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Dissertations / Theses on the topic 'Insulin role in lactation'

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Published: 4 June 2021

Last updated: 16 February 2022

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1

Jones, R. G. "The role of insulin in short-term regulation of mammary-gland lipogenesis : Its relevance to substrate partitioning during lactation." Thesis, University of Oxford, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382547.

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2

Deleo, Domenica. "Structure and function of the insulin receptor: its role during lactation and foetal development." Curtin University of Technology, School of Biomedical Sciences, 1994. http://espace.library.curtin.edu.au:80/R/?func=dbin-jump-full&object_id=14833.

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Prior to the commencement of this study in 1990, a number of reports had appeared in the literature describing the importance of insulin action during lactation in mammals (see Chapter 1). These studies investigated the changes in circulating insulin and glucagon concentrations during lactation, the relative numbers of insulin receptors in insulin-sensitive tissues, and glucose utilisation by these tissues. However, at that time, no information was available on the structure of the mammary insulin receptor. The rationale for undertaking this study was to characterise the structure of the rat mammary insulin receptor as a means of furthering our understanding of the role insulin plays during lactation.An initial requirement of this study was the development of a method for the convenient and inexpensive preparation of A14-tyrosyl[125I]iodoinsulin. A14-tyrosyl[125I]iodoinsulin displays binding characteristics which are virtually indistinguishable from the native hormone, which is a necessary requirement for tracers which are to be used in binding studies. In Chapter 2, I describe a method for the purification of A14-tyrosyl[125I]iodoinsulin from a mixture of iodinated insulin molecules which are produced following oxidation by chloramine-T in the presence of Na125iodine. In this method I employed disposable cartridges packed with a C18 support matrix to which the iodinated insulin molecules are readily adsorbed when in an aqueous solution.A 14-tyrosyl[125I]iodoinsulin absorbed most strongly to the C18 matrix and unwanted products were removed through a sequence of washes prior to the elution of the A14-tyrosyl[125I]iodoinsulin derivative using a buffer containing 50% (v/v) acetonitrile. This prodct was unambiguously shown to be A14-tyrosyl[125I]iodoinsulin by N-terminal amino acid sequencing. The quality of this radiolabel compared favourably with commercially ++
available A14-tyrosyl[125I]iodoinsulin preparations both in terms of specific activity and stability upon storage at -20C. Furthermore, a modified method based on this protocol has been used in our and other laboratories for the isolation of other iodinated peptides with highly satisfactory results.I have established that the size of the a-subunit of the rat mammary insulin receptor is significantly diminished compared with the liver insulin receptor (125 kDa versus 130 kDa). This difference in size was present throughout all stages of lactation and was not due to proteolysis of a larger form. Furthermore, I demonstrated that both the mammary and liver insulin receptor a-subunits migrated equally on PAGE following treatment with neuraminidase, indicating that the apparent size difference may be accounted for by a variation in the extent of receptor sialation. Treatment of the mammary insulin receptor a-subunit with glycopeptidase F demonstrated that the size of the aglycoreceptor (100 kDa) was similar to that described for insulin receptors from other insulin-sensitive tissues.I characterised the distribution of mRNA encoding the two, naturally-occurring insulin receptor isoforms in mammary tissue throughout all stages of pregnancy and lactation. These insulin receptor isoforms differ due to the absence (IR-A) or presence (IR-B) of a 12 amino acid peptide, encoded by exon 11 of the insulin receptor gene, and located near the C-terminus of the insulin receptor a-subunit. Mammary tissue predominantly expressed IR-A mRNA in contrast to liver tissue, which almost exclusively expressed IRB mRNA. Furthermore, the ratio of IR-A to IR-B mRNA in mammary tissue changed significantly during the first week post-partum whilst the distribution of IR-A and IR-B mRNA in the liver remained constant throughout pregnancy and lactation. This difference in insulin receptor isoform ++
expression between mammary and liver tissue also contributed to the estimated size difference between the insulin receptor a-subunits from these two tissues. In addition, I characterised the expression of IR-A and IR-B mRNA in several different tissues obtained from rats on day 14 of gestation through to 7 days post partum. I established that the splicing mechanism is functional at least as early as day 14 of gestation, suggesting a possible role for the preferential expression of a particular insulin receptor isoform during organogenesis. I observed that IR-A mRNA was the predominant isoform in all foetal tissue studied, and the proportion of this isoform declined as the animal matured. These changes were significant in cardiac muscle, kidney and most dramatic in the liver where the expression of IR-A mRNA changed from 53% in the 21 day old foetus (the day before parturition) to 13% in the 1 day old neonate. These results suggest that the splicing mechanism which generates the receptor isoforms is subject to acute hormonal and/or metabolic control.The current literature suggests that the carbohydrate moieties of the insulin receptor affects its affinity for insulin. Furthermore, the IR-A and IR-B isoforms have been shown to display a 2-fold difference in their insulin binding affinity when expressed in heterologous cell lines such at CHO cells or Rat-1 fibroblasts. Since both glycosylational and isoform distribution differences were evident between mammary and liver tissues, the insulin binding affinities of these receptors were compared. Estimates of the binding affinity parameters were performed at both 4 C and 37 C. At both temperatures the equilibrium binding constants for mammary and liver tissues were not significantly different suggesting that structural variations of the mammary insulin receptor had no effect on the insulin binding affinity under the ++
conditions described in this study. Comparison of the 4 C and 37 C binding data showed that the mammary insulin receptor exhibited complex, temperature-dependent binding characteristics, similar to those previously described for the liver insulin receptor, and entirely consistent with the presence of a temperature-dependent regulatory protein that affects insulin binding.

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3

Metcalf, J. A. "The effect of insulin on glucose metabolism during lactation in the ewe." Thesis, University of Newcastle Upon Tyne, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.378850.

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4

Knights, Penelope Anne. "Magnesium status in normal and diabetic pregnancy : pregnancy outcome and lactation." Thesis, University of Wolverhampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263332.

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5

Kim, Tae-gyu. "Effects of #beta#-casomorphins on metabolism of dairy cows." Thesis, University of Glasgow, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301620.

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6

Tavare, J. M. "The insulin receptor and insulin stimulated protein kinase : Their role in insulin action." Thesis, University of Bristol, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.370675.

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7

Almutairi, Mohammed Mashari. "Role of Bumetanide on Insulin Secretion." Wright State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=wright1408377608.

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8

Denis, RaphaeÌˆl Georges Philippe. "Role of the leptin-hypothalmic axis in the hyperphagia of lactation." Thesis, University of Liverpool, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268899.

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9

Basson, Annelie. "Circulating glucose responses in early lactation dairy cows to dietary restriction and rbST treatment." Diss., University of Pretoria, 2008. http://hdl.handle.net/2263/28939.

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Galactopoietic effects of somatotropin are the result of IGF-I and require high-quality nutrient intake. This study investigated short-term partitioning effects during recombinant bovine somatotropin (bST) administration in high yielding early lactation dairy cows. Administration of recombinant bST has been shown generally to alter results of metabolic tests in the face of unchanged basal glucose and insulin concentrations. Ten multiparous Holstein cows were subjected to rbST (Lactotropin®) and/or feed intake restriction to 80% of predicted ME requirement (80% ME). Responses to insulin challenge (0.1 IU porcine insulin/kg BW. 210 min) and hyperglycaemic clamp (+50 mg/dL whole blood, 120 min) were tested during weeks 8 (control), 9 (rbST ), 11 (80% ME) and 12 (rbST + 80% ME) postpartum. Plasma and whole blood samples were assayed for glucose concentrations. The rbST treatment decreased fasting whole-blood glucose concentration by 9.4% (P<0.0001), which was likely a remnant of control hyperglycaemia. Maximum glucose response was 4.0 mg/dL (21.7%) lower (P<0.0038) and took 6.5 minutes longer to attain (P<0.0037). Steady-state glucose infusion rate (SSGIR) decreased by 8.1 % (P<0.0001). The 80% ME treatment decreased glucose availability by 5 to 6% (P<0.0100), while no glucose responses were affected. Restricted energy intake during treatment with rbST resulted in plasma glucose increase by 5.5% (P<0.0001). Peripheral uptake and utilization of glucose increased by 5.1 % (P<0.0005). Compared to energy restriction, 80%ME + rbST did not alter effects of nutrient restriction on responses to exogenous insulin challenge. Effects were small and inconsistent. SSGIR decreased by 5.0% in the 80% ME + rbST compared to the 80% ME period (P<0.0004) and the change in the hyperglycaemic clamp in the absence of an effect in the insulin challenge may be due to differences in endogenous insulin secretion. The conclusion was that rbST treatment resulted in altered glucose metabolic responses, even with restricted energy intake.
Dissertation (MSc(Agric))--University of Pretoria, 2008.
Animal and Wildlife Sciences
unrestricted

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10

Hoppa, Michael Blake. "The role of calcium in Insulin exocytosis." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.510976.

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11

Ribó, Gené Sílvia. "Role of early postnatal nutrition during lactation in offspring metabolic health programming." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/462066.

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Childhood obesity and overweight can often cause severe complications, including hypertension, dyslipidemia, insulin resistance, type 2 diabetes, and non-alcoholic fatty liver disease, amongst other disorders. Several studies have shown that early postnatal nutrition is of great importance in modulating newborn health outcomes. In this work, we have studied the role of nutrition during early stages of life in long-term metabolic health applying two different approaches: a) transgenerational transmission of impaired metabolic health induced by accelerated early weight gain caused by postnatal overnutrition and b) short and long-term metabolic effects on offspring of maternal diet supplementation with betaine. Rapid weight gain during early life has been associated with several components of the Metabolic Syndrome. Previously we developed a mouse model of neonatal overfeeding and rapid weight gain by litter size reduction. Neonatal overnutrition (ON) altered the metabolism of the exposed individuals (F0). Furthermore, offspring (F1) and grand-offspring (F2) of postnatal overfed male mice also developed metabolic complications during adulthood. In agreement, it has been shown that environmental exposure on males can affect health in subsequent generations. Here, we hypothesized that epigenetic modifications, including DNA methylation, histone modifications, and noncoding-RNA, might be involved in the inheritance of diabetes risk in our model. We analyzed sperm methylome of F0 and F1 generations, and in the liver of 8-day-old mice of F1 and F2 generations, observing significant changes in methylation of specific DNA regions. We found 912 probes differentially methylated when comparing control and ON mice throughout the three generations, between the two tissues. Our results suggest that methylation of the male germ line caused by nutritional challenges during early life may carry information that influence metabolism across multiple generations. We then analyzed gene expression by qPCR of these genes in the liver of 8-days-old mice finding differences in some genes. Breast milk composition is important in modulating growth and health of the infant. Amongst the many nutrients that breast milk contains one worth highlighting is glycine betaine (or betaine). In addition to decreasing levels of fat in the liver, previous data demonstrated that maternal supplementation with betaine during breastfeeding also improves glucose homeostasis and modulates offspring early-life gut microbiota composition. Gut microbiota in the newborn is defined at birth and during early nutrition. Breast milk also contains essential bacteria that can influence gut microbiota composition of the breastfed infant. Changes in the microbiome caused by antibiotic administration during early life were significantly correlated to higher adiposity and development of obesity during adulthood. We observed beneficial short and long-term metabolic effects of betaine on offspring and protection against adult diet-induced obesity. We have analyzed ilea and gut microbiota of mice supplemented with betaine, and with or without antibiotics at different stages of life. Analyzing the microbiome we found that microbial community composition was modulated by betaine supplementation in 2-week-old offspring. Antibiotic treatment annulled completely long-term betaine-induced effects on body weight. Moreover, glucose tolerance was no longer improved when combining antibiotics with betaine treatment.
L'obesitat i el sobrepès infantil poden causar sovint complicacions greus en la salut, incloent hipertensió, dislipèmia, resistència a la insulina, diabetis tipus 2 i esteatosis hepàtica no alcohòlica, entre d’altres. Diversos estudis han demostrat que la nutrició post-natal precoç és de gran importància en la modulació de la salut del nounat. En aquesta tesis, hem estudiat el paper de la nutrició durant les primeres etapes de la vida en la salut metabòlica a llarg termini aplicant dos enfocaments diferents: a) efectes metabòlics de suplementar de la dieta materna durant la lactància amb betaïna sobre la descendència a curt i llarg termini i b) transmissió transgeneracional del fenotip d’intolerància a la glucosa induïda per un augment accelerat de pes en etapes primerenques de la vida, causat per l'excés de nutrició post-natal. La composició de la llet materna és important per modular el creixement i la salut metabòlica de l'infant. Entre els nutrients que conté la llet materna, cal destacar la glicina betaïna (o betaïna). A més de disminuir els nivells de greix en fetge, diverses publicacions demostren que suplementar la dieta materna amb betaïna durant la lactància també millora l'homeòstasi de la glucosa i modula la composició de la microbiota intestinal del nounat. Al suplementar amb betaïna l’aigua de femelles durant la lactància vam observar efectes beneficiosos en la descendència a nivell metabòlic a curt i llarg termini. També vam poder observar que la betaïna protegia contra l'obesitat induïda per una dieta rica en greixos en l’etapa adulta. Se sap que la llet materna també conté bacteris essencials que poden influir en la composició de microbiota intestinal del lactant. S'ha analitzat la microbiota de l’ili i cec de ratolins suplementats amb betaïna, i amb o sense antibiòtics en diferents etapes de la vida. Analitzant el microbioma trobem que la composició de la comunitat microbiana dels ratolins de dues setmanes de vida estava modulada per la suplementació de betaina. Els canvis en el microbioma causats per l'administració d'antibiòtics durant la lactància estan significativament correlacionats amb una major adipositat i risc de desenvolupar obesitat durant l'edat adulta. El tractament amb antibiòtics en els nostres ratolins va anul·lar els efectes induïts per betaïna a llarg termini sobre el pes corporal. A més, la tolerància a la glucosa no estava millorarada quan es combinaven els antibiòtics amb el tractament amb betaïna. L'augment ràpid de pes durant les primeres etapes de la vida s'ha associat a diversos components de la Síndrome Metabòlica en l’adult. Prèviament en aquest laboratori hem desenvolupat un model murí de sobrealimentació neonatal i augment de pes ràpid a partir d’una reducció de la mida de la ventrada. L'excés d'alimentació neonatal (ON) va alterar el metabolisme dels mascles exposats (F0). A més, els fills (F1) i els néts (F2) dels ratolins exposats a la sobrenutrició també van desenvolupar un metabolisme alterat durant l'edat adulta. En acord, s'ha demostrat que l'exposició ambiental sobre els mascles pot afectar la salut de generacions posteriors. Així, ens vam plantejar que les modificacions epigenètiques, incloses la metilació de l'ADN, les modificacions de l'histona i l'ARN no codificant, podrien estar implicades en l'herència del risc de diabetis en el nostre model. Es va analitzar el metilma d’esperma de les generacions F0 i F1, i el metiloma de fetges de ratolins de 8 dies d'edat de les generacions F1 i F2, observant canvis significatius en la metilació de regions específiques d'ADN. Al comparar els ratolins control amb ON de cada generació i teixit, vam trobar 912 sondes diferentment metiladas. Els nostres resultats suggereixen que la metilació de la línia germinal masculina provocada per reptes nutricionals durant etapes primerenques de la vida pot portar informació que influeixi en el metabolisme en les següents generacions.

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12

Baba, Reizo, Masaaki Koketsu, Masami Nagashima, Akiko Tamakoshi, and Hiroshi Inasaka. "Role of Insulin Resistance in Non-Obese Adolescents." Nagoya University School of Medicine, 2010. http://hdl.handle.net/2237/14178.

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13

Holt, L. J. "The role of Grb10 in insulin receptor signalling." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604199.

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To facilitate the study of Grb10 function, polyclonal antibodies were produced. They were directed against the SH2 domain of Grb10, which is common to all isoforms. The purified antibody was highly specific for Grb10 and able to detect both mouse and human forms of the protein. To examine the effects of Grb10 proteins on the insulin signalling pathway, they were expressed exogenously in CHO-T cells, in both a transient and stable manner. Comparison were made of the mouse and human isoforms of Grb10 at the genomic, RNA and protein levels. Differential expression of isoforms was observed in murine cells. Use of the information generated by the Human Genome Project allowed the genomic organisation of the human Grb10 isoforms to be determined. Bioinformatics tools were also employed to predict binding motifs and phosphorylation sites within Grb10. These elucidated similarities between the isoforms, and differences, in their potential regulation. In examining its effects on the insulin signalling system in CHO-T cells, hGrb10x was shown to associate with the activated insulin receptor in a rapid and sustained manner. Various isoforms of Grb10 bound equally well to the receptor. The global tyrosine phosphorylation state of the insulin receptor was not altered in the presence of hGrb10x. However, insulin-stimulated activation of IRS-1 and ERK were inhibited. The tyrosine phosphorylation state of a broad array of proteins was also affected by the expression of hGrb10x in CHO-T cells. hGrb10x induced an apparent increase in total IRS-1 protein level. The studies presented in this thesis are consistent with hGrb10x acting as a negative regulator of the insulin signalling pathway in CHO-T cells.

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14

Ling, Alisha Viva. "The Role of Hepatic FoxO1 in Insulin Resistance." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17463131.

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Metabolic syndrome is a major health concern in the US, affecting a third of all adults and amplifying the risk of cardiovascular disease and diabetes. The central pathophysiological root of metabolic syndrome is widely considered to be insulin resistance, though the mechanisms linking insulin resistance to this clinical constellation of obesity, dyslipidemia, hypertension and hepatic steatosis are poorly understood. In insulin resistance, insulin suppression of the forkhead box protein O1 (FOXO1) transcription factor is lost, and FoxO1 remains inappropriately over-active. FoxO1 has an established role activating gluconeogenesis, however, its regulation of lipid metabolism, especially of cholesterol metabolism, has remained largely unstudied. Here, we investigate the role of hepatic FoxO1 in mediating the dysregulation of lipid metabolism. Using a mouse model liver-specific knockout of the insulin receptor and FoxO1, we show that loss of hepatic FoxO1 restores normal gene expression of gluconeogenic and cholesterologenic, but not lipogenic genes. We identify Cyp8b1 as a target of exquisitely sensitive control by FoxO1. Cyp8b1 expression is increased in a mouse model of metabolic syndrome and decreased with acute knockdown of FoxO1, and also increased in humans with metabolic syndrome. Via Cyp8b1, FoxO1 controls cholic acid synthesis, which in turn increases dietary cholesterol absorption, intrahepatic cholesterol, and secretion of FGF15 and GLP1 from the small intestine. To confirm this extrahepatic role of hepatic FoxO1 as a regulator of cholesterol metabolism, we re-introduced CYP8B1 in the absence of FoxO1. To further investigate the well-documented association between insulin resistance and cardiovascular disease, we used non-biased profiling methods to identify the enzyme flavin-containing monooxygenase 3 (Fmo3) to be a target of insulin. FMO3 produces trimethylamine N-oxide (TMAO), which has recently been suggested to promote atherosclerosis in mice and humans. We show that FMO3 is suppressed by insulin in vitro, increased in obese/insulin resistant mice, and increased in obese/insulin resistant humans. Knockdown of FMO3 in insulin-resistant mice suppressed FoxO1, and entirely prevented the development of hyperglycemia, hyperlipidemia, and atherosclerosis. Overall, this dissertation examines the role of hepatic FoxO1 as a potent mediator of the metabolic dysfunction in insulin resistance and metabolic syndrome, and the development of cardiovascular disease.
Medical Sciences

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15

Beith, Jennifer Lynn. "The role of insulin on beta-cell proliferation." Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/32143.

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A relative decrease in β-cell mass is key in the pathogenesis of type 1 diabetes, type 2 diabetes and in the failure of transplanted islet grafts. It is now clear that β-cell duplication plays a dominant role in the regulation of adult β-cell mass. Knowledge of the endogenous regulators of β-cell replication is therefore critical for understanding the physiological control of β-cell mass and for harnessing this process therapeutically. We have shown that physiological concentrations of insulin act directly on β-cells to promote survival. Whether insulin stimulates adult β-cell proliferation remains unclear. We tested this hypothesis using dispersed primary mouse islet cells double-labeled with BrdU and insulin antisera. Treating cells with 200 pM insulin significantly increased proliferation from a baseline rate of 0.15% per day. Elevating glucose from 5 mM to 15 mM did not significantly increase β-cell replication. β-cell proliferation was inhibited by somatostatin, as well as inhibitors of insulin signalling. Interestingly, inhibiting Raf-1 kinase blocked proliferation stimulated by physiological, but not super-physiological insulin doses. Insulin-stimulated MIN6 cell proliferation was dependent on both PI3-kinase/Akt and the Raf-l/MEK pathways. Examination of the effects of insulin and its receptor pathway on cell cycle molecules was inconclusive. Together, these results demonstrate for the first time that insulin, at physiological levels, can directly stimulate β-cell proliferation and that Raf-l kinase is involved in this process. These findings have significant implications for the understanding of the regulation of β-cell mass in both the hyperinsulinemic and insulindeficient states that occur in the various forms of diabetes.
Medicine, Faculty of
Cellular and Physiological Sciences, Department of
Graduate

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16

Caravaggio, Justin W. "Insulin Degrading Enzyme And Its Role In Atherosclerosis." Thesis, University of Ottawa (Canada), 2010. http://hdl.handle.net/10393/28818.

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The type-A scavenger receptor (SR-A) plays a major role in the uptake of modified lipoproteins leading to foam cell formation and fatty streak development in artery walls. Our lab previously showed that a peptide known as insulin degrading enzyme (IDE) is able to bind the SR-A cytoplasmic domain in vitro. The present study provides evidence that male low density lipoprotein receptor-null (LDLr-/-) mice on a high fat diet, generate significantly more atherosclerotic lesion in aortic root and the aortic intimal surface when reconstituted with IDE-null (IDE-/-) bone marrow derived cells compared to those reconstituted with wild type bone marrow. Total serum cholesterol and the LDLr cholesterol fraction was also significantly increased in male LDLr-/- mice reconstituted with IDE-/- bone marrow. Macrophages procured from IDE-/- mice showed no difference in uptake of modified LDL compared to wild type cells but may be able to accumulate more cholestertyl ester than wild type cells. Our findings reveal that IDE expression likely exerts an anti-atherogenic effect via cholesterol metabolism, although further in vitro experiments are required to elucidate an exact mechanism.

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17

Irshad-ul-Haq. "The role of insulin and insulin related factors on lipoprotein utilization by bovine luteal cells /." The Ohio State University, 1992. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487776210792447.

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18

Stairiker, Patricia A. "The role of cathepsin L in involution and the termination of lactation in the mouse mammary gland." Click here for download, 2006. http://wwwlib.umi.com/cr/villanova/fullcit?p1432836.

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19

Dai, Tong. "Differential role of CEACAM1 and CEACAM2 in insulin metabolism." Connect to full-text via OhioLINK ETD Center, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1139336269.

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Thesis (Ph.D.)--Medical University of Ohio, 2004.
"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Medical Sciences." Major advisor: Sonia M. Najjar. Includes abstract. Document formatted into pages: v, 217 p. Title from title page of PDF document. Bibliography: pages 158-216.

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20

Parpal, Santiago. "Mechanisms of insulin signaling and the role of caveolae /." Linköping : Univ, 2001. http://www.bibl.liu.se/liupubl/disp/disp2001/med684s.pdf.

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21

Tyler-Rubinstein, Nadia. "The role of insulin receptor substrate signalling in metabolism." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/54894.

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Background/Aims: In order to mediate a diverse range of growth and metabolic functions, insulin receptor substrate (IRS) proteins recruit a complex network of intracellular signalling molecules including PI3-kinase and the Grb2 adaptor protein. These studies proposed to answer the question to what extent are the different phenotypes observed in Irs1 and Irs2 knockout mice due to the loss of the whole protein or due to the loss of specific signalling interactions between IRS proteins and either p85 (the regulatory subunit of PI3K) or Grb2? Determining which interactions mediate which biological responses is of interest to our understanding of insulin resistance and its associated pathologies. Methods: The strategy utilised for these studies was to mutagenise the IRS proteins in vivo with specific signalling defects with the aim of disrupting IRS1 or IRS2 signalling via two major insulin mediated pathways, the PI3K-Akt axis and the Grb2-Ras-Raf-MAPK cascade. The phenotypes of the mice were assessed in five main areas: growth, glucose homeostasis, energy homeostasis, cognitive behaviour and fertility. Results: The IRS1-PI3K mutants presented with a severe growth-defect and acute insulin resistance, though through compensatory β-cell expansion maintained normal glycaemia. They were also lean with low circulating leptin levels and displayed a severe defect in learning and memory. IRS2-PI3K mutants were glucose intolerant and insulin resistant with a reduction in β-cell area that resulted in hyperglycaemia and onset of diabetes around 3-months of age. Additionally, the mice had increased fat mass and high circulating leptin levels. In contrast, the Grb2 mutants displayed normal metabolic phenotypes. Conclusion: The data presented here revealed a primary role for IRS signalling via PI3K in regulating metabolic functions. Both the IRS-PI3K mutants largely phenocopy the corresponding Irs knockout mice. In contrast, the Grb2 mutants appeared metabolically normal, suggesting a relatively minor role for IRS-Grb2 interactions in metabolic and growth control.

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22

Weimershaus, Mirjana Léona. "The Role of Insulin-Regulated Aminopeptidase in Cross-Presentation." Paris 5, 2011. http://www.theses.fr/2011PA05T036.

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L’aminopeptidase IRAP est localisée dans des endosomes du type de stockage dans divers types cellulaires. Dans les cellules dendritiques (CD), IRAP est impliquée dans l’élagage des ligands des molécules du CMH de classe I (CMH-I). L’absence d’IRAP provoque un défaut de la présentation d’antigènes internalisés sur le CMH-I (connue comme la “présentation croisée”). Par contre, IRAP n’est pas nécessaire dans les voies “classiques” de présentation antigéniques. Au vue de la colocalisation et interaction d’IRAP avec les CMH-I, nos observations suggèrent qu’IRAP marque un compartiment spécialisé à la dernière étape d’élagage et associations de peptides sur les CMH-I dans la présentation croisée. Nous avons pu mettre en évidence que ce compartiment, caractérisé par la présence de Rab14 et STX6, est fonctionnel dans les soustypes CD8+ et CD8- des CD. L’internalisation d’antigène est accompagné par le recrutement rapide des endosomes IRAP au phagosome. En l’absence d’IRAP la maturation phagosomale est accélérée, ce qui est manifesté par une acquisition plus rapide des marqueurs des endosomes tardifs et des lysosomes, ainsi qu’une dégradation plus importante de l’antigène. En conclusion, les endosomes d’IRAP ont au moins deux rôles distincts dans la physiologie des CD: l’elagage de peptides antigéniques et le ralentissement de la maturation phagosomale, un mécanisme connu pour être bénéfique pour la présentation croisée. La meilleure caractérisation des stimuli qui interviennent dans la mobilisation d’IRAP pourrait être pertinente pour mieux comprendre la régulation de différentes fonctions des CD, y compris la présentation antigénique
Insulin-regulated aminopeptidase (IRAP) localizes to storage-type endosomes in many non-immune and immune cell types. In dendritic cells (DCs), IRAP functions as trimming peptidase to generate peptide ligands for MHC class I molecules (MHC-I). Absence of IRAP led to a defect in the presentation of internalized antigen on MHC-I (referred to as cross-presentation) in vitro and in vivo. Importantly, IRAP was not required for the “classical” presentation pathways (i. E. Presentation of extracellular antigens on MHC-II as well as presentation of intracellular antigens on MHC-I). Further supported by the colocalization and physical interaction of MHC-I with IRAP, these observations suggest that IRAP marks a cross-presentation compartment in which final trimming and loading on MHC-I can take place. We show that this compartment, marked by STX6 and Rab14, is functional in both CD8+ and CD8- DC subsets. In DCs, upon antigen internalization, IRAP vesicles are rapidly recruited to the phagosome. Additional to its function in antigen trimming, IRAP seems to regulate phagosome dynamics. In IRAP-deficient cells, phagosome maturation was accelerated, as shown by the rapid acquirement of late endosomal and lysosomal markers to the phagosome and increased antigen degradation. Thus, IRAP endosomes have at least two important roles in the DCs physiology: the trimming of antigenic peptides and the delay of phagosome maturation that is beneficial for cross-presentation. Understanding the stimuli that regulate IRAP mobilization, and possibly cross-presentation, could be relevant in order to understand if and how DCs control their different functions, including antigen presentation

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23

Dai, Tong. "Differential Role of CEACAM Proteins in Regulating Insulin Metabolism." University of Toledo Health Science Campus / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=mco1139336269.

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24

Patel, Payal R. "A Role for CEACAM2 in Insulin Homeostasis and Action." University of Toledo Health Science Campus / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=mco1279320879.

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25

Alexander, Lindsey Ann. "The Role of Inflammation in Diet-Induced Insulin Resistance." University of Toledo / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1260808416.

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26

Andersen, Ditte K. "The role of microRNAs in skeletal muscle insulin resistance." Thesis, Royal Veterinary College (University of London), 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.701676.

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27

Camba-Colón, Joanna Irene Rosa. "Role of the maternal liver in lactating mice." Diss., [Riverside, Calif.] : University of California, Riverside, 2010. http://proquest.umi.com/pqdweb?index=0&did=2019822721&SrchMode=1&sid=2&Fmt=2&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1274111729&clientId=48051.

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Thesis (Ph. D.)--University of California, Riverside, 2010.
Includes abstract. Available via ProQuest Digital Dissertations. Title from first page of PDF file (viewed May 17, 2010). Includes bibliographical references. Also issued in print.

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28

Cleland, Stephen Jackson. "Insulin's role as a vascular hormone in health and disease." Thesis, University of Glasgow, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301835.

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29

Walker, Andrew Michael Nicholas. "Exploring the role of the insulin and insulin-like growth factor receptors in vascular regeneration and aging." Thesis, University of Leeds, 2017. http://etheses.whiterose.ac.uk/19117/.

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Insulin resistance is a key independent risk factor for cardiovascular disease. Our group has previously shown that the insulin-like growth factor-1 receptor (IGF-1R) is a negative regulator of insulin receptor (IR) signalling, by sequestering IR subunits in insulin resistant IR:IGF1R ‘hybrid receptors’. By crossing IR haploinsufficient (IRKO) mice with IGF-1R haploinsufficient (IGF1Rko) mice (producing “double knockout” or DKO mice), our group has previously demonstrated rescue of the endothelial dysfunction caused by insulin resistance. Whether this is associated with wider benefits in vascular biology or aging is unclear. Our hypothesis was that reduced expression of the IGF-1R in whole body insulin resistance would improve vascular repair and regeneration and prolong healthspan. Metabolic assessment included measurement of weight gain and glucose and insulin tolerance testing. We studied vascular repair and regeneration with in vivo models, complementing these studies with mechanistic work in vitro. 15 animals per group were aged until they met healthspan endpoints, with monitoring of metabolic status throughout. Glucose and insulin tolerance tests were similar in young DKO and IRKO mice, with DKO and IRKO having improved glucose tolerance and insulin sensitivity compared with WT and IGF1Rko when tested at ≥80 weeks of age. Body weight was significantly lower in young DKO than IRKO, with IRKO and DKO remaining lighter than WT and IGF-1Rko littermates as they aged. DKO had superior recovery after induction of hind-limb ischemia versus both IRKO and WT. Re- endothelialisation after denuding femoral artery wire injury was improved in the DKO group compared with IRKO. Healthspan was significantly prolonged in DKO versus WT. In conclusion, reduced IGF-1R expression improves vascular repair and regeneration in the context of whole-body insulin resistance, and also appears to promote healthy aging. Further work will aim to elucidate the possible mechanisms for these observations.

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30

Voisin, Daniel. "Le controle central du reflexe d'ejection de lait : mise en evidence du role du gaba." Toulouse 3, 1992. http://www.theses.fr/1992TOU31564.

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31

Obese, Frederick Yeboah. "Concentrations of insulin-like growth factor-I (IGF-I) and insulin-like growth factor binding protein-3 (IGFBP-3) in the plasma and milk of pasture-fed dairy cows in early lactation /." Connect to thesis, 2003. http://eprints.unimelb.edu.au/archive/00000549.

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32

Heinrich, Garrett. "A role for CEACAM proteins in energy balance and peripheral insulin action." Toledo, Ohio : University of Toledo, 2010. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1272976279.

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Dissertation (Ph.D.)--University of Toledo, 2010.
"Submitted to the Graduate Faculty as partial fulfillment of the requirements for the Doctor of Philosophy Degree in Biomedical Sciences." Title from title page of PDF document. "A Dissertation entitled"--at head of file. Bibliography: p. 37-41, 77-82, 102-107, 124-125, 153-160, 195-199, 221-254.

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33

Purushotham, Aparna. "Role of bioactive compounds in the regulation of insulin sensitivity." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1173108971.

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34

Ahmed, Zamal. "The role of SH2-BÎ± and APS in insulin signalling." Thesis, University of Nottingham, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269693.

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35

Mahood, I. Kim. "Glycated insulin and its role in the pathogenesis of diabetes." Thesis, University of Ulster, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274037.

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36

Suckow, Arthur T. "The role of synaptogenic synaptic adhesion molecules in insulin secretion." Diss., [La Jolla] : University of California, San Diego, 2010. http://wwwlib.umi.com/cr/ucsd/fullcit?p3390978.

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Thesis (Ph. D.)--University of California, San Diego, 2010.
Title from first page of PDF file (viewed Feb. 19, 2010). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 170-188).

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37

Kawamoto, Kazuyuki. "Role of Insulin-like growth factor-2 in colorectal cancer." Kyoto University, 1998. http://hdl.handle.net/2433/156995.

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本文データは平成22年度国立国会図書館の学位論文(博士)のデジタル化実施により作成された画像ファイルを基にpdf変換したものである
Kyoto University (京都大学)
0048
新制・課程博士
博士(医学)
甲第7548号
医博第2058号
新制||医||702(附属図書館)
UT51-99-A234
京都大学大学院医学研究科分子医学系専攻
(主査)教授下遠野邦忠, 教授日合弘, 教授今村正之
学位規則第4条第1項該当

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38

Alshahrani, Saeed. "Role of Na+K+2Cl¿¿¿¿¿¿ Co-transporters in Insulin Secretion." Wright State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=wright1347832847.

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39

Marchã, Penha Maria Alexandra [Verfasser], and Frank [Akademischer Betreuer] Schaeffel. "The Role of Insulin and Insulin Signaling in Eye Growth Regulation / Maria Alexandra Marchã Penha ; Betreuer: Frank Schaeffel." Tübingen : Universitätsbibliothek Tübingen, 2014. http://d-nb.info/1162897201/34.

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40

Fatani, Sameer Hasan M. "The effects of diet-induced obesity on metabolic and vascular functions : role of insulin signalling and insulin resistance." Thesis, University of Liverpool, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.437519.

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41

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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42

Kulkarni, Rohit N. "Role of regulatory peptides in the control of #beta#-cell function." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388123.

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43

Cowley, Elizabeth Asenath. "A study into the role of insulin and insulin-like growth factor I (IGF-I) in rat embryonic development." Thesis, University of Leicester, 1992. http://hdl.handle.net/2381/34313.

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Insulin, and the structurally related insulin-like growth factors (IGFs), are peptide growth factors believed to play a role in embryonic development. In addition to factors produced by the embryo, certain maternally derived growth factors may also be important during development. These are likely to act upon the extraembryonic membranes which surround the embryo throughout gestation, before they, or their breakdown products, are transported to the developing embryo. This thesis examines the processing of both insulin and insulin-like growth factor I (IGF-I) by the visceral yolk sac, an extraembryonic membrane in the rat. Both radiolabelled and fluorescently labelled ligands have been examined in 17.5 day yolk sacs, and their cultured equivalent. It appears that both factors are digested by this tissue very rapidly, which may involve receptor-mediated pinocytosis or surface digestion. Further, the role of the IGF-I receptor during rat embryonic development has been examined using a monoclonal antibody reported to block this receptor. When this antibody was applied to rat embryos cultured from 9.5 to 11.5 days of gestation, it resulted in growth retardation plus an associated increase in morphological abnormalities. These effects were largely reversed by the addition of an excess of IGF-I to the culture medium in the presence of this antibody, while the addition of insulin or IGF-II had no effect. In conclusion, receptors mediating insulin and IGF-I uptake appear to be present on the surface of the rat visceral yolk sac. The growth inhibition seen in the presence of the antibody also implicates that IGF-I plays a role in the normal development of post-implantation rat embryos.

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44

Stairiker, Patricia A. "The role of L in involution and the termination of lactation in the mouse mammary gland." Click here for download, 2007. http://proquest.umi.com/pqdweb?did=1075710531&sid=3&Fmt=2&clientId=3260&RQT=309&VName=PQD.

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45

Bode-Rhoads, Michelle Lynn. "Regulation of the growth hormone receptor, insulin-like growth factor (IGF) I and IGF binding protein 2 in reproductive tissues of dairy cattle during lactation and associated effects on fertility." free to MU campus, to others for purchase, 2004. http://wwwlib.umi.com/cr/mo/fullcit?p3164490.

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46

Lin, Jian-Man. "Islet insulin secretory patterns in diabetes and the role of UCP2." Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2989.

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During development of type 1 and type 2 diabetes plasma insulin patterns are altered. Since the islet insulin release pattern has been implicated in this development, insulin secretion from single islets was studied and linked to the islet protein levels of uncoupling protein-2 (UCP2). Islets were isolated from NOD- and KKA^y- mice, GK- and GK-derived congenic rats, which are animal models of diabetes, and three human subjects with type 2 diabetes. At basal glucose (3 mM), insulin release from such islets was pulsatile and the amount released was comparable to that of control islets. When the glucose concentration was raised to 11 mM insulin release was essentially unchanged in islets isolated from older NOD- and KKA^y- mice, GK- and Niddm1i congenic rats, and NIDDM persons. In islets from Niddm1f congenic rats, younger NOD- and KKA^y-mice, control animals and normal human donors the secretion rate increased 2-9 fold when the glucose concentration was raised. This rise in secretion was manifested as increase of the amplitude of the insulin oscillations without affecting their frequency. Impaired glucose-induced insulin release was associated with reduction in glucose oxidation measured in NOD-islets, unaffected respiration measured in GK-islets and higher protein level of UCP2 measured in KKA^y-islets. When the UCP2 amounts in KKA^y-islets were reduced by culture to those of control islets, glucose-induced insulin secretion was essentially normalized. Our studies suggest that the deranged plasma insulin patterns observed in diabetes are related to decrease in the amplitude of insulin oscillations from the islets rather than loss of the oscillatory activity. This reduction of pulse amplitude may be related to impaired glucose metabolism and/or increased mitochondrial uncoupling.

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47

Pinnameneni, Srijan Kumar, and s3083722@student rmit edu au. "Role of stearoyl-CoA desaturase1 in fatty acid-induced insulin resistance." RMIT University. Medical Sciences, 2006. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20070119.162450.

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Recent investigations suggest that reducing stearoyl CoA desaturase (SCD) 1 expression confers protection against obesity and insulin resistance, whereas others show that increasing SCD1 expression protects cells from lipotoxicity. The overall aim of this thesis was to establish the role of SCD1 expression in fatty acid metabolism and insulin stimulated glucose disposal in skeletal muscle. In vitro and in vivo studies were conducted to investigate the relationship between fatty acid subtype, SCD1 expression and fuel metabolism. The role of fatty acid subtype on fatty acid metabolite accumulation and insulin resistance was initially examined in rats. Rats were provided with a low fat diet or a high fat diet consisting of predominantly saturated (SAT) or polyunsaturated fatty acids (PUFA). Rats fed a SAT diet were insulin resistant and had increased skeletal muscle diacylglycerol content whereas rats fed a PUFA diet retained insulin sensitivity and accumulated triacylglycerol rather than diacylglycerol. Interestingly, SCD1 mRNA and protein content were elevated in SAT rats compared with PUFA fed and control fed rats, indicating a possible involvement of SCD1 in the aetiology of insulin resistance. Subsequently, SCD1 expression was examined in the skeletal muscle of various rodent models of genetic and diet-induced obesity. SCD1 content was consistently upregulated in the skeletal muscle of obese rodents. To determine whether SCD1 contributes to or protects from fatty-acid induced insulin resistance, SCD1 levels were transiently altered in L6 skeletal muscle myotubes. Short interfering (si) RNA was used to decrease SCD1 content and a pcDNA3.1/HygromSCD1 vector was introduced to increase SCD1 content. Reducing SCD1 protein resulted in marked esterification of exogenous fatty acids into diacylglycerol and ceramide. Insulin-stimulated Akt (acute transforming retrovirus thymoma) phosphorylation and 2-deoxyglucose uptake were reduced with SCD1 siRNA. Exposure of L6 myotubes to palmitate abolished insulin-stimulated glucose uptake in both control and SCD1 siRNA myotubes. Transient overexpression of SCD1 resulted in triacylglycerol esterification but attenuated ceramide and diacylglycerol accumulation and protected myotubes from fatty acid-induced insulin resistance. Further, these changes were associated with reduced phosphorylation of c-Jun Amino-Terminal Kinase (JNK) and the inhibitor of IêB kinase (IKK), both of which impair insulin signalling. These studies indicated that SCD1 protects from cellular toxicity in L6 myotubes by preventing excessive accumulation of bioactive lipid metabolites. Collectively, these experiments indicate that increasing SCD1 expression may be a protective mechanism designed to prevent insulin resistance in obese phenotypes.

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48

Shen, Yvonne Yun Hwa Clinical School St George Hospital Faculty of Medicine UNSW. "Insulin resistance in patients with kidney disease: the role of adiponectin." Awarded by:University of New South Wales. Clinical School - St George Hospital, 2009. http://handle.unsw.edu.au/1959.4/44567.

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The multifunctional glycoprotein, adiponectin has insulin-sensitising, anti-atherogenic and anti-inflammatory properties. However, despite the prevalence of both insulin resistance (IR) and vascular disease in patients with end-stage kidney disease (ESKD), I found levels of adiponectin in these subjects to be high. The high molecular weight (HMW) isoform of adiponeclin is thought to be the most insulin-sensitising form and binds to two receptors, adiponectin receptor 1 (AdipoR1) and adiponectin receptor 2 (AdipoR2). I found that both the proportion of the HMW moiety and AdipoR expression on peripheral blood mononuclear cells (PBMC) were increased in patients on haemodialysis, Further studies showed equivalent phosphorylation of AMP-kinase by recombinant adiponectin implying that AdipoR on PBMC from controls and patients with ESKD were equally functional. Thus, IR in ESKD was not explained by a change in isoform distribution nor by AdipoR down-regulation or dysfunction. Rather, this receptor-ligand axis is up-regulated and may be a beneficial response to the inflammatory milieu of ESKD After successful renal transplantation, IR (measured as HOMA-R) was lower compared to the group on haemodialysis and this coincided with lower levels of total adiponeclin, the absolute amount of the HMW isoform and of AdipoR on PBMCs. Lower AdipoR post-transplantation may be secondary to immunosuppression and/or an improvement in the glomerular filtration rate (GFR) and the uraemic milieu. Exposure to uraemic sera in vitro resulted in greater up-regulation of AdipoR on PBMC than that observed with sera from healthy controls. Uraemic sera fractionated by fast protein liquid chromatography {FPLC} showed siginificant up-regulation of AdipoR with each fraction. These results suggested that there may be multiple compounds in uraemic sera that up-regulate AdipoR on PBMC. However, there was discordant induction of AdipoR on PBMC from healthy controls in-vitro after exposure to uraemic sera in comparison to the "native" expression of AdipoR on PBMC from these same individuals with ESKD, This suggested that AdipoR expression is influenced by both serum and serum-independent factors. Functional AdipoR were also identified on cultured proximal tubular cells, Ligation of AdipoR by recombinant adiponectin on these cells increased phosphorylation of AMPK, and specifically down-regulated the secretion of monocyte chemoattractant protein-' (MCP-') showing that the adiponeetin/AdipoR system may also be involved in the regulation of inflammatory processes in the kidney. Together, these results show that adiponectin and its receptors may have a protective role in subjects with kidney disease and that these effects may extend to local effects within the kidney itself.

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49

Nickerson, Tara. "A role for insulin-like growth factor binding proteins in apoptosis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0022/NQ50229.pdf.

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50

Fryer, Lee George Daniel. "Studies into the role of glucose transporter function in insulin resistance." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265007.

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