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Dissertations / Theses on the topic 'Insulin; Insulin-like growth factors'

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Published: 4 June 2021

Last updated: 1 February 2022

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1

Robertson, James Gray. "Insulin-like growth factors and insulin-like growth factor binding proteins in wounds /." Title page, contents and abstract only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09phr6509.pdf.

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2

Clark, Sarah Jane. "The growth hormone, insulin-like growth factor, insulin-like growth factor binding proteins and insulin axis in acute liver failure." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397943.

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3

Watanabe, Shin. "Insulin-like growth factor axis (insulin-like growth factor-I/insulin-like growth factor-binding protein-3) as a prognostic predictor of heart failure: association with adiponectin." Kyoto University, 2011. http://hdl.handle.net/2433/142074.

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4

Kind, Karen Lee. "Insulin-like growth factors and growth of the fetal sheep /." Title page, contents and abstract only, 1995. http://web4.library.adelaide.edu.au/theses/09PH/09phk525.pdf.

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5

Kampman, Kimberly A. "The insulin-like growth factors in intrauterine growth retarded swine /." The Ohio State University, 1992. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487759914760326.

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6

Mörth, Corinna. "Consequences of postnatal insulin-like growth factor II overexpression in insulin-like growth factor I deficient mice." Diss., lmu, 2005. http://nbn-resolving.de/urn:nbn:de:bvb:19-46307.

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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.

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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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8

Upton, Zee. "Production and characterization of nonmammalian insulin-like growth factors /." Title page, table of contents and summary only, 1993. http://web4.library.adelaide.edu.au/theses/09PH/09phu71.pdf.

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9

Perks, Claire Marie. "The insulin-like growth factors in the ovine ovary." Thesis, University of Bristol, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.259444.

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10

Burns, Jason Lee. "Growth control by insulin-like growth factor II." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270285.

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11

Odoom, Joseph E. "Creatine transport and its regulation in skeletal and smooth muscle." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294345.

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12

Dodson, Michael Verne. "EFFECTS OF INSULIN AND INSULIN-LIKE GROWTH FACTORS ON SATELLITE CELL PROLIFERATION IN VITRO (SOMATOMEDINS, RECEPTORS)." Diss., The University of Arizona, 1985. http://hdl.handle.net/10150/188065.

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Primary cultures of skeletal muscle satellite cells were induced to proliferate by exposure to physiologic levels of somatomedins and pharmacologic levels of insulin. Dexamethasone inclusion in serum containing medium facilitated the ovine somatomedin (oSm) (P < 0.05), but that both were different than the proliferation induced by MSA/rIGF-II (P < 0.05). In the presence of insulin concentrations that promote maximum proliferation, addition of oSm did not produce an additive effect, whereas the addition of MSA/rIGF-II did produce a significant increase in satellite cell proliferation above that induced by insulin. A more, in depth, analysis of the interaction of MSA/rIGF-II with its satellite cell receptor under a variety of experimental conditions revealed that binding of ¹²⁵I-MSA/rIGF-II was inhibited by oSm and MSA/rIGF-II, but not by insulin. Migration, and localization of ¹²⁵I-MSA/rIGF-II-receptor complexes in 7% sodium dodecyl sulfate polyacrylamide gels suggest that these complexes are Type II IGF receptors. In addition, this receptor system of satellite cells was shown to be modulated by other hormones; notably, pre-exposure of cells with insulin increased ¹²⁵I-MSA/rIGF-II binding, while oSm, or MSA/rIGF-II preincubation decreased the binding of ¹²⁵I-MSA/rIGF-II. Therefore, the proliferative effects of MSA/rIGF-II appeared not as a consequence of MSA/rIGF-II induction of other receptor types such as the insulin, or Type I IGF receptor systems. Concommitant to the previous experimentation, oSm was further examined in an initial attempt to elucidate its biologic binding mechanism in myogenic satellite cells. Binding of ¹²⁵I-oSm was inhibited by MSA/rIGF-II, insulin and IGF-I; thus these data suggest that oSm may be the ovine analog to human IGF-I. In addition, pre-exposure of cells to MSA/rIGF-II and oSm down-regulated the ability of satellite cells to bind oSm, while only concentrations of insulin greater than 550 ng insulin had this ability. Collectively, these data support the hypothesis that somatomedins play an important role in the control of postnatal muscle growth by providing a link between these hormones and satellite cells, one of the significant target cells involved in the growth process.

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13

Alsabban, Abdulrahman Essam. "Establishing methods to screen novel small molecules targeting insulin-like growth factor/insulin-like growth factor binding protein interaction." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/45046.

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Insulin-like growth factors (IGFs) are important systemic mediators of growth and survival that suppress apoptosis and promote cell cycle progression, angiogenesis and metastatic activities in various cancers by activating IGF-IR tyrosine kinase-mediated signaling. These effects depend on the bioavailability of IGFs, which is regulated by IGF binding proteins (IGFBPs). Increased IGFBP-2 and IGFBP-5 expression observed in castration-resistant prostate cancer is thought to promote tumor progression by enhancing IGF-mediated signaling. IGFBPs have cooperative carboxy-terminal and amino-terminal low and a high affinity IGF binding sites. I hypothesize that blocking the high affinity IGF binding site can affect the bioavailability of IGFs to target tissues and thus be used for treatment of various IGF-responsive diseases including prostate cancer. I initially characterized immunologic reagents capable of being used in sandwich ELISA formats to detect IGF-I and IGFBP-5 and attempted several configurations to establish an IGF-I/IGFBP-5 “bridged” sandwich ELISA platform to measure association and dissociation of IGF-I/IGFBP-5 complex formation. The inability of all bridged ELISA formats tested to measure IGF-I/IGFBP-5 binding, lead me to developed a Bio-Layer Interferometry-based assay that measures IGF-I/ IGFBP-5 binding kinetics that will allow for screening of factors that can affect this intermolecular interaction. I demonstrated that biotinylated IGF-I bound to streptavidin-coated biosensors can be used to measure binding of recombinant IGFBP-5 [2.24 nm shift in optical density (Response)]. I also demonstrated that IGF-I could efficiently disrupt this interaction (0.21 nm shift), while the amino-terminal IGF-I mutant, E3R, exhibits an intermediate competitive activity (1.47 nm shift) and insulin exhibits a low competitive activity (1.83 nm shift). In addition, I demonstrated that IGF-I can competitively disrupted this interaction, resulting in a dissociation rate constant (Kdis 1.5-³ 1/s), In contrast, the amino terminal IGF-I mutant, E3R binds with an intermediate affinity (Kdis 5.6-⁴ 1/s), and buffer free sample results in a (Kdis) of 1.5-⁴ (1/s). These results demonstrate the capacity of this BLI-based assay to differentiate relative competitive activity of compounds that target the high affinity IGF-I binding site of IGFBPs and establish a platform to screen for factors that might be developed as rationale therapeutics to disrupt sequestration of IGF-I by IGFBPs.

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14

Campbell-McNulty, Maeli Judith. "Isoflavone effects on insulin like growth factors and breast cancer." Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1444132/.

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An increased concentration of insulin-like growth factor-1 (IGF-1) is recognized to be an independent risk factor for pre-menopausal breast cancer. Tamoxifen is thought to initially reduce IGF-1 concentrations and increase levels of the IGF binding proteins 1 and 3. Isoflavones are oestrogen-like plant compounds, which may, because of their structural similarities to tamoxifen, also alter IGF status. This thesis first compares IGF-1, IGF binding protein 1(BP-1) and IGF binding protein 3 (BP-3) levels in breast cancer patients (n=14) compared with control subjects (n=23) and then assesses the effect of tamoxifen on IGF status after 9, 18 and 27 months of treatment. Concentrations of IGF-1, BP-1 and BP-3 at baseline did not differ between cases and controls. However on tamoxifen treatment, BP-1 and BP-3 were both significantly increased after 18 and 27 months while the IGF-1/BP-3 ratio was significantly decreased after 9 and 18 months. A feasibility study was then conducted to compare the effects of acute (single 80 mg load) versus chronic (80 mg/day for 7 days) administration of isoflavone- containing soy and linseed cereal bars on IGF-1, IGFBP-1 and IGFBP-3 in healthy female volunteers (n=10). Assays were established for the analyses of serum IGF-1, BP1 and BP3 concentrations and GCMS analysis of isoflavones in urine. Concentrations of IGF-1 were unchanged following the single 80 mg load. However, IGF-1 and BP-3 concentrations were significantly elevated after a week of supplementation with the soy and linseed bar. A larger study was then carried out to assess the effect of one-month isoflavone supplementation (80 mg/d) in tablet form, on IGF status in healthy pre- (n=16) and post-menopausal (n=7) women. This was a randomized, placebo-controlled crossover study with a minimum two-month washout period. Hormonal, antioxidant and lipid altering effects of the supplement were also examined, as was background diet. For pre-menopausal subjects, while there was an effect of time on IGF-1 (p=0.005), BP-1 (p=0.004), and BP-3 (p<0.001) confirming that IGF profile is influenced by menstrual cycle, this did not differ between placebo and isoflavone supplement. When the change in IGF-1 over the whole supplementation period was compared between the supplement and placebo phases, there was a non-significant reduction in change in IGF-1 (p=0.06) on isoflavone supplement compared to placebo. However, this may have been due to the non-significantly higher baseline concentrations of IGF-1 during the supplement phase. In post-menopausal subjects, there was no effect of isoflavone supplementation in comparison with placebo on IGF-1, BP-1 or BP-3. Finally, experiments were done in vitro to study the effect of isoflavones on DNA synthesis and proliferation in ERa positive MCF-7 and ERa negative MDA-MB 231 human breast cancer cells. In MCF-7 cells, low concentrations of isoflavones (0.1uM-10uM) stimulated DNA synthesis while high concentrations of genistein and equol were able to inhibit DNA synthesis with IC50 values of 93uM and 55uM respectively compared with 1.17uM tamoxifen. In MDA-MB231 cells the Isoflavones did not stimulate DNA synthesis at any concentrations but significantly inhibited DNA synthesis with IC50 values of 114uM, 14.1 uM and 14.55uM for daidzein, genistein and equol respectively compared with 1.35uM tamoxifen. This work suggests that isoflavone supplementation may alter IGF profile in pre menopausal women, and could suggest a role for these dietary compounds in breast cancer prevention. This should be further investigated in long term intervention studies with isolated isoflavone supplements.

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15

Al-Zahrani, Ali Saeed. "Insulin-like growth factors and genetic susceptibility to breast cancer." Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615155.

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16

Ekman, Bertil. "IGF-I in growth hormone deficiency and in type 1 diabetes /." Linköping : Univ, 2002. http://www.bibl.liu.se/liupubl/disp/disp2002/med757s.pdf.

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17

Hale, Lorna Jessica. "The roles of insulin and insulin-like growth factors in the podocyte cells of the kidney." Thesis, University of Bristol, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.535175.

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18

Wang, Jing. "Novel insulin-like growth factor-binding protein proteases: detection and characterization /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-942-4/.

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19

Cheetham, Tim D. "The growth hormone/insulin-like growth factor I axis in insulin-dependent diabetes mellitus during adolescence : studies of recombinant human insulin-like growth factor I (rhIGF-I) administration." Thesis, University of Leicester, 1996. http://hdl.handle.net/2381/34300.

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The fall in insulin sensitivity during adolescence is accentuated in insulin-dependent diabetes mellitus (IDDM) and has been linked to enhanced growth hormone (GH) secretion. The rise in GH release is related to low insulin-like growth factor I (IGF-I) levels and low IGF bioactivity. Abnormalities of the IGF binding proteins (IGFBP's), including low insulin-like growth factor binding protein-3 (IGFBP-3) and elevated insulin-like growth factor binding protein-1 (IGFBP-1) concentrations are also observed. The rise in GH concentrations may lead to increased insulin requirements that cannot easily be met by current treatment regimens and can result in deteriorating blood glucose control. GH release also enhances ketogenesis and has been linked to the development of microvascular complications. The impact of a subcutaneous injection of rhIGF-I (40 mug/kg) on GH concentrations, insulin sensitivity and the IGFBP's was studied in adolescents with IDDM (n=17). A control night was compared with a night when rhIGF-I was administered at 18.00h. Blood samples were taken regularly overnight and glucose concentrations controlled by a variable-rate insulin infusion. GH concentrations on the control night correlated with glycated haemoglobin levels. The administration of rhIGF-I led to a sustained increase in IGF-I levels, IGF bioactivity and reductions in GH secretion and the insulin infusion requirements to maintain euglycaemia. The change in GH secretion was due to reduced pulse amplitude rather than pulse frequency. The attributes assessing GH release correlated with free insulin concentations on control and rhIGF-I nights, and the reduction in GH release was related to the fall in insulin levels. The concentrations of IGFBP-3 did not fall after rhIGF-I as they did during the control study, but IGFBP-1 levels were unchanged. In longer term studies (n=6), daily rhIGF-I administration (40 ug/kg) for one month led to a reduced isophane insulin dose and a fall in glycated haemoglobin concentrations. GH levels were reduced and IGFBP-3 concentrations rose in 5 of the 6 subjects studied. The administration of rhIGF-I may have a therapeutic role in IDDM during adolescence by reducing GH concentrations and increasing insulin sensitivity.

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20

Schaffer, Andrea. "Insulin-like growth factor-I, insulin-like growth factor binding protein-3 and the risk of cervical squamous intraepithelial lesions." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=81435.

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Insulin-like growth factors (IGFs) and their binding proteins (IGFBPs) have been associated with an increased risk of several cancers. This case-control study investigated the relationship between IGF-I and IGFBP-3 plasma levels and the risk of squamous intraepithelial lesions (SILs) of the cervix, as well as the risk of HPV infection in women. 366 cases and 366 controls were recruited from five Montreal area hospitals. There was a significantly decreased risk of LSIL for the highest quartile of IGFBP-3 relative to the lowest quartile (Odds Ratio (OR)=0.25, 95% confidence interval (CI) 0.08-0.77), adjusted for age, HPV status and IGF-I. Also, there was a significantly increased risk of being positive for HPV, specifically high-risk types, for the highest quartiles of IGFBP-3 relative to the lowest quartile in controls (OR=4.53, 95% CI 1.33-15.40), adjusted for age and IGF-I. IGF-I was not significantly associated with SILs or HPV infection.

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21

Sitar, Tomasz. "Structural basis for the inhibition of insulin-like growth factors by insulin-like growth factor-binding proteins and structural and biochemical characterization of formins - the actin nucleating factors." kostenfrei, 2007. http://mediatum2.ub.tum.de/doc/652583/652583.pdf.

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22

Glassford, Janet. "Regulation of insulin-like growth factor-I bioactivity." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624728.

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23

Treiber, Kimberly Hoffer. "Glucose regulation in Thoroughbred weanlings: Regulation by insulin, growth hormone and insulin-like growth factor-I." Thesis, Virginia Tech, 2003. http://hdl.handle.net/10919/31221.

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Diets rich in hydrolyzable carbohydrates induce a hyperglycemic/insulinemic response and may increase the incidence of metabolic disorders associated with some types of laminitis, exertional rhabdomyolysis and osteochondrosis in horses. This study applied the minimal model of glucose and insulin dynamics to determine the effect of diet on metabolites and hormones that regulate glucose metabolism in young horses. Twelve Thoroughbred foals were raised on pasture and supplemented twice daily with a feed high in either sugar and starch (SS) or fat and fiber (FF). As weanlings (age 199 Â± 19 d, weight 274 Â± 18 kg), the subjects underwent a modified frequent sampling intravenous glucose tolerance test during which they remained in stalls and had access to grass hay and water ad libitum. Samples were colleted at -60, -45, 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 14, 16, 19, 22, 23, 24, 25, 27, 30, 35, 40, 50, 60 , 70 , 80, 90, 100, 120, 150, 180, 210, 240, 270, 300, 330 and 360 min with a glucose bolus of 300 mg/kg BW at 0 min and an insulin bolus of 1.5 mU/kg BW at 20 min. Plasma was analyzed for glucose, insulin, growth hormone (GH) and insulin-like growth factor-I (IGF-I) concentrations. Insulin sensitivity, glucose effectiveness, acute insulin response to glucose and disposition index were derived using Minmod Millennium and WinSAAM software. Diet groups were compared using the non-parametric Kruskal-Wallis test or the sign test. Time interactions were compared using a mixed model with repeated effects. Rank-ordered linear regression was used for correlations. Basal glucose did not differ between groups (P = 0.75). There was nearly a trend towards higher basal (P = 0.11), and median insulin was higher in the sugar and starch foals at all 36 sample points (P = 0.030). The basal glucose:basal insulin ratio for the sugar and starch supplemented foals was lower than for fat and fiber foals (P = 0.025). Insulin sensitivity (SI) was lower in foals fed sugar and starch than foals fed fat and fiber (P = 0.007). Acute insulin response to glucose was directly correlated to weight (r = 0.78; P = 0.003) and inversely correlated with SI (r = -0.55; P = 0.067). The glucose:insulin ratio was directly correlated to SI (r = 0.92; P < 0.001). Growth hormone concentrations were increased from basal from 19 to 180 min after the glucose dose (P < 0.05). Basal IGF-I was higher (P = 0.006) in the SS group compared to the FF group. Concentrations of total IGF-I increased with time (P = 0.002) in the SS group. The change in IGF-I concentration from baseline to the end of the study was positively correlated (r = 0.72; P = 0.008) to the area under the insulin curve from 0 to 80 min. Basal IGF-I was inversely correlated to SI (r = 0.71; P = 0.015). These results show that the metabolic response to a diet high in hydrolyzable carbohydrates differs from the response to a fat and fiber meal resembling forage. Weanlings adapted to meals high in glucose equivalents have higher insulin and IGF-I secretion as compared to foals adapted to a fat and fiber feed, possibly contributing to lower insulin sensitivity observed in these foals. Such deviations may contribute to metabolic dysfunction and osteochondrosis in horses fed grain diets.
Master of Science

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24

Miyamoto, Shinichi. "Matrix Metalloproteinase-7 Facilitates Insulin-like Growth Factor Bioavailability through its Proteinase Activity on Insulin-like Growth Factor Binding Protein-3." Kyoto University, 2004. http://hdl.handle.net/2433/147465.

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25

Xu, Su. "Insulin-like growth factors and their binding proteins in human skin." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343351.

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26

Szász, Nóra 1977. "Transport and binding of insulin-like growth factors to articular cartilage." Thesis, Massachusetts Institute of Technology, 1999. http://hdl.handle.net/1721.1/80129.

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Thesis (S.B. and M.Eng.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 1999.
Includes bibliographical references (leaves 68-71).
by Nóra Szász.
S.B.and M.Eng.

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27

Kiefer, Julie Christine. "Analysis of myogenic regulatory factors and insulin-like growth factors in early somite myogenesis /." Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/9227.

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28

Holmes, Robert. "The maternal insulin-like growth factor system and fetal growth." Thesis, University of Bristol, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265467.

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29

Hyde, Carolyn Elizabeth. "The functional consequences of the interactions between insulin-like growth factors (IGFs), insulin-like growth factor binding proteins (IGFBPs) and vitronectin (VN) and their involvement in skin." Queensland University of Technology, 2006. http://eprints.qut.edu.au/16197/.

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The insulin-like growth factor (IGF) system plays an important role in a number of disease states, such as cancer, and has also been implicated in wound and burn healing processes. Two IGF receptors, the type-1 IGF and type-2 IGF receptors, as well as six insulin-like growth factor binding proteins (IGFBP-1 to 6), have well established roles in mediating IGF activity. Earlier studies in this laboratory demonstrated that IGF-II binds to the extracellular matrix (ECM) protein vitronectin (VN), and although IGF-I does not bind directly to VN it can bind indirectly via specific IGFBPs. Therefore the aim of the research described in this thesis was to determine whether binary and ternary complexes of IGF-I/II, IGFBPs and VN affect human keratinocyte cell function. The strategy of pre-binding these complexes to the culture dishes was adopted in this study in an attempt to more accurately reflect the extracellular environment in vivo. These studies demonstrated that the binary complex of IGF-II and VN and the ternary complexes comprised of IGF-I, IGFBP-2, or 3, or 4, or 5 and VN significantly stimulated HaCaT de novo cell protein synthesis in the human keratinocyte cell line. Interestingly, these latter experiments demonstrated that although large increases in protein synthesis were observed using the ternary complexes, IGF-I/IGFBP complexes alone were responsible for the significant increases in protein synthesis and these responses are mediated via the MAPK signaling pathway. In addition, both the dimeric and trimeric complexes significantly enhanced cell migration through 12 μm TranswellsTM. Unlike the protein synthesis assays, VN was critically important in these migratory responses and highlighting the important role that integrins play in cell migration. Cell attachment assays on the other hand demonstrated that the interactions of IGFs with IGFBPs and VN did not affect cell attachment. The data encompassed within this thesis represent the first studies to provide a functional role for the interaction between IGFs, IGFBPs and VN in human keratinocytes. Taken together these results suggest that IGF/IGFBP/VN complexes may hold great potential in situations where enhanced keratinocyte cell migration and proliferation is required, such as in wound healing and skin engineering applications.

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30

Ohlsen, Susan M. "Cloning and characterization of ovine insulin, insulin-like growth factor-I and -II genes." Diss., This resource online, 1993. http://scholar.lib.vt.edu/theses/available/etd-06062008-165729/.

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31

Wang, Mengjie. "Brain Insulin-Like Growth Factor 1 Receptor and Insulin Receptor in Metabolism and Reproduction." University of Toledo Health Science Campus / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=mco1564676824418256.

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32

Dickey, Lindsey Ann. "Peripheral Hormone Interactions with the Growth Hormone-Insulin-Like Growth Factor (GH-IGF) System in Rainbow Trout." Diss., North Dakota State University, 2019. https://hdl.handle.net/10365/31353.

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The growth of vertebrates is primarily regulated by the growth hormone-insulin-like growth factor (GH-IGF) system, but not in isolation. The central question of this dissertation was how do other hormones peripheral to the GH-IGF system interact with the system, including feedbacks by GH and IGF themselves on various tissues in rainbow trout (Oncorhynchus mykiss)? The representative hormones selected were thyroxine, cortisol, and the sex steroids testosterone and estrogen, along with GH and IGF. These hormones were chosen because they are known to affect overall growth and development during specific life events, but exactly what target genes and what mechanisms are involved are only at the early stages of being delineated in fish. Liver and gill tissues were selected as representative tissues to assess the in vitro effects on growth-related genes of the GH-IGF system. A total of more than thirty experiments were conducted, including time- and concentration-response, inhibitory studies, hormone combination studies, and radio-receptor binding assays. Hormones were applied to whole tissue cultures and real-time quantitative-PCR was used to measure hormonal effects on GHR, IGF, and IGFR1 genes. Microsomal preparations were treated with selected hormones and radio-labeled GH or IGF. A gamma counter was used to measure receptor-ligand activity. GH and IGF were found to possess autocrine and/or paracrine actions in self-regulating target growth genes. Thyroxine had no direct effects on targeted growth genes but may interact with other molecules or hormones to elicit its effects on growth and development. Cortisol directly influenced target growth genes in a tissue-specific and isoform-specific manner. Finally, sex steroids differentially regulated the growth genes: estradiol inhibited growth genes while testosterone directly stimulated growth genes. These findings contribute to understanding how hormones peripheral to the GH-IGF system interact with the growth system.
National Science Foundation grant IOS 0920116 to Dr. Mark Sheridan

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33

Clayton, Simon James. "Regulation of oestrogen receptor and oestrogen responsive genes by insulin, IGF-I, oestrogen and antioestrogens in breast cancer cells." Thesis, University of Newcastle Upon Tyne, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283743.

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34

Daws, Michael Rory. "Hormone responsiveness in breast cancer cell growth : the role of the type I IGF receptor." Thesis, University of Newcastle Upon Tyne, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284225.

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35

Khan, Frances R. "The role of insulin and the insulin-like growth factors in the proliferation of the rat thymic lymphocyte." Thesis, Aston University, 1989. http://publications.aston.ac.uk/12518/.

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Concanavalin A, provoked a 35-fold increase in the rate of proliferation of rat thymocytes. Insulin (10-6M), and insulin-like growth factor I (10-10M) approximately doubled the rate of DNA synthesis. Both of these structurally related molecules acted through the type I insulin-like growth factor receptor. The sequential addition of Concanavalin A and insulin, promoted a much greater proliferative response than to either of the two agonists alone. Insulin also increased the uptake of glucose and amino acids by the cells. Glucose uptake was enhanced at insulin concentrations of 10-6M and 10-10M. Amino acid uptake was more strongly affected at the higher concentration. Insulin-like growth factor I (10-11M) also enhanced amino acid uptake. The effects of insulin on metabolism were mediated by both insulin and type I insulin-like growth factor receptors. These effects were greatly enhanced after a pre-treatment with Concanavalin A. Concanavalin A provided a primary mitogenic signal to the cells. Amongst the responses was an increased expression of insulin and/or type I insulin-like growth factor receptors. The consequent enhanced cellular sensitivity to these agonists, enabled them to facilitate the passage of the cells through the cell cycle by: i) providing a secondary mitogenic signal, and ii) promoting the uptake of raw materials and energy substrates. The initiation of DNA synthesis and passage through the cell cycle was thus punctuated by the sequential expression of various cell surface receptors. This regulated cellular sensitivity, enabling them to react in a precisely orchestrated fashion to hormones and other molecules in their environment. The intracellular mechanism of insulin action remains an enigma. Although the presence of extracellular calcium was essential for insulin stimulation of amino acid uptake and DNA synthesis, the cation did not subserve a direct mediator function. Insulin promoted an increase in intracellular pH, which was mediated by the Na+/H+ antiport. Other mechanisms were probably also involved in mediating the full cellular response to insulin.

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36

Lucic, Melinda Robin. "Characterisation of the molecular interactions between insulin-like growth factors and their binding proteins." Title page, contents and abstract only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phl9375.pdf.

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Addenda inserted in back. Includes bibliographical references (leaves 139-160) Assesses the importance of amino acids 221 to 236 of bIGFBP-2 for IGF binding activity, by creating amino acid substitutions.

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37

Levitt, Randy J. "Aspects of insulin-like growth factor physiology in cancer." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111826.

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The insulin-like growth factor (IGF) pathway consists of two ligands (IGF-I and IGF-II), two receptors (IGF-IR and IGF-IIR) and six IGF binding proteins (IGFBP-I through -6). There is considerable evidence from both laboratory and population studies that IGF physiology is relevant to neoplastic growth. For example, it has been shown that IGF-I and/or IGF-II act as mitogens and anti-apoptotic agents for both normal and malignant cells by binding to the IGF-IR and activating downstream signalling pathways. Consistent with this data, IGF-IR inhibition by a variety of strategies inhibits cancer cell proliferation and/or induces apoptosis both in vitro and in animal models of neoplasia. Furthermore, epidemiological studies have demonstrated a positive correlation between serum IGF-I levels and risk of subsequent cancer. Classically, the IGFBPs were considered to be growth inhibitors, as they had a well-defined role in sequestering the mitogens IGF-I and IGF-II, therefore preventing binding and subsequent activation of mitogenic and anti-apoptotic pathways downstream of the IGF-IR. However, increasing evidence indicates that under certain conditions, IGFBPs can act as growth stimulators, and both IGF-dependent and -independent mechanisms have been proposed.
Although the roles of the IGFs, IGF-IR and IGFBPs in cancer have been studied extensively, this thesis describes several new links between IGF physiology and neoplasia. In the first section, we demonstrate that IGF-I can attenuate growth inhibition and apoptosis induced by a class of drugs called COX-2 inhibitors in BxPC-3 pancreatic cancer cells. This effect could be attributed to opposite influences of IGF-IR signalling and COX-2 inhibitors on activation of Akt, with IGF-IR signalling increasing activity and COX-2 inhibitors decreasing activity. In the second section, we demonstrate that in 184htert cells, an immortal but untransformed breast epithelial cell line, COX-2 inhibitors can induce IGFBP-3 expression. We go on to show that IGFBP-3 can inhibit growth of this cell line in an IGF-dependent manner, and speculate that this action of COX-2 inhibitors may be relevant to data linking use of this class of drugs to decreased breast cancer risk. In the third section, we demonstrate that the expression of IGFBP-2 in U251 glioma cells is inhibited by the induction of the tumor suppressor PTEN. Furthermore, IGFBP-2 does not effect the growth of this cell line, indicating that published associations between tumor IGFBP-2 expression and grade of glioma may be a result of IGFBP-2 acting as a marker for loss of function of PTEN. In the fourth and final section, we demonstrate that in MDA-MB-231 breast cancer cells, over-expression of IGFBP-2 can enhance growth, indicating that the effect of IGFBP-2 on growth of neoplastic cells is tissue specific. Furthermore, antisense strategies targeting IGFBP-2 mRNA (antisense oligonucleotides and siRNA) can inhibit growth of IGFBP-2-expressing breast cancer cells both in vitro and in vivo.
Taken together, these results extend the existing body of evidence demonstrating that IGF physiology contributes to neoplastic growth, and suggest that strategies to inhibit IGF-IR signalling and/or IGFBP-2 expression may have therapeutic value for some types of cancers.

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38

Girnita, Ada. "Targeting insulin-like growth factor-1 receptor in cancer /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-041-9/.

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39

Hopkins, Nicholas John. "Insulin-like growth factor-I and its binding proteins." Thesis, University of Reading, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240702.

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40

Williams, Nolann G. "Myostatin regulation of the insulin-like growth factor axis." Pullman, Wash. : Washington State University, 2009. http://www.dissertations.wsu.edu/Thesis/Spring2009/n_williams_042009.pdf.

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Thesis (M.S. in genetics and cell biology)--Washington State University, May 2009.
Title from PDF title page (viewed on Apr. 5, 2010). "School of Molecular Biosciences." Includes bibliographical references (p. 39-45).

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41

Ong, Kenneth Kian Leong. "Longitudinal analysis of the insulin gene minisatellite and insulin-like growth factors in human size at birth and early childhood growth." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619807.

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42

Gustafsson, Sara. "The insulin-like growth factor system - effects of circulating proteases /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-436-8/.

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43

Balderson, Stephanie D. "Investigations of Insulin-Like Growth Factor I Cell Surface Binding: Regulation by Insulin-Like Growth Factor Binding Protein-3 and Heparan Sulfate Proteoglycan." Thesis, Virginia Tech, 1997. http://hdl.handle.net/10919/30494.

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The primary aim of this text is to gain insight on how cellular activation by a insulin-like growth factor (IGF-I), in the presence of insulin-like growth factor binding protein-3 (IGFBP-3), is influenced by heparan sulfate proteoglycans (HSPG). Initial research will be presented, assumptions and hypotheses that were included in the development of mathematical models will be discussed, and the future enhancements of the models will be explored. There are many potential scenarios for how each component might influence the others. Mathematical modeling techniques will highlight the contributions made by numerous extracellular parameters on IGF-I cell surface binding. Tentative assumptions can be applied to modeling techniques and predictions may aid in the direction of future experiments. Experimentally, it was found that IGFBP-3 inhibited IGF-I Bovine Aortic Endothelial (BAE) cell surface binding while p9 HS slightly increased IGF-I BAE cell surface binding. IGFBP-3 has a higher binding affinity for IGF-I (3 x 10-9 M) than p9 HS has for IGF-I (1.5 x 10-8 M) as determined with cell-free binding assays. The presence of p9 HS countered the inhibiting effect of IGFBP-3 on IGF-I BAE cell surface binding. Although preliminary experiments with labeled p9 HS and IGFBP-3 indicated little to no cell surface binding, later experiments indicated that both IGFBP-3 and p9 HS do bind to the BAE cell surface. Pre-incubation of BAE cells with either IGFBP-3 or p9 HS resulted in an increase of IGF-I BAE cell surface binding . There was a more substantial increase of IGF-I surface binding when cells were pre-incubated with IGFBP- 3 than p9 HS. There was a larger increase of IGF-I BAE cell surface binding when cells were pre-incubated with p9 HS than when p9 HS and IGF-I were added simultaneously. This suggests that IGFBP-3 and p9 HS surface binding plays key role in IGF-I surface binding, however, p9 HS surface binding does not alter IGF-I surface binding as much as IGFBP-3 surface binding seems to. Experimental work helps further the understanding of IGF-I cellular activation as regulated by IGFBP-3 and p9 HS. Developing mathematical models allows the researcher to focus on individual elements in a complex systems and gain insight on how the real system will respond to individual changes. Discrepancies between the model results and the experimental data presented indicate that soluble receptor inhibition is not sufficient to account for experimental results. The alliance of engineering analysis and molecular biology helps to clarify significant principles relevant to the conveyance of growth factors into tissue. Awareness of the effects of individual parameters in the delivery system, made possible with mathematical models, will provide guidance and save time in the design of future therapeutics involving growth factors.
Master of Science

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44

Miell, John Patrick. "Glucocorticoid modulation of growth hormone/insulin - like growth factor - 1 relationships." Thesis, University of Southampton, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386657.

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45

Edwall, Dan. "Insulin-like growth factor-I in tissue regeneration and growth control." Stockholm : Karolinska Institute, 1993. http://catalog.hathitrust.org/api/volumes/oclc/28296811.html.

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46

Guernec, Anthony. "Insulin-like growth factors (IGFs), myostatine et croissance musculaire chez le poulet." Tours, 2003. http://www.theses.fr/2003TOUR4024.

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Les Insulin-like Growth Factors (IGF-I et IGF-II) et la myostatine (MSTN) sont des facteurs produits dans le muscle qui exercent une action antagoniste sur sa croissance, respectivement stimulatrice et inhibitrice. Pour tester l'hypothèse selon laquelle l'équilibre d'expression entre eux déterminerait la quantité de muscles déposée chez le poulet, nous avons cherché à relier les niveaux d'ARN messagers codant pour ces régulateurs avec les performances de croissance musculaire au cours du développement, en fonction du génotype et de l'état nutritionnel. Le modèle génétique que nous avons choisi est constitué de poulets sélectionnés spécifiquement pour des rendements accrus en filets, et de leurs contrôles. L'effet de l'état nutritionnel a été étudié sur des poulets de type chair industriel, juste après l'éclosion et à l'âge de 4 semaines. Dans ces deux modèles, nous avons observé une relation positive entre le développement musculaire et les niveaux de messagers codant pour IGF-I, suggérant un rôle causal pour stimuler la croissance hypertrophique des fibres musculaires chez le poulet. La relation négative attendue pour MSTN a été observée juste autour de l'éclosion au moment où démarre la croissance explosive du muscle pectoral. Dans tous les autres cas, la relation était plutôt positive. Une connaissance plus approfondie du mode d'action de ce facteur est requise pour interpréter les conséquences des variations de son ARN messager
Insulin-like growth factors (IGF-I and IGF-II) and myostatin (MSTN) are paracrine regulators which respectively stimulate and inhibit muscle development. The present study was conducted to evaluate if the balance between muscle IGF-I or IGF-II and MSTN mRNA levels could control muscle growth at different stages of development in relation with genotype and nutritional status. The genetic model consisted of chickens selected for increased breast meat yield and their controls. The effect of nutritional state was studied in industrial broiler chickens just after hatching and at four weeks of age. In both models, a positive relation was observed between IGF-I mRNA and muscle development, suggesting that IGF-I could participate to induce muscle fibres hypertrophy. The expected negative relation with MSTN was only observed around hatch when breast muscle yield markedly increased. In the other conditions, the relation between MSTN and muscle growth appeared positive. Further understanding of MSTN's mechanism of action is required before using MSTN mRNA levels as a predictor of muscle growth

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47

Niemann, Inga [Verfasser]. "Die Assoziation zwischen Insulin-like Growth Factor I sowie Insulin-like Growth Factor Binding Protein 3 und Knochenumbaumarkern in der Allgemeinbevölkerung / Inga Niemann." Greifswald : Universitätsbibliothek Greifswald, 2016. http://d-nb.info/1115357387/34.

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48

Schmid, Uwe. "Untersuchungen zur Rezeptorbindung und biologischen Wirkung von Insulin, Lispro-Insulin und Insulin-Like Growth Factor-1 (IGF-1) an proximalen Nierentubuluszellen." Ulm : Universität Ulm, Medizinische Fakultät, 1999. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB8473239.

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49

Kallincos, Nicholas Campbell. "Growth hormone (GH) and insulin-like growth factor-I (IGF-I) in vivo: investigation via transgenesis in rats /." Adelaide : Thesis (Ph.D.) -- University of Adelaide, Department of Biochemistry, 1993. http://web4.library.adelaide.edu.au/theses/09PH/09phk143.pdf.

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50

Hedman, Christina A. "Insulin and IGF-I in type 1 diabetes /." Linköping : Univ, 2005. http://www.bibl.liu.se/liupubl/disp/disp2005/med915s.pdf.

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