Relevant bibliographies by topics / Insuling signalling

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Insuling signalling'

Author: Grafiati
Published: 19 February 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Insuling signalling.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Insuling signalling"

1

Bevan, Paul. "Insulin signalling." Journal of Cell Science 114, no. 8 (January 1, 2001): 1429–30. http://dx.doi.org/10.1242/jcs.114.8.1429.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Nystrom, Fredrik H., and Michael J. Quon. "Insulin Signalling." Cellular Signalling 11, no. 8 (August 1999): 563–74. http://dx.doi.org/10.1016/s0898-6568(99)00025-x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

SHEPHERD, Peter R., Dominic J. WITHERS, and Kenneth SIDDLE. "Phosphoinositide 3-kinase: the key switch mechanism in insulin signalling." Biochemical Journal 333, no. 3 (August 1, 1998): 471–90. http://dx.doi.org/10.1042/bj3330471.

Full text
Abstract:
Insulin plays a key role in regulating a wide range of cellular processes. However, until recently little was known about the signalling pathways that are involved in linking the insulin receptor with downstream responses. It is now apparent that the activation of class 1a phosphoinositide 3-kinase (PI 3-kinase) is necessary and in some cases sufficient to elicit many of insulin's effects on glucose and lipid metabolism. The lipid products of PI 3-kinase act as both membrane anchors and allosteric regulators, serving to localize and activate downstream enzymes and their protein substrates. One of the major ways these lipid products of PI 3-kinase act in insulin signalling is by binding to pleckstrin homology (PH) domains of phosphoinositide-dependent protein kinase (PDK) and protein kinase B (PKB) and in the process regulating the phosphorylation of PKB by PDK. Using mechanisms such as this, PI 3-kinase is able to act as a molecular switch to regulate the activity of serine/threonine-specific kinase cascades important in mediating insulin's effects on endpoint responses.
APA, Harvard, Vancouver, ISO, and other styles
4

Persaud, Shanta J., Dany Muller, and Peter M. Jones. "Insulin signalling in islets." Biochemical Society Transactions 36, no. 3 (May 21, 2008): 290–93. http://dx.doi.org/10.1042/bst0360290.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
5

Pathak, Himani, and Jishy Varghese. "Edem1 activity in the fat body regulates insulin signalling and metabolic homeostasis in Drosophila." Life Science Alliance 4, no. 8 (June 17, 2021): e202101079. http://dx.doi.org/10.26508/lsa.202101079.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
6

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
7

Heinrichs, Arianne. "PTEN and insulin signalling." Trends in Molecular Medicine 7, no. 5 (May 2001): 200. http://dx.doi.org/10.1016/s1471-4914(01)02037-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Lizcano, Jose M., and Dario R. Alessi. "The insulin signalling pathway." Current Biology 12, no. 7 (April 2002): R236—R238. http://dx.doi.org/10.1016/s0960-9822(02)00777-7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Buren, J., HX Liu, J. Lauritz, and JW Eriksson. "High glucose and insulin in combination cause insulin receptor substrate-1 and -2 depletion and protein kinase B desensitisation in primary cultured rat adipocytes: possible implications for insulin resistance in type 2 diabetes." European Journal of Endocrinology 148, no. 1 (January 1, 2003): 157–67. http://dx.doi.org/10.1530/eje.0.1480157.

Full text
Abstract:
OBJECTIVE: The purpose of this study was to investigate the cellular effects of long-term exposure to high insulin and glucose levels on glucose transport and insulin signalling proteins. DESIGN AND METHODS: Rat adipocytes were cultured for 24 h in different glucose concentrations with 10(4) microU/ml of insulin or without insulin. After washing, (125)I-insulin binding, basal and acutely insulin-stimulated d-[(14)C]glucose uptake, and insulin signalling proteins and glucose transporter 4 (GLUT4) were assessed. RESULTS: High glucose (15 and 25 mmol/l) for 24 h induced a decrease in basal and insulin-stimulated glucose uptake compared with control cells incubated in low glucose (5 or 10 mmol/l). Twenty-four hours of insulin treatment decreased insulin binding capacity by approximately 40%, and shifted the dose-response curve for insulin's acute effect on glucose uptake 2- to 3-fold to the right. Twenty-four hours of insulin treatment reduced basal and insulin-stimulated glucose uptake only in the presence of high glucose (by approximately 30-50%). At high glucose, insulin receptor substrate-1 (IRS-1) expression was downregulated by approximately 20-50%, whereas IRS-2 was strongly upregulated by glucose levels of 10 mmol/l or more (by 100-400%). Insulin treatment amplified the suppression of IRS-1 when combined with high glucose and also IRS-2 expression was almost abolished. Twenty-four hours of treatment with high glucose or insulin, alone or in combination, shifted the dose-response curve for insulin's effect to acutely phosphorylate protein kinase B (PKB) to the right. Fifteen mmol/l glucose increased GLUT4 in cellular membranes (by approximately 140%) compared with 5 mmol/l but this was prevented by a high insulin concentration. CONCLUSIONS: Long-term exposure to high glucose per se decreases IRS-1 but increases IRS-2 content in rat adipocytes and it impairs glucose transport capacity. Treatment with high insulin downregulates insulin binding capacity and, when combined with high glucose, it produces a marked depletion of IRS-1 and -2 content together with an impaired sensitivity to insulin stimulation of PKB activity. These mechanisms may potentially contribute to insulin resistance in type 2 diabetes.
APA, Harvard, Vancouver, ISO, and other styles
10

Bergantin, Leandro B. "A Link Between Brain Insulin Resistance and Cognitive Dysfunctions: Targeting Ca2+/cAMP Signalling." Central Nervous System Agents in Medicinal Chemistry 20, no. 2 (September 29, 2020): 103–9. http://dx.doi.org/10.2174/1871524920666200129121232.

Full text
Abstract:
Background: A correlation between cognitive dysfunctions and brain insulin resistance has been established by several clinical and experimental studies. Consistent data support that people diagnosed with brain insulin resistance, resulted from diabetes, have shown an increased risk of presenting cognitive dysfunctions, clinical signs of dementia and depression, then speculating a role of dysregulations related to insulin signalling in these diseases. Furthermore, it is currently discussed that Ca2+ signalling, and its dysregulations, may be a factor which could correlate with brain insulin resistance and cognitive dysfunctions. Objective: Following this, revealing this interplay between these diseases may provide novel insights into the pathogenesis of such diseases. Methods: Publications covering topics such as Ca2+ signalling, diabetes, depression and dementia (alone or combined) were collected by searching PubMed and EMBASE. Results: The controlling of both neurotransmitters/hormones release and neuronal death could be achieved through modulating Ca2+ and cAMP signalling pathways (Ca2+/cAMP signalling). Conclusion: Taking into account our previous reports on Ca2+/cAMP signalling, and considering a limited discussion in the literature on the role of Ca2+/cAMP signalling in the link between cognitive dysfunctions and brain insulin resistance, this article has comprehensively discussed the role of these signalling pathways in this link (between cognitive dysfunctions and brain insulin resistance).
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Insuling signalling"

1

Nield, Alex. "The role of Zinc Transporters in modulating Insulin signalling." Thesis, Federation University Australia, 2015. http://researchonline.federation.edu.au/vital/access/HandleResolver/1959.17/99999.

Full text
Abstract:
Zinc is a cell impermeable transition metal with a large number of biological functions, and is an essential component of the insulin signalling pathway. Cellular free zinc increases insulin sensitivity though it is also toxic at high levels, making it essential for cells to tightly regulate bioavailable levels. This homeostasis is maintained by three groups of proteins known as Zips, ZnTs and metallothioneins (MTs). Zips and ZnTs are zinc transporters with Zips increasing cytosolic zinc by pumping it outside the cell or from organelle stores, while the ZnTs decrease cytosolic zinc. The MTs bind to free zinc in the cytosol, reducing its bioavailability. The rapid release of zinc mediated by these proteins has been implicated as a mechanism of signal pathway activation, through zinc activating and deactivating various signalling proteins. This thesis investigated one zinc transporter in particular, known as Zip7. Zip7 is a novel Zip transporter localised to the endoplasmic reticulum and has been implicated in cell signalling in breast cancer cells through release of zinc from cellular stores in response to extracellular stimuli. The aim of this thesis was to investigate the potential role of this zinc transporter in modulating the insulin signalling pathway. The human Zip7 protein sequence was analysed using various bioinformatics tools to identify regions that may contribute to the proposed novel function of this transporter. The loop regions of Zip7 were found to be poorly conserved between species with the exception of histidine rich regions, which showed a high level of conservation when compared to a diverse series of species and so are suspected to have an essential role in modulating the transport function of Zip7 by binding to zinc. These findings implicate histidine residues as an important functional component of Zip7. In order to identify whether Zip7 expression is essential for a normal insulin response, Zip7 mRNA was reduced via transfection of siRNA in mouse skeletal muscle cells and measurement of markers of insulin signalling. When Zip7 expression was reduced there was a subsequent decrease in the expression of several markers of insulin signalling including Glut4 protein levels, Akt phosphorylation and insulin-mediated glycogen synthesis, indicating that the cells were insulin resistant compared to the control. It was hypothesised that given the proposed role for Zip7 in mediating rapid zinc release and that Zip7 expression is important for normal insulin signalling, Zip7 activation is stimulated by insulin treatment to temporarily increase cytosolic zinc bioavailability as a positive feedback mechanism for prolonging pathway activation. To test this, live cell imaging of zinc flux in cells was performed in cells with reduced Zip7 expression compared to controls. Insulin was shown to cause an increase in cytosolic zinc in C2C12 cells. However when Zip7 expression was reduced, even though the cells showed signs of insulin resistance, there was still an increase in zinc levels mediated by insulin. Insulin treatment is known to induce cellular ROS production and hydrogen peroxide has been suggested to cause a release of zinc due to oxidation of MTs leading to a release of bound zinc. These findings indicate that insulin-stimulated zinc flux is the result of MT oxidation rather than Zip7 activation. Taken together, these results highlight an important role for Zip7 in the insulin signalling pathway and show a previously undescribed positive feedback loop whereby insulin mediates a release of zinc to potentially inhibit PTP1B and other phosphatases to prolong insulin signalling activation. Further work is needed to fully elucidate the role of Zip7 in this pathway.
Doctor of Philosophy
APA, Harvard, Vancouver, ISO, and other styles
2

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
3

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
4

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

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
5

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
7

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
8

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

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
9

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Cherif-Feildel, Maëva. "Structure et fonctionnement de la niche germinale chez un Lophotrochozoaire, l'huître creuse Crassostrea gigas." Thesis, Normandie, 2018. http://www.theses.fr/2018NORMC282/document.

Full text
Abstract:
L’huître creuse Crassostrea gigas est un mollusque hermaphrodite alternatif dont le cycle dereproduction est annuel. Sa gamétogenèse est soutenue par des réserves énergétiques, stockées dansun tissu conjonctif de réserve entourant la gonade. Des travaux antérieurs ont montré l’implication dusystème insuline dans ce processus liant étroitement alimentation, énergie stockée et gamétogenèse.Le fonctionnement des étapes précoces de gamétogenèse reste encore méconnu chez l’huître. Cetravail a permis d’identifier les cellules germinales souches (GSC) et les progéniteurs potentiels en sebasant sur une approche d’histologie quantitative couplée au marquage des cellules germinales par unanticorps homologie anti-Oyvlg (Oyster vasa-like gene). Certains éléments constitutionnels de la nichegerminale ont également été identifiés, notamment la présence d’une cellule somatique associée à lacellule germinale souche potentielle qui présente un marquage par un anticorps hétérologue anti-BMP2/4. En amont de l’étude concernant la régulation des étapes précoces de gamétogenèse par lesvoies des insulines, le criblage in silico des bases de données a permis d’identifier des ligands, unrécepteur et de nombreux effecteurs du signal insuline conservés chez C. gigas. Six IRPs (InsulinRelated Peptides) ont été caractérisés ce qui a permis de retracer l’histoire évolutive des IRPs chez lesmollusques. D’après leur profil d’expression en qPCR et HIS, Cg-mip123 et Cg-ilp sont susceptiblesd’être impliqués dans le contrôle de la reproduction. Ces IRPs peuvent se lier à un récepteur CIR (C.gigas Insulin Receptor) dont la séquence complète a été décrite. Les acteurs des voies de signalisationde l’insuline sont également conservés chez l’huître et exprimés dans la gonade. Pour aller plus loin surle rôle de ces IRPs dans les étapes précoces de gamétogenèse, un conditionnement alimentaire (à jeunvs alimentés en Isochrysis galbana) a été réalisé sur des huîtres en première gamétogenèse. Lesrésultats de ce conditionnement montrent que l’apport nutritif augmente la différenciation des GSCainsi que les proliférations goniales. L’implication du signal insuline dans ce contrôle devra êtreprécisée
The Pacific oyster Crassostrea gigas is an alternative hermaphrodite mollusc with an annualreproduction cycle. Its gametogenesis is supported by energy reserves, store in a conjunctive storagetissue surrounding the gonad. Previous studies have shown the insulin system involvement in thisprocess closely connecting diet, energy reserves and gametogenesis. The functioning of earlygametogenetic stages stays unknown in the oyster. This work allows the identification of putative germstem cells (GSC) et progenitors on the basis of histological quantitative approach combined with agerm cells labelling by homologous antibody against Oyvlg (Oyster vasa-like gene). The maincomponents of the germinal niche have also been identified including a somatic cell, associated to theputative germ stem cell, with a heterologous antibody against BMP2/4 labelling. Above the study ofthe early gametogenetic stages regulation by insulin signalling, the genomic and transcriptomic-widescreening allows the identification of ligands, receptor et several effectors conserved in C. gigas. SixIRPs (Insulin Related Peptides) have been characterized which inform about the evolutionary history ofmolluscan IRPs. According to the expression profiles, in qPCR and ISH, Cg-mip123 and Cg-ilp may beinvolved in the reproduction process. These IRPs are able to bind the CIR (C. gigas Insulin Receptor)receptor whose sequence has been described. The insulin signalling effectors are also conserved in C.gigas and expressed in the gonad. To better understand the involvement of IRPs in the early stagesfunctioning, a food conditioning (unfed vs fed with Isochrysis galbana) has been done with oysters intheir first gametogenesis. The results showed that nutrient intake increases GSC and gonial mitosis.The involvement of insulin signalling has to be clarified
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Insuling signalling"

1

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

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

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Insuling signalling"

1

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Guglielmo, Gianni M. Di, Paul G. Drake, Patricia C. Baass, François Authier, Barry I. Posner, and 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Ogawa, Wataru, Takashi Matozaki, and 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Goldstein, Barry J., Faiyaz Ahmad, Wendi Ding, Pei-Ming Li, and 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Liu, Feng, and 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

An, Seon Woo A., Murat Artan, Sangsoon Park, Ozlem Altintas, and 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Varela, Isabel, Jose F. Alvarez, Jose Puerta, Rosa Clemente, Ana Guadaño, Matias Avila, Francisco Estevez, Susana Alemany, and 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Insuling signalling"

1

Vlahos, R., C. Mastronardo, H. J. Seow, and 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Dodd, MS, Mdl Sousa Fialho, CN Montes Aparico, M. Kerr, KN Timm, JL Griffin, JJFP Luiken, JFC Glatz, DJ Tyler, and 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Erlandsson, M., M. Nadali, S. Silfverswärd Töyrä, MN Svensson, I.-M. Jonsson, KM Andersson, and 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Insuling signalling"

1

Lekhanya, Portia Keabetswe, and 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, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0167.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Insuling signalling' for particular source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography