Tesis: "Insulin-like growth factor I Physiology"

1

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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2

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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3

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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4

Bibollet-Bahena, Olivia. "The insulin-like growth factor-1 stimulates protein synthesis in oligodendrocyte progenitors /." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112382.

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Insulin-like growth factor-1 (IGF-1) is essential for oligodendrocyte (OL) development, promoting their survival, proliferation and differentiation. Furthermore, IGF-1 null mutant mice have a decrease in CNS myelination and in the number of OL progenitors (OLPs). IGF-1 interacts with the Type I IGF receptor to activate two main downstream signalling pathways, the PI3K/Akt and the Ras-Raf-MEK/ERK cascades, which mediate survival or proliferation of OLPs. The objective of this study is to elucidate the transduction pathways involved in IGF-I-stimulated protein synthesis, important for growth and differentiation of OLs. In other cellular systems, the PI3K/Akt pathway is involved in protein translation. mTOR and the p70 S6 kinase are downstream effectors that phosphorylate translation initiation factors (e.g. eIF-4E) and their regulators (e.g. 4E-BP1). OLPs were obtained from primary cultures and were treated with IGF-1 with or without inhibitors LY294002 or wortmannin (PI3K), rapamycin (mTOR), Akt III or IV, an adenovirus with a dominant negative form of Akt or PD98059 (ERK). Protein synthesis was assessed by metabolic labeling with [35S]-methionine, and protein phosphorylation by Western blotting. Results from the former showed that IGF-1 stimulates protein synthesis in a dose-dependent manner. Moreover, IGF-1 increases protein synthesis in OLPs through PI3K, mTOR, Akt and ERK activation. Concordantly, Western blot analysis reveals that IGF-1 stimulates phosphorylation of Akt, mTOR, ERK, S6 and 4E-BP 1. Activation of S6 and inactivation of 4E-BP1 occur through phosphorylation and are required for protein synthesis to take place. These events are dependent on the upstream activation of PI3K, Akt and mTOR.

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5

Robertson, Katherine. "The role of the growth hormone/IGF-I system on islet cell growth and insulin action /." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103288.

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The study of diabetes mellitus is vital in this day and age because its incidence is increasing at an alarming rate. Diabetes results in the loss of function of beta-cells within the pancreas. Insulin resistance contributes to diabetes but the human body can compensate in various ways such as increasing the islet cell mass, glucose disposal and insulin secretion, in order to prevent the onset of diabetes. Growth hormone (GH) and insulin-like growth factor-I (IGF-I) are two integral hormones important in both glucose homeostasis and islet cell growth. Early studies using cultured islet cells have demonstrated positive regulation of beta-cell growth by both GH and IGF-I. To evaluate their relevance on normal beta-cell growth, compensatory growth, as well as in insulin responsiveness, we have used two mouse models that represent opposite manipulations of the GH/IGF-I axis. Specifically, the growth hormone receptor gene deficient (GHR-/-) and the IGF-I overexpression (MT-IGF) mice, to help understand the role of glucose homeostasis and islet cell growth in the GH/IGF-I axis. GH is essential for somatic growth and development as well as maintaining metabolic homeostasis. It is known that GH stimulates normal islet cell growth. Moreover, GH may also participate in islet cell overgrowth and compensate for insulin resistance induced by obesity. To determine whether the islet cell overgrowth is dependent on GH signaling, we studied the response of GHR-/- mice to high-fat diet (HFD)-induced obesity. We also studied the insulin responsiveness in GHR-/- mice. On the other hand, IGF-I promotes embryonic development, postnatal growth and the maturation of various organ systems. The notion that IGF-I stimulates islet cell growth has been challenged in recent years by results from IGF-I and receptor gene targeted models. We have characterized MT-IGF mice which overexpress the IGF-I gene. The results of our studies indicate that (1) GH is essential for normal islet cell growth, but not required for compensatory overgrowth of the islets in response to obesity, (2) GHR gene deficiency caused delayed insulin responsiveness in skeletal muscle; in contrast to elevated insulin sensitivity in the liver; (3) although overexpression does not stimulate islet cell growth, a chronic IGF-I elevation caused significant hypoglycemia, hypoinsulinemia, and improved glucose tolerance, (4) finally IGF-I overexpression mice are resistant to experimental diabetes.

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6

Kallincos, Nicholas Campbell. "Growth hormone (GH) and insulin-like growth factor-I (IGF-I) in vivo: investigation via transgenesis in rats." Thesis, Adelaide, 1993. http://hdl.handle.net/2440/21602.

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7

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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8

Lu, Yarong 1971. "Pancreatic-specific insulin-like growth factor I gene deficiency on islet cell growth and protection." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111827.

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The role of insulin-like growth factor I (IGF-I) in pancreatic islet cell growth and development has been debated in recent years. The dogma that IGF-I stimulates pancreatic islet growth has been challenged by combinational targeting of IGF or IGF-IR genes, as well as beta-cell-specific IGF-IR gene deficiency. In order to assess the physiological role of locally produced IGF-I, we have developed pancreatic-specific IGF-I gene deficiency (PID) by crossing Pdx1-Cre and IGF-I/loxP mice. PID mice were normal except for decreased blood glucose level and a 2.3-fold enlarged islet cell mass. When challenged with low doses of streptozotocin, control mice developed hyperglycemia after 6 days that was maintained at high levels for at least 2 months. In contrast, PID mice only exhibited marginal hyperglycemia after 12 days, maintained throughout the experiment. Furthermore, streptozotocin-induced beta-cell apoptosis (TUNEL assay) was significantly prevented in PID mice. PID mice also exhibited a delayed onset of type 2 diabetes induced by a high-fat diet, accompanied by super enlarged pancreatic islets and preserved sensitivity to insulin. As the phenotype is unlikely a direct consequence of IGF-I deficiency, we used oligonucleotide DNA microarray to explore possible activation of pro-islet genes in PID mice, which revealed upregulation of multiple new members of the Reg family genes (Reg2, 3alpha and 3beta) in the pancreas. The results were subsequently confirmed by Northern blot and/or realtime PCR, which exhibited 2 to 8 fold increases in the level of their mRNAs. Moreover, these Reg family genes were also activated following streptozotocin-induced beta-cell damage and diabetes. Our results reveal a possible mechanism of islet growth and protection in PID mice, thus serving a potential strategy in combating diabetes.

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9

Lok, Fong. "Role of IGF-I in ovine fetal and placental growth and development /." Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phl836.pdf.

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10

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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11

Degger, Brian. "Fish insulin-like growth factors : their role in growth from a functional perspective." Thesis, Queensland University of Technology, 2001.

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12

Bos, Petra Marianne. "Regional differences in adipose tissue development : effects of nutritional challenges on genes involved in insulin, insulin like growth factor and glucocorticoid signalling." Thesis, University of Nottingham, 2010. http://eprints.nottingham.ac.uk/11360/.

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Adipose tissue development is regulated by a complex interaction between the local actions of insulin, glucocorticoids and insulin like growth factors (IGFs). A series of experiments was undertaken in which the normal development of individual adipose tissue depots and their development following periconceptional under- and overnutrition, formula feeding and juvenile obesity was investigated in sheep. Expression and abundance of glucocorticoid receptor (GR), 11β-hydroxysteroid dehydrogenases (11β-HSDs), insulin receptor, p85 subunit of phosphatidylinositol 3-kinase (p85), glucose transporter 4 (Glut4), insulin like growth factor (IGF) 1 and 2 and their receptors (IGF-R) were measured as markers of sensitivity to glucocorticoids, insulin and IGFs in individual adipose tissue depots. It was found that during early postnatal life omental adipose tissue grows faster than other depots. In all investigated groups there were marked differences in the expression of all investigated genes between adipose tissue depots. No effect was found of periconceptional nutrition on expression of the investigated genes. Weight of the mother prior to conception was negatively associated with omental GR and 11β-HSD1. Free fatty acid levels at 4 months of age were related to omental and subcutaneous 11β-HSD1 expression. Perirenal expression of IGF1R at 4 months was negatively correlated with perirenal and subcutaneous adipose tissue mass. IGF1R expression correlated with IR and GR expression. Formula feeding resulted in reduced expression of Glut4 and increased 11β-HSD1 expression. A combination of formula feeding and juvenile obesity resulted in a redistribution of adipose tissue in favour of the perirenal depot. Obesity per se resulted in a reduction of the expression of all genes and proteins examined. We have shown significant differences in markers of tissue sensitivity to the actions of insulin, glucocorticoids and insulin like growth factors between different adipose tissue depots in the body, highlighting the importance of examining those depots individually in future studies.

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13

Mukherjee, Aditi. "Studies on the Role of Insulin Like Growth Factor-I on Bone Formation and Mineralization." University of Cincinnati / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1109173865.

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14

Steeb, Corinna-Britta. "Effects of insulin-like growth factor-I (IGF-I) peptides on the growth and function of the gastrointestinal tract in adult and sucking rats /." Title page, abstract and contents only, 1995. http://web4.library.adelaide.edu.au/theses/09PH/09phs813.pdf.

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15

Ritter, Ashlyn D. "The Influence of the Insulin-Like Gene Family and Diet-Drug Interactions on Caenorhabditis elegans Physiology: A Dissertation." eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/872.

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Aging can be defined as the accumulation of changes affecting the maintenance of homeostatic processes over time, leading to functional decline and increased risk for disease and death. In its simplicity, aging is the systemwide deterioration of an organism. Genetic studies have identified many potential molecular mechanisms of aging including DNA damage, telomere shortening, mitochondrial dysfunction, increased oxidative stress, uncontrolled inflammation, and hormone dysregulation (reviewed in [1]). However, in reality, aging is likely to be a combination of some (or potentially all) of these mechanisms. Interestingly, aging and metabolism are tightly coordinated. Aging is a major contributor to metabolic decline and related diseases, including type 2 diabetes, metabolic syndrome, and cancer. One of the best characterized metabolic pathways implicated in aging is the insulin/IGF-1 signaling (IIS) pathway. Downstream signaling components of the IIS pathway receptor have been well studied and include an interconnected network of signaling events that regulate many physiological outputs. However, less is known about the role of upstream signaling components and how intracellular pathways and physiology are regulated accordingly. In Part I, I present my work towards understanding upstream IIS pathway components using a systems biology approach. The goal of this study is to gain insight into the redundancy and specificity of the insulin gene family responsible for initiating IIS pathway activity in Caenorhabditis elegans. The information gained will serve as a foundation for future studies dissecting the molecular mechanisms of this pathway in efforts to uncouple the downstream signaling and physiological outputs. The clear impact of metabolism on aging and disease stimulated questions regarding the potential of promoting health and longevity through diet and dietary mimetics. Recent findings indicate reduced food intake, meal timing and nutritional modulation of the gut microbiome can ameliorate signs of aging and age-associated diseases. Aging, therefore, is also the result of dynamic and complex interplay between genes of an organism and its environment. In Part II, I will discuss my efforts to gain insight into how diet influences aging. This preliminary study has demonstrated that diet can affect lifespan in the model organism, C. elegans. Additionally, we observe diet-specific effects on drug efficacy that, in turn, modulates C. elegans lifespan and reproduction. The implications of these experiments, while limited, illustrate a potentially greater role in diet- and drug-mediated effects on lifespan.

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16

Ritter, Ashlyn D. "The Influence of the Insulin-Like Gene Family and Diet-Drug Interactions on Caenorhabditis elegans Physiology: A Dissertation." eScholarship@UMMS, 2008. http://escholarship.umassmed.edu/gsbs_diss/872.

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Aging can be defined as the accumulation of changes affecting the maintenance of homeostatic processes over time, leading to functional decline and increased risk for disease and death. In its simplicity, aging is the systemwide deterioration of an organism. Genetic studies have identified many potential molecular mechanisms of aging including DNA damage, telomere shortening, mitochondrial dysfunction, increased oxidative stress, uncontrolled inflammation, and hormone dysregulation (reviewed in [1]). However, in reality, aging is likely to be a combination of some (or potentially all) of these mechanisms. Interestingly, aging and metabolism are tightly coordinated. Aging is a major contributor to metabolic decline and related diseases, including type 2 diabetes, metabolic syndrome, and cancer. One of the best characterized metabolic pathways implicated in aging is the insulin/IGF-1 signaling (IIS) pathway. Downstream signaling components of the IIS pathway receptor have been well studied and include an interconnected network of signaling events that regulate many physiological outputs. However, less is known about the role of upstream signaling components and how intracellular pathways and physiology are regulated accordingly. In Part I, I present my work towards understanding upstream IIS pathway components using a systems biology approach. The goal of this study is to gain insight into the redundancy and specificity of the insulin gene family responsible for initiating IIS pathway activity in Caenorhabditis elegans. The information gained will serve as a foundation for future studies dissecting the molecular mechanisms of this pathway in efforts to uncouple the downstream signaling and physiological outputs. The clear impact of metabolism on aging and disease stimulated questions regarding the potential of promoting health and longevity through diet and dietary mimetics. Recent findings indicate reduced food intake, meal timing and nutritional modulation of the gut microbiome can ameliorate signs of aging and age-associated diseases. Aging, therefore, is also the result of dynamic and complex interplay between genes of an organism and its environment. In Part II, I will discuss my efforts to gain insight into how diet influences aging. This preliminary study has demonstrated that diet can affect lifespan in the model organism, C. elegans. Additionally, we observe diet-specific effects on drug efficacy that, in turn, modulates C. elegans lifespan and reproduction. The implications of these experiments, while limited, illustrate a potentially greater role in diet- and drug-mediated effects on lifespan.

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17

Doyle, Kharen Leigh. "The control of insulin-like growth factor-1 (IGF-1) in the spinal cord of the rat." Thesis, Queensland University of Technology, 1999.

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18

Wang, Min. "Importance of insulin-like growth factor-1 receptor and EWS/FLI-1 fusion protein in growth and survival of two different types of neuroectodermal tumor cells /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3293-X/.

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19

Marshall, Nicholas John. "The influence of insulin-like growth factor 1 and its analogues on fibroblasts and dermal wound healing." Title page, table of contents and synopsis only, 1998. http://web4.library.adelaide.edu.au/theses/09MD/09mdm3685.pdf.

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Includes bibliography (leaves 191-219). Examines the levels of insulin-like growth factor and the presence of IGF binding proteins in human wound fluid. Tests the potency of IGF-1 and 2 analogues in in vitro models of fibroblast activity and their effect on healing in normal and diabetic rodent wounds. Shows that IGF-1, IGF-2 and their binding proteins are present in fluid from a partial thickness cutaneous wound; that the binding proteins negatively modulate the activity of insulin-like growth factors in vitro, but that the IGFs do not necessarily show enhanced activity in vivo at the wound site if binding protein affinity is decreased. Discusses possible roles of these binding proteins in wound repair.

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20

Kachra, Zarin. "Regulation of insulin-like growth factor-I (IGF-I) and IGF-binding protein-1 (IGFBP-1) mRNA levels in cultured rat hepatocytes." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=41300.

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The liver is a major site of production of circulating levels of insulin-like growth factor-I (IGF-I) and IGF-binding proteins (IGFBPs). We have used primary cultured rat hepatocytes maintained under serum free conditions to explore the regulatory role of various hormones on hepatic IGF-I and IGFBP-1 mRNA levels. IGF-I mRNA levels were stimulated 2.0 to 2.5 fold by bovine growth hormone (bGH) and 1.8 to 2.0 fold by glucagon but on combining bGH and glucagon, a synergistic effect was observed and IGF-I mRNA level was augmented 10 to 12 fold. Octreotide blocked the hGH induced stimulation of IGF-I production in serum and hepatic IGF-I mRNA levels in hypophysectomized rats. This effect could have been partly due to the low levels of glucagon in serum when hypophysectomized rats were treated with hGH and octreotide. Octreotide was also found to inhibit GH stimulated IGF-I mRNA levels in rat hepatocytes. The unique synergy observed with glucagon and bGH on IGF-I mRNA levels in hepatocytes was not reproduced by T$ sb3$, oPRL, dexamethasone, EGF or insulin when each was added in combination with bGH or glucagon. Like glucagon, the addition of IBMX or (Bu)$ sb2$cAMP stimulated IGF-I mRNA levels 1.8 to 2.0 fold, but in the presence of bGH, IGF-I mRNA levels were stimulated 10 to 12 fold. PMA stimulated IGF-I mRNA levels 1.2 to 1.4 fold but displayed no synergism when added with bGH. The stimulatory effect of bGH plus glucagon on IGF-I mRNA levels was inhibited in PKC depleted cells, in the presence of inhibitors of PKC and in the presence of cycloheximide. bGH had no posttranscriptional effect on IGF-I mRNA stability whereas glucagon or (Bu)$ sb2$cAMP stabilized IGF-I mRNA at a posttranscriptional level. In summary, the major hormonal regulators of hepatic IGF-I mRNA levels appear to be GH and glucagon. Hepatic IGF-I mRNA levels are regulated by pathways involving protein kinase C and, protein kinase A as well as by synthesis of one or more protein(s). Glucagon and dexamethasone each stimulated IGFBP-1 mRNA levels 3 to 4 fold whereas bGH and T$ sb3$ each inhibited IGFBP-1 mRNA levels 45 to 70%. Insulin, which inhibited IGFBP-1 mRNA levels 95%, was the most powerful inhibitor and was also found to inhibit IGFBP-1 mRNA levels in the presence of dexamethasone. IBMX and (Bu)$ sb2$cAMP stimulated IGFBP-1 mRNA levels 6 to 8 fold whereas PMA inhibited IGFBP-1 mRNA levels 40 to 50%. The inhibitory effect of bGH on IGFBP-1 mRNA levels was abolished in PKC depleted cells and also in the presence of inhibitors of PKC. In the presence of cycloheximide, IGFBP-1 mRNA was superinduced by bGH. bGH had no posttranscriptional effect on IGFBP-1 mRNA whereas glucagon and (Bu)$ sb2$cAMP stabilized IGFBP-1 mRNA at a postranscriptional level. In summary, bGH, T$ sb3$ and insulin inhibited whereas dexamethasone and glucagon stimulated IGFBP-1 mRNA levels in hepatocytes. Effect of glucagon may be via elevation of cAMP levels, whereas the effect of bGH may be via activation of PKC levels. The inhibitory effect of bGH appears to require synthesis of one or more protein(s) besides stimulation of PKC levels.

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21

Zhang, Fenz. "Regulation of erythropoiesis in a murine model of chronic renal failure : the relative role of erythropoietin and insulin-like growth factor 1." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=69733.

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Anemia is an almost invariable manifestation of chronic renal failure (CRF) and it often contributes substantially to the morbidity of the condition. In its uncomplicated form, this anemia is due primarily to reduced production of erythropoietin (EPO) by the diseased kidney. The present study was carried out in order to determine the relative role in the anemia secondary to CRF of EPO and insulin-like growth factor-1 (IGF-1), a recently recognized important regulatory factor of erythropoiesis in the normal physiological state. A mouse model of CRF was employed in this investigation. Six weeks after the surgical induction of renal failure, the mice were characterized in terms of biochemical and hematological parameters which included the response to a 3-week treatment with recombinant human EPO (r-HuEPO). Additionally the kidneys, liver and bone marrow were harvested for the determination of the mRNA expression of EPO and IGF-1 as assessed by the reverse transcription polymerase chain reaction followed by Southern blotting. Normal mice and mice rendered anemic by phlebotomy were included in all experiments. (Abstract shortened by UMI.)

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22

Lemmey, Andrew Bruce. "Effects of insulin-like growth factors (IGFS) on recovery from gut resection in rats : a thesis submitted to the University of Adelaide, South Australia for the degree of Doctor of Philosophy." 1992, 1993. http://web4.library.adelaide.edu.au/theses/09PH/09phl554.pdf.

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Includes bibliographical references (leaves 159-213) Shows that IGF-I peptides are effective in diminishing post-surgical catabolism and enhancing adaptive gut hyperplasia in rats recovering from massive small bowel resection.

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23

Scamurra, Ronald W. "Development of a technique for measuring insulin-like growth factor-I in swine:application to the study of the IN VIVO and IN VITRO effects of growth hormone in neonatal pigs." Thesis, Virginia Polytechnic Institute and State University, 1986. http://hdl.handle.net/10919/91042.

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The relationship between porcine growth hormone (pGH) and insulin-like growth factor-I (IGF-I) in swine was investigated. IGF-I levels were measured by radioimmunoassay (RIA) with an antisera specific for human IGF-I after ultrafiltration of acidified samples. Ultrafiltration quantitatively separated carrier proteins and IGF-I. Failure to separate these species interfered with the RIA. Using this assay, swine chronically treated with pGH had 2.6-fold higher sera levels of IGF-I than controls, whereas, serum IGF-I from a hypophysectomized animal was only 4% that of normal animals. The ultrafiltration procedure was incorporated into a protocol to measure IGF-I in sera from neonatal swine treated with pGH (5O ug •kg BWt⁻¹•d⁻¹). Treatment of neonatal pigs with pGH for one or two weeks elevated pGH in sera, but did not significantly affect either growth or serum IGF-I concentrations. Preliminary studies were performed to determine if neonatal swine hepatocytes secreted IGF-I in vitro. Results indicated that neonatal hepatocytes synthesized limited quantities of IGF-I that approached the detection limits of the RIA. Furthermore, pGH did not stimulate hepatocyte IGF-I synthesis in vitro or in vivo. Neonatal hepatocytes synthesized a protein species that bound labeled IGF-I and had a molecular weight similar to a carrier protein in swine serum. Estimation of the rate of carrier protein synthesis suggested that IGF-I and carrier proteins are coordinately regulated in isolated neonatal hepatocytes. These results suggest that IGF-I is not inducible in the neonatal pig by GH therapy and that growth in neonatal swine is either maximal or GR-independent. M.S.

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24

Milliken, Laura Ann 1970. "Bone mineral density, bone remodeling, insulin-like growth factors, hormone replacement therapy, and exercise training in postmenopausal women." Diss., The University of Arizona, 1998. http://hdl.handle.net/10150/282746.

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Osteoporosis is a condition of reduced bone mineral density (BMD) resulting in an increased susceptibility to bone fractures. The purpose of this study was to determine the effects of 12 months of weight bearing and resistance exercise on BMD, bone formation, measured by serum osteocalcin (OC) and bone resorption, measured by urinary excretion of deoxypyridinoline crosslinks (Dpd), in 2 groups of postmenopausal women who were either taking or not taking hormone replacement therapy (HRT). Secondary aims were to characterize the changes in insulin-like growth factors-l and -2 (IGF-l and -2) and IGF binding protein 3 (IGFBP3) in response to exercise training, and to determine the contribution of these growth factors in predicting changes in bone mineral density in the 2 populations of postmenopausal women. Women who were three to ten years postmenopausal and aged 40-65 years were included in the study. Women in HRT and no HRT groups were randomized into the exercise intervention resulting in four groups: (1) women not taking HRT, not exercising; (2) women taking HRT, not exercising; (3) women exercising, not taking HRT; and (4) women exercising, taking HRT. The number of subjects per group after one year was 27, 21, 25, and 16, respectively. Exercise training and HRT increase BMD similarly at most BMD sites whereas the combination of exercise and HRT produced increases in BMD greater than either treatment alone. Bone remodeling was surpressed in the groups taking HRT regardless of exercise status. The bone remodeling response to exercise training in women not taking HRT was not significantly different from those not exercising but the direction of change suggests an elevation in bone remodeling in response to exercise training. Exercise training does not stimulate a change in IGF-1, IGF-2, IGF-1:IGF-2, and IGFBP3. Markers of bone remodeling and IGF-1 are significant predictors of BMD changes but the overall amount of variation in BMD changes accounted for is low. Exercise and HRT status were significant predictors of changes in BMD even after accounting for variation due to bone remodeling indicating that bone changes are regulated by factors not addressed in this study.

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25

Van, Renen Margaret Jean. "Effects of GH on the IGF's and IGFBP's in children with chronic renal failure and transplantation /." Title page, contents and abstract only, 1996. http://web4.library.adelaide.edu.au/theses/09MD/09mdv274.pdf.

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26

Greer, Katarina Brenkusova. "THE ROLE OF THE INSULIN GROWTH FACTOR FAMILY IN DEVELOPMENT OF BARRETT’S ESOPHAGUS: A CASE-CONTROL STUDY." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1244125383.

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27

Castellanos, Amber. "The Role of IGF-1 In Geriatric Skin." Wright State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=wright1588759288275605.

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28

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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29

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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30

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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31

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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32

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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33

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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34

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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35

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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36

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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37

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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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

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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42

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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43

Heinichen, Markus Gerd. "Insulin-like Growth Factor-1, Mechano Growth Factor und Myosin Schwerketten Transformation beim Krafttraining." [S.l. : s.n.], 2006. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-55900.

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44

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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45

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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46

Ferguson, Rhea. "The role of insulin-like growth factor-I and insulin-like growth factor binding protein-3 in the development of cervical squamous intraepithelial lesions." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=95203.

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Abstract Objectives: Higher levels of circulating insulin-like growth factor-I (IGF-I) and lower levels of its binding protein (IGFBP-3) have been linked to an increased risk of certain epithelial cancers. It is unclear whether IGF-1 plays a similar role in the development of cervical squamous intraepithelial lesions (SIL). I investigated the association between circulating levels IGF-1 and IGFBP-3 and development of SIL. Methods: Blood serum samples from a nested case-control study were analyzed. Two controls were age and risk-set matched to each case. Conditional logistic regression was used for the statistical analysis and potential confounders, such as age, education, salary and smoking history were included in the model. Results: While the odds ratios of higher quartiles of circulating IGF-1 showed a higher risk of developing SIL, as compared to baseline, none of the associations were significant. The same was found for both IGFBP-3 and the molar ratio IGF-1:IGFBP-3. Conclusions: IGF-1 and IGFBP-3 may play at most a minor role in the development of cervical SIL. Objectifs: Des niveaux élevés de circulation du facteur de croissance analogue à l'insuline (IGF-I) et des niveaux inférieurs de sa protéine de liaison (IGFBP-3) sont associés à un risque accru de certains cancers épithéliaux, mais leur rôle dans le développement lésions squameuses intraépithéliales cervicales (SIL) demeure incertain. L'association entre les taux circulatoires d'IGF-1 et d'IGFBP-3 et le développement de SIL a été évaluée. Méthodes: Des échantillons de sérum sanguin d'une étude cas-témoins nichée dans une cohorte ont été analysés. Deux sujets du groupe contrôle ont été pairés quand à l'âge et certains facteurs de risque à chaque cas. L'analyse statistique a été effectuée par régression logistique conditionnelle. Résultats: Bien que les rapports de cotes des quartiles supérieurs d'IGF-1, d'IGFBP-3 et le rapport molaire IGF-1: l'IGFBP-3 suggèrent un risque accru de développer des SIL, par rapport aux valeurs initiales, aucune des associations ne sont statistiquement significatives. Conclusions: IGF-1 et IGFBP-3 pourraient jouer tout au plus un rôle mineur dans le développement de SIL du col de l'utérus.

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47

Jones, Tiffany Celeste. "Syndecan-4 binds insulin-like growth factor binding protein-4." Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2010r/jones.pdf.

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48

Bagley, Christopher James. "Analogues of Insulin-Like Growth Factor-1 / Christopher James Bagley." Title page, table of contents and summary only, 1989. http://web4.library.adelaide.edu.au/theses/09PH/09phb146.pdf.

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49

Horn, Henrik von. "Regulation of insulin-like growth factor-II in human liver /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-880-0/.

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50

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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Tesis sobre el tema "Insulin-like growth factor I Physiology"

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