Relevant bibliographies by topics / Insulin signaling-Resistance

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Academic literature on the topic 'Insulin signaling-Resistance'

Author: Grafiati
Published: 6 September 2023

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Journal articles on the topic "Insulin signaling-Resistance"

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Beale, Elmus G. "Insulin Signaling and Insulin Resistance." Journal of Investigative Medicine 61, no. 1 (January 1, 2013): 11–14. http://dx.doi.org/10.2310/jim.0b013e3182746f95.

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Martz, Lauren. "Signaling insulin resistance in obesity." Science-Business eXchange 2, no. 30 (August 2009): 1166. http://dx.doi.org/10.1038/scibx.2009.1166.

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Randriamboavonjy, V., and I. Fleming. "Insulin, Insulin Resistance, and Platelet Signaling in Diabetes." Diabetes Care 32, no. 4 (March 31, 2009): 528–30. http://dx.doi.org/10.2337/dc08-1942.

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Zick, Yehiel. "Insulin resistance: a phosphorylation-based uncoupling of insulin signaling." Trends in Cell Biology 11, no. 11 (November 2001): 437–41. http://dx.doi.org/10.1016/s0962-8924(01)02129-8.

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Zick, Yehiel. "Insulin resistance: a phosphorylation-based uncoupling of insulin signaling." Trends in Cell Biology 11 (November 2001): 437–41. http://dx.doi.org/10.1016/s0962-8924(01)81297-6.

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Horita, Shoko, Motonobu Nakamura, Masashi Suzuki, Nobuhiko Satoh, Atsushi Suzuki, and George Seki. "Selective Insulin Resistance in the Kidney." BioMed Research International 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/5825170.

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Insulin resistance has been characterized as attenuation of insulin sensitivity at target organs and tissues, such as muscle and fat tissues and the liver. The insulin signaling cascade is divided into major pathways such as the PI3K/Akt pathway and the MAPK/MEK pathway. In insulin resistance, however, these pathways are not equally impaired. For example, in the liver, inhibition of gluconeogenesis by the insulin receptor substrate (IRS) 2 pathway is impaired, while lipogenesis by the IRS1 pathway is preserved, thus causing hyperglycemia and hyperlipidemia. It has been recently suggested that selective impairment of insulin signaling cascades in insulin resistance also occurs in the kidney. In the renal proximal tubule, insulin signaling via IRS1 is inhibited, while insulin signaling via IRS2 is preserved. Insulin signaling via IRS2 continues to stimulate sodium reabsorption in the proximal tubule and causes sodium retention, edema, and hypertension. IRS1 signaling deficiency in the proximal tubule may impair IRS1-mediated inhibition of gluconeogenesis, which could induce hyperglycemia by preserving glucose production. In the glomerulus, the impairment of IRS1 signaling deteriorates the structure and function of podocyte and endothelial cells, possibly causing diabetic nephropathy. This paper mainly describes selective insulin resistance in the kidney, focusing on the proximal tubule.
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Chen, Li, Rui Chen, Hua Wang, and Fengxia Liang. "Mechanisms Linking Inflammation to Insulin Resistance." International Journal of Endocrinology 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/508409.

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Obesity is now widespread around the world. Obesity-associated chronic low-grade inflammation is responsible for the decrease of insulin sensitivity, which makes obesity a major risk factor for insulin resistance and related diseases such as type 2 diabetes mellitus and metabolic syndromes. The state of low-grade inflammation is caused by overnutrition which leads to lipid accumulation in adipocytes. Obesity might increase the expression of some inflammatory cytokines and activate several signaling pathways, both of which are involved in the pathogenesis of insulin resistance by interfering with insulin signaling and action. It has been suggested that specific factors and signaling pathways are often correlated with each other; therefore, both of the fluctuation of cytokines and the status of relevant signaling pathways should be considered during studies analyzing inflammation-related insulin resistance. In this paper, we discuss how these factors and signaling pathways contribute to insulin resistance and the therapeutic promise targeting inflammation in insulin resistance based on the latest experimental studies.
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Choi, Cheol S., Young-Bum Kim, Felix N. Lee, Janice M. Zabolotny, Barbara B. Kahn, and Jang H. Youn. "Lactate induces insulin resistance in skeletal muscle by suppressing glycolysis and impairing insulin signaling." American Journal of Physiology-Endocrinology and Metabolism 283, no. 2 (August 1, 2002): E233—E240. http://dx.doi.org/10.1152/ajpendo.00557.2001.

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Elevation of plasma lactate levels induces peripheral insulin resistance, but the underlying mechanisms are unclear. We examined whether lactate infusion in rats suppresses glycolysis preceding insulin resistance and whether lactate-induced insulin resistance is accompanied by altered insulin signaling and/or insulin-stimulated glucose transport in skeletal muscle. Hyperinsulinemic euglycemic clamps were conducted for 6 h in conscious, overnight-fasted rats with or without lactate infusion (120 μmol · kg−1 · min−1) during the final 3.5 h. Lactate infusion increased plasma lactate levels about fourfold. The elevation of plasma lactate had rapid effects to suppress insulin-stimulated glycolysis, which clearly preceded its effect to decrease insulin-stimulated glucose uptake. Both submaximal and maximal insulin-stimulated glucose transport decreased 25–30% ( P < 0.05) in soleus but not in epitrochlearis muscles of lactate-infused rats. Lactate infusion did not alter insulin's ability to phosphorylate the insulin receptor, the insulin receptor substrate (IRS)-1, or IRS-2 but decreased insulin's ability to stimulate IRS-1- and IRS-2-associated phosphatidylinositol 3-kinase activities and Akt/protein kinase B activity by 47, 75, and 55%, respectively ( P < 0.05 for all). In conclusion, elevation of plasma lactate suppressed glycolysis before its effect on insulin-stimulated glucose uptake, consistent with the hypothesis that suppression of glucose metabolism could precede and cause insulin resistance. In addition, lactate-induced insulin resistance was associated with impaired insulin signaling and decreased insulin-stimulated glucose transport in skeletal muscle.
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Boura-Halfon, Sigalit, and Yehiel Zick. "Phosphorylation of IRS proteins, insulin action, and insulin resistance." American Journal of Physiology-Endocrinology and Metabolism 296, no. 4 (April 2009): E581—E591. http://dx.doi.org/10.1152/ajpendo.90437.2008.

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Insulin signaling at target tissues is essential for growth and development and for normal homeostasis of glucose, fat, and protein metabolism. Control over this process is therefore tightly regulated. It can be achieved by a negative feedback control mechanism whereby downstream components inhibit upstream elements along the insulin-signaling pathway (autoregulation) or by signals from apparently unrelated pathways that inhibit insulin signaling thus leading to insulin resistance. Phosphorylation of insulin receptor substrate (IRS) proteins on serine residues has emerged as a key step in these control processes under both physiological and pathological conditions. The list of IRS kinases implicated in the development of insulin resistance is growing rapidly, concomitant with the list of potential Ser/Thr phosphorylation sites in IRS proteins. Here, we review a range of conditions that activate IRS kinases to phosphorylate IRS proteins on “hot spot” domains. The flexibility vs. specificity features of this reaction is discussed and its characteristic as an “array” phosphorylation is suggested. Finally, its implications on insulin signaling, insulin resistance and type 2 diabetes, an emerging epidemic of the 21st century are outlined.
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Li, Hongliang, Jiyeon Lee, Chaoyong He, Ming-Hui Zou, and Zhonglin Xie. "Suppression of the mTORC1/STAT3/Notch1 pathway by activated AMPK prevents hepatic insulin resistance induced by excess amino acids." American Journal of Physiology-Endocrinology and Metabolism 306, no. 2 (January 15, 2014): E197—E209. http://dx.doi.org/10.1152/ajpendo.00202.2013.

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Nutrient overload is associated with the development of obesity, insulin resistance, and type 2 diabetes. However, the underlying mechanisms for developing insulin resistance in the presence of excess nutrients are incompletely understood. We investigated whether activation of AMP-activated protein kinase (AMPK) prevents the hepatic insulin resistance that is induced by the consumption of a high-protein diet (HPD) and the presence of excess amino acids. Exposure of HepG2 cells to excess amino acids reduced AMPK phosphorylation, upregulated Notch1 expression, and impaired the insulin-stimulated phosphorylation of Akt Ser473 and insulin receptor substrate-1 (IRS-1) Tyr612. Inhibition of Notch1 prevented amino acid-induced insulin resistance, which was accompanied by reduced expression of Rbp-Jk, hairy and enhancer of split-1, and forkhead box O1. Mechanistically, mTORC1 signaling was activated by excess amino acids, which then positively regulated Notch1 expression through the activation of the signal transducer and activator of transcription 3 (STAT3). Activation of AMPK by metformin inhibited mTORC1-STAT3 signaling, thereby preventing excess amino acid-impaired insulin signaling. Finally, HPD feeding suppressed AMPK activity, activated mTORC1/STAT3/Notch1 signaling, and induced insulin resistance. Chronic administration of either metformin or rapamycin inhibited the HPD-activated mTORC1/STAT3/Notch1 signaling pathway and prevented hepatic insulin resistance. We conclude that the upregulation of Notch1 expression by hyperactive mTORC1 signaling is an essential event in the development of hepatic insulin resistance in the presence of excess amino acids. Activation of AMPK prevents amino acid-induced insulin resistance through the suppression of the mTORC1/STAT3/Notch1 signaling pathway.
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Dissertations / Theses on the topic "Insulin signaling-Resistance"

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Barber, Collin. "SIRT3: Molecular Signaling in Insulin Resistance." Thesis, The University of Arizona, 2014. http://hdl.handle.net/10150/315823.

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A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.
Post-translational modification of intracellular proteins through acetylation is recognized as an important regulatory mechanism of cellular energy homeostasis. Specific proteins called sirtuins deacetylate other mitochondrial proteins involved in glucose and lipid metabolism, activating them in metabolic processes. SIRT3 is a sirtuin of particular interest as it is found exclusively in mitochondria and has been shown to affect a variety of cellular metabolic processes. The activity of this enzyme is related to cellular insulin sensitivity. This study attempted to identify the relationship between insulin sensitivity and change in amount of SIRT3 following a bout of exercise in non-diabetic individuals. We find a moderate inverse correlation between insulin sensitivity and increase in SIRT3 abundance following exercise. This suggests that this protein may not be involved directly in cells’ ability to regulate energy homeostasis or that it may act through another mechanism not investigated in this study.
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Nyman, Elin. "Insulin signaling dynamics in human adipocytes : Mathematical modeling reveals mechanisms of insulin resistance in type 2 diabetes." Doctoral thesis, Linköpings universitet, Avdelningen för cellbiologi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-104725.

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Type 2 diabetes is characterized by raised blood glucose levels caused by an insufficient insulin control of glucose homeostasis. This lack of control is expressed both through insufficient release of insulin by the pancreatic beta-cells, and through insulin resistance in the insulin-responding tissues. We find insulin resistance of the adipose tissue particularly interesting since it appears to influence other insulin-responding tissues, such as muscle and liver, to also become insulin resistant. The insulin signaling network is highly complex with cross-interacting intermediaries, positive and negative feedbacks, etc. To facilitate the mechanistic understanding of this network, we obtain dynamic, information-rich data and use model-based analysis as a tool to formally test different hypotheses that arise from the experimental observations. With dynamic mathematical models, we are able to combine knowledge and experimental data into mechanistic hypotheses, and draw conclusions such as rejection of hypotheses and prediction of outcomes of new experiments. We aim for an increased understanding of adipocyte insulin signaling and the underlying mechanisms of the insulin resistance that we observe in adipocytes from subjects diagnosed with type 2 diabetes. We also aim for a complete picture of the insulin signaling network in primary human adipocytes from normal and diabetic subjects with a link to relevant clinical parameters: plasma glucose and insulin. Such a complete picture of insulin signaling has not been presented before. Not for adipocytes and not for other types of cells. In this thesis, I present the development of the first comprehensive insulin signaling model that can simulate both normal and diabetic data from adipocytes – and that is linked to a whole-body glucose-insulin model. In the linking process we conclude that at least two glucose uptake parameters differ between the in vivo and in vitro conditions (Paper I). We also perform a model analysis of the early insulin signaling dynamics in rat adipocytes and conclude that internalization is important for an apparent reversed order of phosphorylation seen in these cells (Paper II). In the development of the first version of the comprehensive insulin signaling model, we introduce a key parameter for the diabetic state – an attenuated feedback (Paper III). We finally continue to build on the comprehensive model and include signaling to nuclear transcription via ERK and report substantial crosstalk in the insulin signaling network (Paper IV).
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Franck, Niclas. "On the importance of fat cell size, location and signaling in insulin resistance." Doctoral thesis, Linköping : Linköping University, 2009. http://www.bibl.liu.se/liupubl/disp/disp2009/med1123s.pdf.

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Yamada, Chizumi. "Genetic inactivation of GIP signaling reverses aging-associated insulin resistance through body composition changes." Kyoto University, 2008. http://hdl.handle.net/2433/135794.

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Lee, Nina Louise. "The roles of diet and SirT3 levels in mediating signaling network changes in insulin resistance." Thesis, Massachusetts Institute of Technology, 2013. http://hdl.handle.net/1721.1/81674.

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Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Biological Engineering, 2013.
Title as it appears in MIT Commencement Exercises program, June 2013: Signaling network changes in high fat diet-induced insulin resistance Cataloged from PDF version of thesis.
Includes bibliographical references (p. 73-80).
The goal of my research is to understand the mechanism by which high fat diets mediate insulin sensitivity and the role SirT3 plays in high fat diet-induced insulin resistance. Insulin resistance is defined as the inability of cells and tissues to respond properly to ordinary amounts of insulin and is a precursor to many metabolic diseases such as diabetes and cardiovascular disease. Obesity, brought on in large part by caloric excess from high fat diet feeding, is a major contributor to insulin resistance. The recent drastic increase in the prevalence of obesity makes it imperative that steps are taken to more effectively treat and cure obesity-linked diseases such as diabetes. To identify optimal therapeutic targets, it is crucial to first gain a mechanistic understanding of obesity-induced insulin resistance, and understand how specific changes in the signaling network affect insulin sensitivity. Previous work has demonstrated that levels of SirT3, a mitochondrial protein deacetylase, are diet dependent. Additionally, SirT3 expression levels have been shown to mediate insulin and glucose tolerance in animals in a diet-dependent manner. Perturbations in SirT3 levels also alter the levels of phosphorylation on several canonical insulin signaling proteins. In my research, I further investigated the link between SirT3, diet and insulin resistance from a signaling network perspective. Using mouse liver as a model system, I analyzed liver tissue from mice fed a normal diet (insulin sensitive) or mice fed a high fat diet, thus inducing insulin resistance. Quantification of phenotypic and network events in response to insulin and utilization of computational techniques revealed activated pathways and nodes mediating insulin response, some of which had not been previously associated with the canonical insulin signaling network. I extended the study to analyze the role SirT3 plays in diet-mediated insulin sensitivity by perturbing the level of SirT3 in mice on both normal chow and high fat diets. The results of this research are useful for designing more efficacious therapies to treat insulin resistance-induced diseases.
by Nina Louise Lee.
S.M.
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Papazoglou, Ioannis. "Cross-talk between insulin and serotonin signaling in the brain : Involvement of the PI3K/Akt pathway and behavioral consequences in models of insulin resistance." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T039/document.

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L’insuline et la sérotonine (5-HT) sont deux acteurs majeurs du maintien de l’homéostasie énergétique, fonction placée sous le contrôle de l’hypothalamus. En ciblant cette région, l’insuline remplit de nombreuses fonctions métaboliques via l’activation de la voie PI3K/Akt. La 5-HT exercent des effets biologiques similaires mais les voies de signalisation impliquées dans ces processus étaient jusqu’alors mal connues. De plus, il avait été démontré que la 5-HT est capable d’activer la voie PI3K/Akt/GSK3β dans l’hippocampe, mécanisme sous-tendant potentiellement les effets antidépresseurs du neurotransmetteur. Les principaux objectifs de cette thèse étaient d’étudier 1/ l’activation de la voie PI3K/Akt par la 5-HT dans l’hypothalamus de rats diabétiques (modèle Goto-Kakizaki) et chercher un potentiel dialogue avec l’insuline and 2/ les mécanismes sous-tendant l’induction de la dépression par une alimentation hyperlipidique, par l’analyse de la phosphorylation d’Akt et GSK3β sous l’action de l’insuline, de la leptine et de la 5-HT dans l’hippocampe de rat.Ici on montre que 1/ la 5-HT stimule la voie PI3K/Akt dans l’hypothalamus et que la phosphorylation d’Akt induite par la 5-HT est atténuée dans des conditions d’insulino-résistance, suggérant l’existence d’un dialogue entre les voies de signalisation de l’insuline et de la 5-HT. Par ailleurs, nos résultats indiquent qu’une alimentation hyperlipidique induit un comportement dépressif réversible chez le rat, qui pourrait impliquer la voie PI3K/Akt/GSK3β dans les neurones subgranulaires du gyrus denté. La mise en évidence d’un dialogue entre les voies de signalisation de la 5-HT, de la leptine et de l’insuline au niveau central enrichit nos connaissances sur le rôle de ces facteurs dans la régulation de l’homéostasie énergétique et de l’humeur, et propose un lien moléculaire entre diabète de type 2, obésité et dépression
Insulin and serotonin (5-HT) are two key players in the maintenance of energy homeostasis which is controlled by the hypothalamus. In this brain region, insulin mediates numerous metabolic effects via the activation of the PI3K/Akt signaling pathway. 5-HT exerts similar biological properties by acting in the hypothalamus but the signaling pathways accountable for these effects are still unclear. Moreover, it has been reported that 5-HT induces the activation of the PI3K/Akt pathway in the hippocampus and the inhibition of GSK3β, suggesting this action as a potential mechanism for the antidepressant effects of this neurotransmitter.The main objectives of this thesis were to study 1/ the serotonin-induced activation of the PI3K/Akt in the hypothalamus of wild type and diabetic rats (Goto-Kakizaki model) and search a potential cross-talk with insulin and, 2/ the mechanisms underlying the high-fat diet induced depression by investigating the role of the phosphorylation of Akt and GSK3β by 5-HT, insulin and leptin in the hippocampus of rats.Here, we show that 5-HT triggers the PI3K/Akt signaling pathway in the rat hypothalamus, and that this activation is attenuated in insulin-resistant conditions, suggesting a cross-talk between insulin and 5-HT. Moreover, we reported that high-fat diet feeding induces a reversible depressive-like behavior, which may involve the PI3K/Akt/GSK3β pathway in subgranular neurons of the dentate gyrus. In conclusion, the activation of the PI3K/Akt pathway and its target GSK3β by 5-HT in the hypothalamus and in the dentate gyrus, respectively, can be impaired in insulin-/leptin-resistant states, which may underlie a link between metabolic diseases and depression
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Renström, Frida. "Fat cell insulin resistance : an experimental study focusing on molecular mechanisms in type 2 diabetes." Doctoral thesis, Umeå universitet, Institutionen för folkhälsa och klinisk medicin, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1078.

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The aim of the present thesis was to further increase our understanding of mechanisms contributing to and maintaining cellular insulin resistance in type 2 diabetes (T2D). For this reason, the effects of high glucose and insulin levels on glucose transport capacity and insulin signaling, with emphasis on insulin receptor substrate 1 (IRS-1) were assessed in fat cells. Altered levels of IRS-1 have previously been observed in adipose tissue from insulin-resistant and T2D subjects. A high glucose level (≥15 mM) for 24 h exerted only a minor impairment on glucose transport capacity in human adipocytes, as opposed to rat adipocytes. However, when combined with a high insulin level (104 µU/ml), basal and insulin-stimulated glucose transport was significantly impaired in both human and rat adipocytes. This was associated with a depletion of IRS-1 and IRS-2 protein levels in rat adipocytes, as a result of post-translational changes and altered gene transcription, respectively. In human adipocytes was only IRS-1 protein levels reduced. The high glucose/high insulin setting achieved maximal impairment of glucose transport within 6 h. Subsequent incubations of rat adipocytes under physiological conditions could partially restore insulin sensitivity. Interestingly, in both human and rat fat cells, decreased levels of IRSs occurred after the establishment of impaired glucose transport, suggesting that the observed depletion of IRSs is a consequence rather than a cause of insulin resistance. Nonetheless, IRS depletion is likely to further aggravate insulin resistance. Tyrosine phosphorylation of IRS-1 upon insulin stimulation activates the signaling pathway that mediates glucose transport. Pre-treatment of human adipocytes with high glucose and insulin levels was not associated with any alterations in the total IRS-1 Tyr612 phosphorylation following 10 min insulin stimulation. However, a significant increase in basal Tyr612 phosphorylation was observed. Furthermore, a rise in basal IRS-1 Ser312 phosphorylation was found. This is associated with reduced IRS-1 function and is considered to target IRS-1 to degradation pathways, and thus could potentially explain the observed decrease in IRS-1 protein levels. Our results imply an enhanced activation of insulin’s negative-feedback control mechanism that inhibit IRS-1 function. This could potentially have contributed to the observed impairment of insulin action on glucose transport in these cells. Accordingly, we have also shown that the downstream activation of protein kinase B upon insulin-stimulation is significantly impaired in human adipocytes exposed to the high glucose/high insulin setting, indicating a defect in the signaling pathway mediating glucose transport. We also investigated whether there are humoral factors in the circulation of T2D patients that contribute to peripheral insulin resistance. Human adipocytes cultured for 24 h in medium supplemented with 25% serum from T2D subjects, as compared to serum from non-diabetic subjects, displayed significantly reduced insulin-stimulated glucose uptake capacity. The effect could neither be attributed to glucose, insulin, FFA, TNF-α or IL-6 levels in the serum, but other circulating factor(s) seem to be of importance. In conclusion, chronic conditions of elevated glucose and/or insulin levels all impair insulin action on glucose turnover, but to different extents. A clear distinction between rat and human fat cells in the response to these different milieus was also observed. Alterations in the function of the key insulin signaling protein IRS-1 might be involved in the mechanisms underlying the impaired glucose uptake capacity. IRS-1 reduction however, occurs after but probably aggravates the existing insulin resistance. The effects of high glucose and/or insulin levels may be of importance in T2D, but additional novel factors present in the circulation of T2D patients seem to contribute to cellular insulin resistance.
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Araújo, Michella Soares Coelho. "Obesidade e resistência à insulina induzida pela restrição crônica no consumo de sal em ratos Wistar: efeitos sobre o balanço energético, sistema renina-angiotensina (SRA) e sinalização da insulina." Universidade de São Paulo, 2005. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-15012007-134042/.

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A restrição de sal na dieta está associada com resistência à ação da insulina e obesidade. O mecanismo molecular pelo qual a dieta hipossódica (HO) pode induzir resistência à insulina e obesidade não está totalmente compreendido. O objetivo do presente estudo foi avaliar a influência da ingestão crônica de sal sobre o peso corporal (PC), sinalização da insulina no fígado, músculo e tecido adiposo branco (TAB) e sua associação com adiposidade e resistência à insulina. Com esta finalidade, ratos Wistar foram alimentados com dieta HO, normossódica (NR) ou hipersódica (HR) desde o desmame. O PC foi avaliado desde o desmame. Ao completarem 12 semanas de vida, foram avaliados pressão arterial, balanço energético, consumo de ração, glicemia, angiotensina II (ANGIO II) plasmática e perfil hormonal. A atividade motora espontânea foi estudada em ratos com 8 e 12 semanas. A sensibilidade à insulina foi analisada pelo índice de HOMA. A expressão da proteína desacopladora mitocondrial 1 (UPC-1) foi quantificada no tecido adiposo marrom (TAM) e o conteúdo de ANGIO II no TAM, TAB e hipotálamo. As etapas iniciais da sinalização da insulina foram avaliadas por imunoprecipitação e immunoblotting das proteínas envolvidas como o receptor da insulina (IR), substrato 1 e 2 do IR (IRS-1 e IRS-2), enzima fosfatidilinositol 3 – quinase (PI-3q), proteína quinase B (Akt/PKB), ativação da proteína c-jun NH2-terminal quinase (JNK) e fosforilação em serina 307 do IRS-1. O PC no desmame foi semelhante entre os grupos de dieta. No entanto, na idade adulta os ratos em dieta HO apresentaram maior PC, adiposidade visceral, glicemia e insulinemia de jejum, concentração de ANGIO II plasmática e aumento do conteúdo de ANGIO II no TAM. Por outro lado, nestes mesmos animais a dieta HO diminuiu o consumo de ração, o gasto energético, a expressão da proteína UCP-1, adiponectina plasmática e o conteúdo de ANGIO II no TAB. A atividade motora não foi diferente entre os grupos estudados. A dieta HO diminuiu a via IR/PI-3q/Akt/Foxo1 de sinalização da insulina no fígado e músculo. Por outro lado, parte desta via (IRS-2/Akt/Foxo1) mostrou-se aumentada no TAB. No fígado e músculo houve um aumento da fosforilação da proteína JNK associada com maior fosforilação do IRS-1ser307 no grupo HO. Em conclusão, a restrição ou sobrecarga crônica de sal altera a evolução ponderal associada com modificações no balanço energético e no perfil hormonal na idade adulta. A resistência à insulina induzida pela dieta HO é tecido-específico e foi acompanhada por uma ativação da proteína JNK e um aumento da fosforilação dos resíduos de serina 307 do IRS-1.
Restriction of sodium chloride intake has been associated with insulin resistance (INS-R) and obesity. The molecular mechanisms by which the low salt diet (LSD) can induce INS-R and obesity have not yet been established.The aim of the present study was to evaluate the influences of salt intake on body weight (BW) and on insulin signaling in liver, muscle and white adipose tissue (WAT). Wistar rats were fed a LSD, normal (NSD), or high (HSD) salt diet since weaning. At 12 weeks of age, BW, blood pressure(BP),energy balance, food intake, plasma glucose and angiotesin II (ANGIO II), and hormonal profile were evaluated. Afterward, motor activity, HOMA index, uncoupling protein 1 expression (UCP-1) and tissue adipose ANGIO II content was determined. The early steps of insulin signaling (IR: insulin receptor, IRS-1 and IRS-2: IR substrate 1 and 2, PI-3K: phosphatidylinositol 3-kinase), Akt (protein kinase B) phosphorylation, JNK (c-jun NH2-terminal kinase) activation and IRS-1ser307 (serine 307 of IRS-1) phosphorylation were evaluated by immunoprecipitation and immunoblotting. LSD increased BW, visceral adiposity, blood glucose, insulin, leptin, plasma ANGIO II and its content in BAT. Otherwise, LSD decreased food intake, energy expenditure, UCP-1 expression, adiponectin and ANGIO II content in WAT. Motor activity was not influenced by the dietary salt content. In LSD, a decreasing in IR/PI-3K/Akt/Foxo1 was observed in liver and muscle and an increase in this pathway was showed in adipose tissue. JNK activity and IRS-1ser307 phosphorylation were higher in liver and muscle. In conclusion, LSD induced obesity and insulin resistance due to changes in energy expenditure, SRA and insulin signaling. The INS-R is tissuespecific and is accompanied by JNK activation and IRS-1ser307 phosphorylation.
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Steiler, Tatiana L. "Kinase cascades in the regulation of glucose homeostasis /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-201-2/.

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Schäfer, Alexander [Verfasser], Jerzy [Akademischer Betreuer] Adamski, Bernhard [Akademischer Betreuer] Küster, and Marius [Akademischer Betreuer] Ueffing. "The Epoxyeicosatrienoic Acid Pathway Enhances Hepatic Insulin Signaling and Is Repressed In High Fat Diet Induced Hepatic Insulin Resistance : A proteomic study / Alexander Schäfer. Betreuer: Jerzy Adamski. Gutachter: Bernhard Küster ; Jerzy Adamski ; Marius Ueffing." München : Universitätsbibliothek der TU München, 2015. http://d-nb.info/1085023532/34.

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Books on the topic "Insulin signaling-Resistance"

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Kim, Sang Geon. AMPK-S6K1 signaling pathway as a target for treating hepatic insulin resistance. New York: Nova Science Publishers, 2010.

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Kim, Sang Geon. AMPK-S6K1 signaling pathway as a target for treating hepatic insulin resistance. Hauppauge, N.Y: Nova Science, 2009.

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J, Dietze Guenther, ed. A symposium, autocrine and paracrine signaling between contracting myocardium and coronary endothelium during ischemia: Effect of insulin resistance. New York: Excerpta Medica, 1997.

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Højlund, Kurt. Metabolism and insulin signaling in common metabolic disorders and inherited insulin resistance. 2014.

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Federico, Lisa Marie. Mechanistic link between intestinal insulin signaling and lipoprotein metabolism in a model of insulin resistance. 2004.

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Book chapters on the topic "Insulin signaling-Resistance"

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Kim, Cheorl-Ho. "GM3, Caveolin-1 and Insulin Receptor in Insulin Resistance." In GM3 Signaling, 99–103. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5652-4_18.

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"SER/THR PHOSPHORYLATION OF INSULIN RECEPTOR SIGNALING MOLECULES AND INSULIN RESISTANCE." In Insulin Signaling, 304–28. CRC Press, 2002. http://dx.doi.org/10.1201/b12794-23.

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Tonks, Katherine T., Yvonne Ng, Steven Miller, Adelle CF Coster, Dorit Samocha-Bonet, Tristan J. Iseli, Aimin Xu, Donald J. Chisholm, David E. James, and Jerry R. Greenfield. "Insulin Signaling Paradox Characterizes Human Insulin Resistance." In BASIC/TRANSLATIONAL - Diabetes & Glucose Homeostasis: Genetic & Translational Approaches, P2–518—P2–518. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part3.p6.p2-518.

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Pei, Zhe, Kuo-Chieh Lee, Amber Khan, and Hoau-Yan Wang. "Brain Insulin Resistance, Nitric Oxide and Alzheimer’s Disease Pathology." In The Role of Nitric Oxide in Type 2 Diabetes, 238–59. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815079814122010014.

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Alzheimer’s disease (AD) is a devastating age-related neurodegenerative disease characterized by progressive pathological changes and functional and cognitive impairments. Brain insulin resistance appears to contribute significantly to the pathology and cognitive deficits among several pathological mechanisms. Brain insulin resistance has been demonstrated in animal models of AD and postmortem human brain tissue from patients with AD dementia. Studies conducted in AD models and humans suggest attenuating brain insulin resistance by agents such as glucagon-like peptide1 (GLP-1) analogs and small molecule drug candidate PTI-125 reduces many AD pathologic features and symptoms. Insulin affects NO levels by activating endothelial and neuronal nitric oxide synthase (eNOS, nNOS), and systemic insulin resistance has been linked to reduced nitric oxide (NO) bioavailability. Increasing NO availability reduces systemic insulin resistance, and the insulin signaling pathway is associated with the activation of eNOS, implying a causal relationship. This chapter explores this relationship and the role of impaired NO availability in brain insulin resistance in AD dementia.
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Moruzzi, Noah, and Francesca Lazzeri-Barcelo. "Insulin Receptor Isoforms in Physiology and Metabolic Disease." In Insulin Resistance - Evolving Concepts and Treatment Strategies [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.103036.

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Insulin receptors (IRs) are ubiquitously expressed and essential for all cell types. Their signaling cascades are connected to key pathways involved in cell metabolism, proliferation, and differentiation, amongst others. Thus, dysregulation of IR-mediated signaling can lead to diseases such as metabolic disorders. In mammals, the IR pre-mRNA is alternatively spliced to generate two receptor isoforms, IR-A and IR-B, which differ in 12 amino acids in the α-chain involved in ligand binding. Given the isoforms have different affinities for their ligands insulin, proinsulin, and insulin-like growth factors (IGFs), it is speculated that IR amount and splicing regulation might contribute to a change in IR-mediated effects and/or insulin resistance. The aim of this chapter is to increase awareness of this subject in the research fields of diseases characterized by disturbances in insulin signaling. Here, we will describe the IR isoform distribution and discuss the current knowledge of their expression and ligand binding affinities as well as their signaling in physiology and during obesity and type 2 diabetes in humans and animal models. Moreover, we will discuss the necessary steps to gain a better understanding on the function and regulation of the IR isoforms, which could result in future therapeutic approaches against IR-related dysfunction.
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Bahadoran, Zahra, Parvin Mirmiran, Khosrow Kashfi, and Asghar Ghasemi. "Hyperuricemia, Type 2 Diabetes and Insulin Resistance: Role of Nitric Oxide." In The Role of Nitric Oxide in Type 2 Diabetes, 190–209. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815079814122010012.

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Uric acid (UA) is the end product of purine catabolism in humans. Hyperuricemia, defined as elevated plasma concentrations of UA above 7 mg/dL, is a risk factor for developing hypertension, cardiovascular diseases, chronic kidney disease, and type 2 diabetes. Hyperuricemia can induce pancreatic β-cell death and impaired insulin secretion. It can also disrupt insulin-induced glucose disposal and insulin signaling in different insulin-sensitive tissues, including cardiomyocytes, skeletal muscle cells, adipocytes, hepatocytes, and endothelial cells. These events lead to the development of systemic insulin resistance and impaired glucose metabolism. Induction of inflammation, oxidative stress, and impairment of nitric oxide (NO) metabolism mediate hyperuricemia-induced insulin resistance and dysglycemia. This chapter is focused on the potential mediatory role of NO metabolism on hyperuricemia-induced dysglycemia and insulin resistance.
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Koenig, Aaron M., Zoe Arvanitakis, and Steven E. Arnold. "The Role of Insulin Resistance and Signaling in Dementia." In Type 2 Diabetes and Dementia, 143–68. Elsevier, 2018. http://dx.doi.org/10.1016/b978-0-12-809454-9.00008-1.

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Sengupta, Priyanka, and Debashis Mukhopadhyay. "Possibilities of Combinatorial Therapy: Insulin Dysregulation and the Growth Hormone Perspective on Neurodegeneration." In Tyrosine [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97002.

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RTKs have been reported to be implicated in several neurodegenerative disorders and the roles of insulin receptor family have emerged as a key common pathway across diseases. Thus we focussed on the Insulin receptor family and discussed the irregulation from the growth hormone axis. The signaling, regulation and physiology of the production in liver and CNS has never been discussed in signaling perspectives and is extremely crucial for understanding the possibilities of IGF1 in neurodegeneration specifically. The commonalities across neurodegenerative diseases such as oxidative stress, mitochondrial dysfunction, and protein misfolding and insulin pathway anomalies have been elucidated and correlated with the insulin pathway. The crosstalk possibilities of the pathways, along with other regulatory modes for the development of combinatorial therapy have been discussed to visualize a common platform for neurodegenerative diseases including AD, PD, HD, ALS and FTD. Furthermore, the incretin based therapies that have gradually emerged as alternatives for insulin based therapy due to its inherent drawback of resistance has been briefly discussed.
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Singh, Atamjit, Nikhita Ghai, and PreetMohinder Singh Bedi. "Molecular Mechanisms Involved in Insulin Resistance: Recent Updates and Future Challenges." In Insulin Resistance - Evolving Concepts and Treatment Strategies [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.104806.

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Insulin resistance (IR) is a condition in which insulin-mediated regulation of glucose metabolism in body tissues (primarily liver, adipose tissue and skeletal muscle) becomes disrupted. IR is a characteristic marker of type 2 diabetes and cardiovascular diseases. IR is generally associated with metabolic abnormalities, including hyperinsulinemia, impaired glucose homeostasis, hyperlipidemia and obesity. IR can arise from pathological, genetic and environmental factors or from a combination of these factors. Studies conducted in recent decades showcase the important role of adipose tissue in the development of IR via release of lipids and different circulating factors. These extracellular factors influence the intracellular levels of intermediates including ceramide and various lipids that influence the cell responsiveness to insulin. These intermediates are suggested to promote IR via inhibition of one or more components of insulin signaling pathway (e.g., insulin receptor, insulin receptor substrate proteins). This chapter will shed light on various molecular mechanisms and factors contributing to IR, which will help the researchers to design potential therapeutic strategies and interventions for efficiently managing IR and its related disorders.
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Sacerdote, Alan. "Rare and Underappreciated Causes of Polycystic Ovarian Syndrome." In Polycystic Ovary Syndrome [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.101946.

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While hyperinsulinemia is a common contributing mechanism in the pathogenesis of polycystic ovarian syndrome (PCOS), other mechanisms may give rise to or add to the effects of hyperinsulinemia, as well as other causes of hyperandrogenism, in the pathogenesis of PCOS. Such underappreciated causes may include autoimmune, insulin receptor mutations, mutations of post-receptor insulin signaling response elements, polymorphisms of LH, androgen, and estrogen signaling pathways, epigenetic alterations in hormonal signaling cascade response elements, infestations and infections with organisms capable of endocrine disruption by various mechanisms, as well as drugs and other chemicals which may be endocrine disruptors. In addition, alterations in the gut, oral, or vaginal biome may be associated with PCOS and insulin resistance and may, in some instances, have a role to play in its pathogenesis. In this chapter I plan to review what is known about these lesser-known causes of PCOS, in the hopes of alerting clinicians to consider them and stimulating investigators to better understand PCOS pathogenesis in general and, hopefully, develop more individualized, precision treatment and prevention strategies for the people in our care.
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Conference papers on the topic "Insulin signaling-Resistance"

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Aldali, Sara Haitham, and Sownd Sankaralingam. "Induction of Glyoxalase 1 to prevent Methylglyoxal-Induced Insulin Resistance in Cardiomyocytes." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0230.

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Background: Type 2 Diabetes mellitus is characterized by hyperglycemia and insulin resistance. Methylglyoxal (MG) a highly reactive dicarbonyl compound is also increased in diabetes. MG is detoxified by glyoxalase 1 (Glo-1) enzyme using reduced glutathione (GSH) as a co-factor. MG has been shown to have deleterious effects on cardiovascular cells and impairs insulin signaling. Insulin resistance is associated with diabetic cardiomyopathy. Trans-resveratrol (tRES) and Hesperetin (HES) combination has been shown to increase Glo-1 and improve insulin signaling in obese patients. Aim(s): The aim of this study is to investigate whether tRES-HES combination prevents MG-induced cardiac insulin resistance and the underlying mechanisms in cardiomyocytes in culture. Methodology: (H9C2) rat cardiomyocytes were treated with MG (100 µM) for 24 hours in the presence or absence of tRES-HES (10 µM). Glo-1 activity was determined by the formation of S-D lactoylglutathione; protein expression of P-Akt and P-GSK3b was determined using Western blot. In some experiments, cells were stimulated with insulin (100 nM) for 10 minutes to test insulin sensitivity. Results: MG reduced Glo-1 activity by ~25%, blunted insulin-induced phosphorylation of Akt and Gsk3b and increased the expression of beta-myosin heavy chain by ~50% (a marker of cardiac dysfunction) significantly (P˂0.05) compared to untreated control group of cells. Co-administration of tRES-HES combination restored Glo1 activity, maintained insulin-induced phosphorylation of Akt and GSK3b and prevented the increase in beta myosin heavy chain significantly (P<0.05). Conclusion: Induction of Glo1 prevents MG-induced cardiac insulin resistance and the increase in marker of cardiac dysfunction. This strategy could be helpful in preventing cardiovascular complications associated with diabetes.
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Al-Jaber, Hend Sultan, Layla Jadea Al-Mansoori, and Mohamed Aghar Elrayess. "The Role of GATA3 in Adipogenesis & Insulin Resistance." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0143.

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Background: Impaired adipogenesis plays an important role in the development of obesityassociated insulin resistance and type 2 diabetes. Adipose tissue inflammation is a crucial mediator of this process. In hyperglycemia, immune system is activated partially through upregulation of GATA3, causing exacerbation of the inflammatory state associated with obesity. GATA3 also plays a role as a gatekeeper of terminal adipocyte differentiation. Here we are examining the impact of GATA3 inhibition in adipose tissue on restoring adipogenesis, reversing insulin resistance and potentially lowering the risk of type 2 diabetes. Results: GATA-3 expression was higher in insulin resistant obese individuals compared to their insulin sensitive counterparts. Targeting GATA-3 with GATA-3 specific inhibitors reversed impaired adipogenesis and induced changes in the expression of a number insulin signaling-related genes, including up-regulation of insulin sensitivity-related gene and down-regulation of insulin resistance-related genes. Conclusion: GATA3 expression is higher in differentiating adipocytes from obese insulin resistant. Inhibiting GATA3 improves adipocytes differentiation and rescues insulin sensitivity in insulin resistant cells
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Chen, Jian, Xiaoping Su, Andres Rojas, Robert S. Bresalier, John R. Stroehlein, and Sai-ching Yeung. "Abstract 3054: Targeting TGF-β signaling for obesity/insulin resistance-associated hepatocellular carcinoma." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-3054.

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Qi, Yong, Minghong Xie, Li Wei, and Guangjie Hou. "Insulin resistance exacerbates lung inflammation in obese patients via PI3K/Akt signaling pathway." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa3343.

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Gehrke, N., BK Straub, A. Waisman, D. Schuppan, MA Wörns, PR Galle, and JM Schattenberg. "Hepatic IL-1 signaling in NAFLD is a driver of whole-body insulin resistance and adipose tissue inflammation." In 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402163.

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Kim, Jin-Soo, Sun Phil Choi, Yoo-Shin Kim, Woo-Young Kim, and Ho-Young Lee. "Abstract LB-41: Histone deacetylase (HDAC) inhibition induces a resistance mechanism via the insulin-like growth factor-1 receptor (IGF-1R) signaling pathway: Rational basis for cotargeting of IGF-1R and HDAC in non-small cell lung cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-41.

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Reports on the topic "Insulin signaling-Resistance"

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Boisclair, Yves R., and Arieh Gertler. Development and Use of Leptin Receptor Antagonists to Increase Appetite and Adaptive Metabolism in Ruminants. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7697120.bard.

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Objectives The original project had 2 major objectives: (1) To determine the effects of centrally administered leptin antagonist on appetite and adaptive metabolism in the sheep; (2) To develop and prepare second-generation leptin antagonists combining high binding affinity and prolonged in vivo half-life. Background Periods of suboptimal nutrition or exaggerated metabolic activity demands lead to a state of chronic energy insufficiency. Ruminants remain productive for a surprisingly long period of time under these circumstances by evoking adaptations sparing available energy and nutrients. The mechanism driving these adaptations in ruminant remains unknown, but could involve a reduction in plasma leptin, a hormone acting predominantly in the brain. In laboratory animals, reduced leptin signaling promotes survival during nutritional insufficiency by triggering energy sparing adaptations such as reduced thyroid hormone production and insulin resistance. Our overall hypothesis is that similar adaptations are triggered by reduced leptin signaling in the brain of ruminants. Testing of this hypothesis in ruminants has not been possible due to inability to block the actions of endogenous leptin and access to ruminant models where leptin antagonistic therapy is feasible and effective. Major achievements and conclusions The Israeli team had previously mutated 3 residues in ovine leptin, with no effect on receptor binding. This mutant was renamed ovine leptin antagonist (OLA) because it cannot activate signaling and therefore antagonizes the ability of wild type leptin to activate its receptor. To transform OLA into an effective in vivo antagonist, the Israeli made 2 important technical advances. First, it incorporated an additional mutation into OLA, increasing its binding affinity and thus transforming it into a super ovine leptin antagonist (SOLA). Second, the Israeli team developed a method whereby polyethylene glycol is covalently attached to SOLA (PEG-SOLA) with the goal of extending its half-life in vivo. The US team used OLA and PEG-SOLA in 2 separate animal models. First, OLA was chronically administered directly into the brain of mature sheep via a cannula implanted into the 3rdcerebroventricule. Unexpectedly, OLA had no effect of voluntary feed intake or various indicators of peripheral insulin action but reduced the plasma concentration of thyroid hormones. Second, the US team tested the effect of peripheral PEG-SOLA administration in an energy sensitive, rapidly growing lamb model. PEG-SOLA was administered for 14 consecutive days after birth or for 5 consecutive days before sacrifice on day 40 of life. Plasma PEG-SOLA had a half-life of over 16 h and circulated in 225- to 288-fold excess over endogenous leptin. PEG-SOLA administration reduced plasma thyroid hormones and resulted in a higher fat content in the carcass at slaughter, but had no effects on feed intake, body weight, plasma glucose or insulin. These results show that the team succeeded in developing a leptin antagonist with a long in vivo half-life. Moreover, in vivo results show that reduced leptin signaling promotes energy sparing in ruminants by repressing thyroid hormone production. Scientific and agricultural implications The physiological role of leptin in ruminants has been difficult to resolve because peripheral administration of wild type leptin causes little effects. Our work with leptin antagonists show for the first time in ruminants that reduced leptin signaling induces energy sparing mechanisms involving thyroid hormone production with little effect on peripheral insulin action. Additional work is needed to develop even more potent leptin antagonists, to establish optimal administration protocols and to narrow down phases of the ruminant life cycle when their use will improve productivity.
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Hansen, Peter J., and Amir Arav. Embryo transfer as a tool for improving fertility of heat-stressed dairy cattle. United States Department of Agriculture, September 2007. http://dx.doi.org/10.32747/2007.7587730.bard.

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The overall objective of the current proposal is to develop procedures to improve the pregnancy rate achieved following transfer of fresh or cryopreserved embryos produced in the laboratory into heat-stress recipients. The overall hypothesis is that pregnancy rate in heat-stressed lactating cows can be improved by use of embryo transfer and that additional gains in pregnancy rate can be achieved through development of procedures to cryopreserve embryos, select embryos most likely to establish and maintain pregnancy after transfer, and to enhance embryo competence for post-transfer survival through manipulation of culture conditions. The original specific objectives were to 1) optimize procedures for cryopreservation (Israel/US), 2) develop procedures for identifying embryos with the greatest potential for development and survival using the remote monitoring system called EmbryoGuard (Israel), 3) perform field trials to test the efficacy of cryopreservation and the EmbryoGuard selection system for improving pregnancy rates in heat-stressed, lactating cows (US/Israel), 4) test whether selection of fresh or frozen-thawed blastocysts based on measurement of group II caspase activity is an effective means of increasing survival after cryopreservation and post-transfer pregnancy rate (US), and 5) identify genes in blastocysts induced by insulin-like growth factor-1 (IGF-1) (US). In addition to these objectives, additional work was carried out to determine additional cellular determinants of embryonic resistance to heat shock. There were several major achievements. Results of one experiment indicated that survival of embryos to freezing could be improved by treating embryos with cytochalasin B to disrupt the cytoskeleton. An additional improvement in the efficacy of embryo transfer for achieving pregnancy in heat-stressed cows follows from the finding that IGF-1 can improve post-transfer survival of in vitro produced embryos in the summer but not winter. Expression of several genes in the blastocyst was regulated by IGF-1 including IGF binding protein-3, desmocollin II, Na/K ATPase, Bax, heat shock protein 70 and IGF-1 receptor. These genes are likely candidates 1) for developing assays for selection of embryos for transfer and 2) as marker genes for improving culture conditions for embryo production. The fact that IGF-1 improved survival of embryos in heat-stressed recipients only is consistent with the hypothesis that IGF-1 confers cellular thermotolerance to bovine embryos. Other experiments confirmed this action of IGF-1. One action of IGF-1, the ability to block heat-shock induced apoptosis, was shown to be mediated through activation of the phosphatidylinositol 3-kinase pathway. Other cellular determinants of resistance of embryos to elevated temperature were identified including redox status of the embryo and the ceramide signaling pathway. Developmental changes in embryonic apoptosis responses in response to heat shock were described and found to include alterations in the capacity of the embryo to undergo caspase-9 and caspase-3 activation as well as events downstream from caspase-3 activation. With the exception of IGF-1, other possible treatments to improve pregnancy rate to embryo transfer were not effective including selection of embryos for caspase activity, treatment of recipients with GnRH.and bilateral transfer of twin embryos. In conclusion, accomplishments achieved during the grant period have resulted in methods for improving post-transfer survival of in vitro produced embryos transferred into heat-stressed cows and have lead to additional avenues for research to increase embryo resistance to elevated temperature and improve survival to cryopreservation. In addition, embryo transfer of vitrified IVF embryos increased significantly the pregnancy rate in repeated breeder cows.
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