in helping the organism to endure a fluctuating nutrient environment by managing insulin signalling and metabolic homeostasis.

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Villalobos-Labra, Roberto, Luis Silva, Mario Subiabre, Joaquín Araos, Rocío Salsoso, Bárbara Fuenzalida, Tamara Sáez et al. "Akt/mTOR Role in Human Foetoplacental Vascular Insulin Resistance in Diseases of Pregnancy". Journal of Diabetes Research 2017 (2017): 1–13. http://dx.doi.org/10.1155/2017/5947859.

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Insulin resistance is characteristic of pregnancies where the mother shows metabolic alterations, such as preeclampsia (PE) and gestational diabetes mellitus (GDM), or abnormal maternal conditions such as pregestational maternal obesity (PGMO). Insulin signalling includes activation of insulin receptor substrates 1 and 2 (IRS1/2) as well as Src homology 2 domain-containing transforming protein 1, leading to activation of 44 and 42 kDa mitogen-activated protein kinases and protein kinase B/Akt (Akt) signalling cascades in the human foetoplacental vasculature. PE, GDM, and PGMO are abnormal conditions coursing with reduced insulin signalling, but the possibility of the involvement of similar cell signalling mechanisms is not addressed. This review aimed to determine whether reduced insulin signalling in PE, GDM, and PGMO shares a common mechanism in the human foetoplacental vasculature. Insulin resistance in these pathological conditions results from reduced Akt activation mainly due to inhibition of IRS1/2, likely due to the increased activity of the mammalian target of rapamycin (mTOR) resulting from lower activity of adenosine monophosphate kinase. Thus, a defective signalling via Akt/mTOR in response to insulin is a central and common mechanism of insulin resistance in these diseases of pregnancy. In this review, we summarise the cell signalling mechanisms behind the insulin resistance state in PE, GDM, and PGMO focused in the Akt/mTOR signalling pathway in the human foetoplacental endothelium.

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Bertrand, L., S. Horman, C. Beauloye e J. L. Vanoverschelde. "Insulin signalling in the heart". Cardiovascular Research 79, n. 2 (30 aprile 2008): 238–48. http://dx.doi.org/10.1093/cvr/cvn093.

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Levy, Jonathan C. "Insulin signalling through ultradian oscillations". Growth Hormone & IGF Research 11 (giugno 2001): S17—S23. http://dx.doi.org/10.1016/s1096-6374(01)80004-6.

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Tesi sul tema "Insulin signalling"

Philippeos, Christina. "Insulin signalling in endothelial cells". Thesis, King's College London (University of London), 2014. http://kclpure.kcl.ac.uk/portal/en/theses/insulin-signalling-in-endothelial-cells(8e35db48-dc9c-41be-b1aa-1fbe241fc356).html.

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Insulin is known to act as an anti-inflammatory agent and protect vascular endothelial cells during ischaemic damage in vivo. Although it is known that insulin signals in part through phosphatidylinositol 3-kinases (PI3Ks) and Akt, its effects on endothelial junctions and actin cytoskeleton are unknown. This study aimed to characterise endothelial responses to insulin, identify endothelial insulin-‐induced changes in protein phosphorylation and determine the roles of these changes in regulating endothelial functions. Insulin stimulation induced dose-dependent Akt activation in both primary human umbilical vein endothelial cells (HUVECs) and an endothelial cell line, human bone-marrow endothelial cells (HBMECs). Insulin decreased basal HUVEC permeability, increased angiogenic loop formation in vitro and increased cell migration in a wound-healing model, compared to untreated cells. Insulin-stimulated changes in protein phosphorylation were identified using a 14-3-3 affinity purification proteomic screen, as 14-3-3 proteins interact specifically with phosphorylated Ser/Thr residues within 14-3-3-binding motifs. A total of 390 14-3-3-binding proteins were identified from insulin-stimulated HBMECs, from which 12 proteins were selected based on predicted roles in endothelial cytoskeleton regulation. Validation of these hits, performed by Far-Western overlay analysis, identified 4 IGF-I-regulated 14-3-3-binding proteins: Parg1 (ARHGAP29), RICH-1 (ARHGAP17), LMO7 and Epsin2. Parg1 depletion in HUVECs induced stress fibre formation, increased endothelial permeability, severely decreased angiogenic loop formation and decreased cell migration, compared to siRNA control-treated cells. This suggests that Parg1 regulates contractility and hence could affect endothelial cell-cell junctional stability. Depletion of RICH-1 and LMO7 in HUVECs resulted in mislocalisation of the tight junction protein ZO-1. However, this did not affect endothelial permeability, suggesting that these proteins are important for maintaining tight junction integrity. LMO7 and Epsin2 depletion each resulted in an increase in angiogenic loop formation, but did not detectably affect cell migration. Insulin stimulation of Epsin2 might increase lamellipodium formation, although further studies are required to establish the mechanisms involved. In conclusion, this thesis describes a 14-3-3-based proteomic screen that identified novel regulators of endothelial function. These proteins could contribute to the anti-inflammatory roles of insulin.

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Joharatnam, Jalini. "Insulin signalling in granulosa cells". Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9784.

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Polycystic ovary syndrome (PCOS) is characterised by hyperandrogenism and insulin resistance. Granulosa cells in PCOS demonstrate impaired insulin-induced glucose uptake and lactate accumulation, suggesting a post receptor, signalling pathway-specific impairment of insulin action. Gonadotrophins are also important in the regulation of glucose metabolism by of granulosa cells. The first objective of this project was to use KK1 cells an immortalised mouse granulosa cell line, to characterise insulin, androgen and FSH signalling as well as glucose metabolism. Cell lysates were subjected to western immunoblotting for key proteins in the insulin signalling pathways. Glucose metabolism of KK1 cells was also measured. Surprisingly, androgen alone stimulated glucose uptake and lactate production and augmented insulin-induced glucose metabolism. This suggests that the insulin resistance observed in granulosa cells from women with PCOS is not a direct effect of exposure to androgen. The main part of the thesis was examination of insulin action on human primary ovarian granulosa-lutein (GL) cells to investigate the mechanism of insulin resistance in PCOS. Insulin and FSH signalling in GL cells from women with anovulatory PCOS (anovPCO, n=11) was compared to that in GL cells from ovulatory women with (ovPCO, n=8) and without polycystic ovaries (controls n=12). Primary GL cells were incubated with insulin or FSH and analysed for glucose metabolism and progesterone production. Cell lysates were prepared for identification of signalling pathways, using western immunoblotting. The results confirmed selective impairment of glucose metabolism in cells from anovulatory PCOS. No significant impairment of insulin stimulated PI3K signalling was observed. However there was a reduction of p42/44ERK phosphorylation in the ovulatory PCOS group compared to controls. The significance of this finding with respect to impaired glucose metabolism in granulosa cells remains to be determined. We also showed FSH induced glucose metabolism, but without clear evidence of activation of the PI3-kinase pathway.

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Collison, Mary Williamson. "Insulin signalling in insulin resistance and cardiovascular disease syndromes". Thesis, University of Glasgow, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366184.

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Alves, Steven Ribeiro. "The relevence of insulin signalling in Alzheimer's disease". Master's thesis, Universidade de Aveiro, 2017. http://hdl.handle.net/10773/22020.

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Mestrado em Biologia Molecular e Celular
Alzheimer’s disease (AD) is the most common type of dementia worldwide. It is molecularly characterized by deposition of extracellular senile plaques (SPs) composed by aggregated amyloid beta (Aβ) peptide, the formation of neurofibrillary tangles (NFTs) derived from hyperphosphorylation of the microtubule-associated protein Tau, synaptic dysfunction due to the deposits of SPs and NFTs and oxidative stress induced by impaired metabolic pathways. The insulin signalling pathway can play a major role in diverse AD related pathways, such as APP cleavage, Tau hyperphosphorylation, Apolipoprotein E (ApoE) influence in insulin signalling efficiency and the insulin degrading enzyme, which is also the major Aβ degrading enzyme. Growing evidence links AD with type 2 diabetes (T2D) due to impaired insulin signalling (IS) and brain insulin resistance. In a cohort based study in the Aveiro region, a correlation between diabetes and poor cognitive scores in the Mini Mental State Examination (MMSE) test were observed, with a p-value of 0.072. Additionally, carriers of the allele ApoE-ɛ2 appeared to be protective against diabetes, in the literature the same allele appears to be protective for AD. Posteriorly, the analysis of protein interactions, via the development of interactome networks, identified several proteins involved in both AD and the IS pathways. Also, by correlating these pathways with the synapse proteome, a very high overlap was observed (88% for AD, 79% for IS and 96% for AD and IS coincident proteins), enforcing the importance of both pathways in synaptic signalling and plasticity. From gene ontology studies, it was possible to assess the principal biological processes and molecular functions of the dataset of proteins. For AD, response to stimulus, cellular component organization, cell communication, signalling, protein binding, receptor binding and kinase binding were categories with elevated representation. Regarding coincident proteins between AD and IS pathways, an increase in all categories was observed, meaning that insulin plays a pivotal role in many AD events. Finally, the analysis of SH-SY5Y differentiated cells treated with 0, 1, 10 and 100 nM of insulin for 0, 10 and 60 minutes, showed a decrease on the intracellular total levels of protein Tau and an increase in the phosphorylation at serine 396. Regarding the amyloid precursor protein (APP), increases in intracellular levels were observed, when treated with insulin for 10 minutes, followed by a decrease for 60 minutes exposure. The phosphorylation of APP at threonine 668, has previously been related to increased production of Aβ, by promoting APP cleavage via the amyloidogenic pathway. In cells treated with insulin, a clear increase was detected at the 10-minute time point. At 60 minutes, the levels of phosphorylation were low probably due to low total APP levels.
A doença de Alzheimer (DA) é o tipo mais comum de demência no mundo. É caracterizada molecularmente pela deposição extracelular de placas senis (PS) compostas por agregados do péptido amiloide beta (Aβ), pela formação de emaranhados neurofibrilares (EN) derivados da hiperfosforilação da proteína Tau, pela disfunção sináptica devido aos depósitos de PS e EN e também pelo stress oxidativo induzido pelo enfraquecimento das vias metabólicas. A via de sinalização da insulina desempenha um papel principal em diversas vias da DA, tal como na clivagem da APP, hiperfosforilação da proteína Tau, eficiência da sinalização da insulina influenciada pela Apolipoproteína E (ApoE) e pela enzima envolvida na degradação de insulina que também é a enzima principal na degradação de Aβ. Crescente evidência relaciona a DA com a diabetes de tipo 2 (T2D) devido ao mau funcionamento da sinalização pela insulina e da resistência cerebral à mesma. Num estudo baseado num cohort da região de Aveiro, foi observada uma correlação entre a diabetes e um mau resultado no teste do ‘Mini Mental State Examination’. Adicionalmente, também foi observada uma correlação entre os portadores do alelo ApoE-ɛ2 e um estado protetor contra a T2D. Este alelo também foi observado na literatura como sendo protetor contra a DA. Posteriormente, uma análise de interações entre proteínas, identificou várias proteínas envolvidas tanto na DA como na sinalização da insulina. Correlacionando estes dados com o proteoma da sinapse, foi possível observar que existe uma grande representação das duas condições e também das proteínas coincidentes às duas (88% para a DA, 79% para a sinalização da insulina e 96% para as proteínas relacionadas com ambas), reforçando o papel de ambas as vias na sinalização e plasticidade sináptica. Do estudo de ontologia genética para a DA, foi possível identificar diversas vias importantes, tais como, resposta a um estímulo, organização de componentes celulares, comunicação celular, ligação proteica e ligação a uma cinase. Em relação à sinalização da insulina, as mesmas categorias apareciam com maior representação, significando que a insulina tem um papel importante em muitos eventos da DA. Por fim, o tratamento de SH-SY5Y diferenciadas com 0, 1, 10 e 100 nM de insulina por 0, 10 e 60 minutos mostraram uma diminuição nos níveis intracelulares da proteína Tau e um aumento na sua fosforilação na serina 396. Em relação à proteína percursora amiloide (APP), o tratamento de insulina levou a um aumento nos níveis intracelulares, quando exposta por 10 minutos seguido por uma diminuição aos 60 minutos. Quanto à fosforilação da treonina 668 da APP, foi previamente demonstrado que um aumento na fosforilação desse resíduo, promove a clivagem pela via amiloidogénica, levando à produção de Aβ. Nas células tratadas com insulina, um aumento claro da fosforilação desse resíduo da APP foi observado aos 10 minutos. Aos 60 minutos, os níveis da fosforilação eram baixos provavelmente devido aos baixos níveis de APP total.

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Ng, Foong Loo Yvonne Biotechnology &amp Biomolecular Sciences Faculty of Science UNSW. "Insulin action: unravelling AKT signalling in Adipocytes". Awarded by:University of New South Wales. Biotechnology & Biomolecular Sciences, 2009. http://handle.unsw.edu.au/1959.4/44628.

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The Ser/Thr kinase Akt plays an important role in many of insulin's actions including GLUT4 translocation to the plasma membrane (PM). However, there are several features of Akt's regulation of GLUT4 translocation that remain unclear. The goal of my thesis was to resolve some of the following questions: Is activation of Akt sufficient to stimulate GLUT4 translocation? What is the quantitative relationship in signal transmission between individual components within the Akt cascade? What is the role of Akt in insulin resistance? To determine if activation of Akt is sufficient to mediate GLUT4 translocation, I developed a drug-inducible heterodimerisation strategy to activate Akt2 independently of other potential insulin signalling pathways. These studies revealed that activation of Akt2 resulted in rapid stimulation of GLUT4 translocation to a similar extent with maximum insulin, indicating that Akt2 is sufficient for this event. It was previously observed that maximum effect of insulin on GLUT4 translocation was obtained with minimum activation of Akt. To resolve this discrepancy, the relationship between Akt signalling components was examined using a quantitative kinetic and dose response approach combined with hierarchical cluster analysis. Most notably I observed a strong relationship between Akt at the PM, but not Akt in the whole cell lysate, with its substrate phosphorylation. Active pools of phospho-Akt and -AS160, a major substrate involved in GLUT4 translocation, were found in the lipid raft, highlighting the importance of subcellular partitioning of key signalling components for achieving biological specificity. The involvement of Akt in insulin resistance was investigated using the heterodimerisation strategy. These studies revealed that insulin itself initiates a pathway that causes insulin resistance by converging on target(s) downstream of Akt. This inhibitory pathway emanates from PI3-kinase and is likely induced by a range of insults including chronic insulin and dexamethasone. In conclusion, Akt is a crucial element in the insulin action pathway that exhibits precise spatial regulation. While the role of this nanoregulation of Akt in disease remains to be evaluated, my studies suggest that the major defect contributing to insulin resistance occurs downstream of Akt. The elucidation of this target will have major implications for metabolic diseases.

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Bray, Jonathan Alexander. "Comparing insulin and insulin-like growth factor-1 signalling in myoblasts". Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596876.

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In this study a chimeric receptor system was employed in which the extracellular domain of the TrkC receptor was fused to the intracellular portion of either the insulin (TIR) or IGF-1 (TIGFR) receptor. These chimeric receptors were expressed in separate populations of the skeletal muscle cell line L6. Initial analysis of individual downstream signalling components and assessment of cell proliferation, induced by TIR or TIGFR stimulation revealed little difference between the two chimeras. To more comprehensively screen for potential differences, microarray analysis was used to compare regulation of gene expression by the two chimeric receptors. This led to the identification of several differentially regulated genes. Whilst it was initially hypothesised that skeletal muscle cells might yield several selectively insulin-sensitive genes, the majority of genes selectively regulated by one receptor were preferentially IGF-1 responsive, consistent with previous studies in other cell types. This perhaps reflects the more mitogenic effect of this ligand in vivo, manifest as an increased ability to regulate transcription per se. Of the differentially regulated genes, that encoding Fit-1m was found to be preferentially induced through activation of the TIGFR rather than the TIR. Further characterisation using real-time PCR established that induction of Fit-1 expression required an intact MAPK signalling pathway. Similar effects were observed when the regulation of Fit-1 expression by insulin and IGF-1 was examined. Subsequent work attempted to establish regions of promoter responsible for the preferential induction of Fit-1m expression by IGF-1. Despite defining promoter and putative enhancer regions which are important for Fit-1m transcription, no region was found which confers a response to stimulation with various ligands, including IGF-1. Rather, a high level of constitutive expression was driven by these DNA sequences, suggesting that an IGF-1 response inhibitory factor may control expression of this gene, binding outside the regions examined. Fit-1 joins an increasing list of genes preferentially regulated by the IGF-1R over the IR and provides and end point with which to analyse potential inherent differences in the signalling capacity of these two highly homologous receptors.

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Mercer, Ben N. "Does altered insulin signalling modulate vascular regeneration?" Thesis, University of Leeds, 2014. http://etheses.whiterose.ac.uk/7069/.

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The prevalence of insulin resistant syndromes is rising worldwide. Affected individuals are at increased risk of morbidity and premature mortality, much of which is driven by cardiovascular disease (CVD). Enhancement of vascular regeneration, using pharmacological or cell-based therapies, has been suggested as a strategy to help address these issues. Although many pathophysiological processes associated with insulin resistant syndromes are likely to impair vascular regeneration, the effect of insulin resistance per se is not established. South Asian (SA) ethnicity is associated with increased risk of CVD, and insulin resistance is thought to be a major contributor to this. We compared the angiogenic capacity of late outgrowth endothelial progenitor cells (LEPCs) from young SA men, with those from a matched group white European (WE) men. LEPC have previously been shown to offer potential as an autologous cell therapy in preclinical models of ischaemic CVD. Both groups were well matched, and free of classical cardiovascular risk factors, but the SA group were relatively insulin resistant. SA LEPCs did not augment vascular regeneration in a murine model of limb ischaemia, in contrast with WE LEPC. Akt activity, a critical modulator of angiogenesis, was reduced in SA LEPC, and we were able to rescue SA LEPC dysfunction by enhancing Akt activity. We then established the impact of insulin resistance per se on vascular regeneration, using insulin receptor haploinsufficient mice (IRKO). Indices of angiogenesis were reduced in isolated endothelial cells, aortic ring 5 segments, and ischaemic hind limb muscle. Moreover, this was associated with functional resistance to vascular endothelial growth factor (VEGF), which may have mechanistically contributed to our observations. Together, these data provide insight into how insulin resistance may promote the development of premature CVD, and show that by manipulating key growth factor signalling nodes, we can rescue impaired vascular regeneration. Furthermore, we have established that insulin resistance negatively impacts on the functional response to VEGF, and it will be important to explore the mechanisms underlying this phenomenon in future studies. It is hoped that these findings will help lead to the development of strategies to mitigate the effects of CVD in individuals with insulin resistance.

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Musial, Barbara. "Regulation of insulin signalling during mouse pregnancy". Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708844.

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Wuttke, Anne. "Lipid Signalling Dynamics in Insulin-secreting β-cells". Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-198046.

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Certain membrane lipids are involved in intracellular signalling processes, among them phosphoinositides and diacylglycerol (DAG). They mediate a variety of functions, including the effects of nutrients and neurohormonal stimuli on insulin secretion from pancreatic β-cells. To ensure specificity of the signal, their concentrations are maintained under tight spatial and temporal control. Here, live-cell imaging techniques were employed to investigate spatio-temporal aspects of lipid signalling in the plasma membrane of insulin-secreting β-cells. The concentration of phosphatidylinositol 4-phosphate [PtdIns(4)P] increased after stimulation with glucose or Gq protein-coupled receptor agonists. The glucose effect was Ca2+-dependent, whereas the receptor response was mediated by isoforms of novel protein kinase C (PKC). The increases in PtdIns(4)P were paralleled by lowerings of the phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] concentration. This relationship was not caused by conversion of PtdIns(4,5)P2 to PtdIns(4)P but rather reflected independent regulation of the two lipids. Stimulation of β-cells with glucose or a high K+ concentration induced pronounced, repetitive increases in plasma-membrane DAG concentration, which were locally restricted and lasted only for a few seconds. This pattern was caused by exocytotic release of ATP, which feedback-activates purinergic P2Y1-receptors and stimulates local phospholipase C-mediated DAG generation. Despite their short durations the DAG spikes triggered local activation of PKC. Novel PKCs were recruited to the plasma membrane both after glucose and muscarinic receptor stimulation. While the glucose-induced translocation was synchronized with DAG spiking, muscarinic stimulation induced sustained elevation of the DAG concentration and stable membrane association of the kinase. Also conventional PKCs translocated to the membrane after glucose and receptor stimulation. The glucose-induced response was complex with sustained membrane association mirroring the cytoplasmic Ca2+ concentration, and superimposed brief recurring translocations caused by DAG. Interruption of the purinergic feedback loop underlying DAG spiking suppressed insulin secretion. Since the DAG spikes reflected exocytosis events, a single-cell secretion assay was established, which allowed continuous recording of secretion dynamics from many cells in parallel over extended periods of time. With this approach it was possible to demonstrate that insulin exerts negative feedback on its own release via a phosphatidylinositol 3,4,5-trisphosphate-dependent mechanism.

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Wiggins, Emma Louise. "Regulation of myogenesis by IGF- and insulin-signalling". Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608747.

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Libri sul tema "Insulin signalling"

Au, Crystal Suet Ying. Modulation of insulin signalling molecules and hepatic lipoprotein production. Ottawa: National Library of Canada, 2003.

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Yang, Shen-Hsui. Insulin signalling pathways involved in selective control of hepatic gene expression. Manchester: University of Manchester, 1995.

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Belbrahem, Atika. Characterisation of protein Kinase C in chick embryo tissues and hepatocytes: Role in insulin signalling. Manchester: University of Manchester, 1994.

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Vafopoulou, Xanthe, e Colin G. H. Steel, a cura di. The Coming of Age of Insulin-Signalling in Insects. Frontiers SA Media, 2015. http://dx.doi.org/10.3389/978-2-88919-314-1.

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(Editor), Derek LeRoith, Walter Zumkeller (Editor) e Robert C. Baxter (Editor), a cura di. Insulin-like Growth Factor Receptor Signalling (Molecular Biology Intelligence Unit). Springer, 2003.

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Patel, Nish. Insulin-induced actin remodelling and the localization of signalling molecules. 2006.

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Function of receptor tyrosine kinases in Gi-deficient cells: Preferential suppression of insulin signalling. Ottawa: National Library of Canada, 2000.

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Capitoli di libri sul tema "Insulin signalling"

Hollenberg, M. D. "Insulin Receptor-Mediated Transmembrane Signalling". In Insulin, 183–207. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5_10.

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Guglielmo, Gianni M. Di, Paul G. Drake, Patricia C. Baass, François Authier, Barry I. Posner e John J. M. Bergeron. "Insulin receptor internalization and signalling". In Insulin Action, 59–63. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5647-3_6.

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Siddle, Ken. "The Insulin Receptor and Downstream Signalling". In Insulin Resistance, 1–62. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470011327.ch1.

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Ogawa, Wataru, Takashi Matozaki e Masato Kasuga. "Role of binding proteins to IRS-1 in insulin signalling". In Insulin Action, 13–22. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5647-3_2.

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Goldstein, Barry J., Faiyaz Ahmad, Wendi Ding, Pei-Ming Li e Wei-Ren Zhang. "Regulation of the insulin signalling pathway by cellular protein-tyrosine phosphatases". In Insulin Action, 91–99. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5647-3_10.

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White, Morris F. "The IRS-signalling system: A network of docking proteins that mediate insulin action". In Insulin Action, 3–11. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5647-3_1.

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Khadka, Deegendra. "Ameliorating Insulin Signalling Pathway by Phytotherapy". In Ethnopharmacology of Wild Plants, 317–42. First edition. | Boca Raton : CRC Press, 2021.: CRC Press, 2021. http://dx.doi.org/10.1201/9781003052814-17.

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Liu, Feng, e Richard A. Roth. "Binding of SH2 containing proteins to the insulin receptor: A new way for modulating insulin signalling". In Insulin Action, 73–78. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5647-3_8.

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An, Seon Woo A., Murat Artan, Sangsoon Park, Ozlem Altintas e Seung-Jae V. Lee. "Longevity Regulation by Insulin/IGF-1 Signalling". In Healthy Ageing and Longevity, 63–81. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-44703-2_4.

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Varela, Isabel, Jose F. Alvarez, Jose Puerta, Rosa Clemente, Ana Guadaño, Matias Avila, Francisco Estevez, Susana Alemany e Jose M. Mato. "Role of Glycosyl-Phosphatidylinositols in Insulin Signalling". In Activation and Desensitization of Transducing Pathways, 167–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83618-3_10.

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Atti di convegni sul tema "Insulin signalling"

Vlahos, R., C. Mastronardo, H. J. Seow e S. M. Chan. "Apocynin Opposes Oxidative Stress-Induced Atrophy by Preserving Insulin Like Growth Factor (IGF)-1 Signalling in C2C12 Myotubes". In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2376.

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Dodd, MS, Mdl Sousa Fialho, CN Montes Aparico, M. Kerr, KN Timm, JL Griffin, JJFP Luiken, JFC Glatz, DJ Tyler e LC Heather. "P27 Depletion of cardiac succinate mediates impaired hypoxia-inducible factor 1Α signalling by long chain fatty acids in insulin resistance". In British Society for Cardiovascular Research, Autumn Meeting 2017 ‘Cardiac Metabolic Disorders and Mitochondrial Dysfunction’, 11–12 September 2017, University of Oxford. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bscr.32.

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Erlandsson, M., M. Nadali, S. Silfverswärd Töyrä, MN Svensson, I.-M. Jonsson, KM Andersson e MI Bokarewa. "SAT0026 Signalling through insulin-like growth factor 1 receptor contributes to il-6 production and supports t cell dependent inflammation in rheumatoid arthritis". In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.6191.

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Rapporti di organizzazioni sul tema "Insulin signalling"

Lekhanya, Portia Keabetswe, e Kabelo Mokgalaboni. Exploring the effectiveness of vitamin B12 complex and alpha-lipoic acid as a treatment for diabetic neuropathy. Protocol for systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, maggio 2022. http://dx.doi.org/10.37766/inplasy2022.5.0167.

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Abstract (sommario):

Review question / Objective: Does Alpha-Lipoic acid increase the uptake of glucose for better glycaemic control? Does vitamin B12 and Alpha-Lipoic acid improve inflammation? The aim of the study is to explore the effectiveness of Vitamin B12 and Alpha-Lipoic Acid as a possible treatment for diabetic neuropathy with major emphasis on markers of inflammation and glucose metabolism. Condition being studied: Diabetic Neuropathy (DN) is a heterogeneous type of nerve damage associated with diabetes mellitus, the condition most often damages nerves in the legs and feet. It presents both clinically and sub-clinically affecting the peripheral nervous system as a result of an increase in glucose concentration which interferes with nerve signalling. After the discovery of insulin as a treatment for Diabetes Mellitus (DM), the prevalence of DN has since increased significantly due to DM patients having a longer life expectancy. It has been estimated that atleast 50% of DM patients will develop DN in their life, with approximately 20% of these patients experiencing neuropathic pain. Nerves are susceptible to changes in glucose concentrations and insulin makes it impossible for neurons to continue regulating glucose uptake.

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