Relevant bibliographies by topics / Glucose metabolism

Academic literature on the topic 'Glucose metabolism'

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Published: 4 June 2021
Last updated: 28 July 2024

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Journal articles on the topic "Glucose metabolism"

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Kumar, B. Hemanth. "Regulation of Glucose Metabolism by Glucagon: A Review." Indian Journal of Applied Research 3, no. 9 (October 1, 2011): 524–26. http://dx.doi.org/10.15373/2249555x/sept2013/159.

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HAWKINS, JOSIAH Z. S., and DEBORAH WING. "Abnormal Glucose Metabolism." Clinical Obstetrics and Gynecology 55, no. 3 (September 2012): 731–43. http://dx.doi.org/10.1097/grf.0b013e31825cf731.

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Ray, L. B. "Glucose Metabolism Revisited." Science Signaling 3, no. 140 (September 21, 2010): ec289-ec289. http://dx.doi.org/10.1126/scisignal.3140ec289.

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Madhok, Brijesh M., Sashidhar Yeluri, Sarah L. Perry, Thomas A. Hughes, and David G. Jayne. "Targeting Glucose Metabolism." American Journal of Clinical Oncology 34, no. 6 (December 2011): 628–35. http://dx.doi.org/10.1097/coc.0b013e3181e84dec.

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Delgado Mendoza, Roberth Fernando, Dayana Jamileth Aguayo Palma, and Nereida Josefina Valero Cedeño. "CORTISOL Y METABOLISMO GLUCÍDICO EN ADULTOS." Enfermería Investiga 7, no. 4 (December 3, 2022): 68–73. http://dx.doi.org/10.31243/ei.uta.v7i4.1870.2022.

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El cortisol, es una hormona esteroidea secretada por la corteza suprarrenal, liberada al torrente sanguíneo realiza su función en los tejidos periféricos y regula una amplia gama de procesos corporales, entre ellos la intolerancia de la glucosa y reducción de la sensibilidad a la insulina. La finalidad del presente estudio fue analizar la relación entre los niveles de cortisol y el metabolismo glucídico en adultos. Estudio de diseño documental descriptivo, llevado a cabo mediante una revisión bibliográfica de artículos originales, de revisión, de casos clínicos, entre otros, en revistas indexadas en las diferentes bases de datos científicas, publicados en los últimos diez años, seleccionados bajos criterios de inclusión y exclusión. En general, se evidencio que el cortisol es un glucocorticoide secretado por la glándula suprarrenal, cumple una importante función en el metabolismo glucídico, inhibiendo la secreción de la insulina cuando ya no es necesaria y regula la capacidad de transporte de la glucosa hacia las células. Palabras claves: glucocorticoides, metabolismo, glucosa, diabetes mellitus, homeostasis, prevalencia. ABSTRACT Cortisol is a steroid hormone secreted by the human adrenal cortex. When released into the bloodstream, performs its function in the peripheral tissues and regulates a wide range of body processes, including glucose intolerance and reduced insulin sensitivity. The purpose of this study was to analyze the relationship between the cortisol levels and glucose metabolism in adults, emphasizing the physiological processes of secretion and assimilation of these analytes. A documental study design was applied and carried out through a bibliographic review, clinical cases, indexed journals from scientific database, among others, all published within the past ten years. All these were selected under inclusion and exclusion criteria. Generally, cortisol is a glucocorticoid secreted by the adrenal gland. It plays an important role in glucose metabolism by inhibiting the secretion of insulin when it is no longer needed, and thus, regulating the ability to transport glucose into cells. Keywords: cortisol, glycogenesis, glucocorticoids, metabolism, glucose, diabetes mellitus, homeostasis, prevalence
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Vlad, Mihaela, Daniela Amzar, Diana Bănică, Ioana Golu, Melania Balaș, Adrian Vlad, Romulus Timar, and Ioana Zosin. "Glucose and Lipid Abnormalities in Newly Diagnosed Acromegalic Patients." Romanian Journal of Diabetes Nutrition and Metabolic Diseases 22, no. 1 (March 1, 2015): 47–51. http://dx.doi.org/10.1515/rjdnmd-2015-0006.

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AbstractBackground and Aims. Acromegaly is frequently associated with abnormalities of glucose and lipid metabolism. The aim of our study was to analyze the prevalence of glucose and lipid metabolism abnormalities in newly diagnosed acromegaly patients. Material and Methods. This retrospective study included 14 patients (F/M=10/4), mean age 49.5 ± 10.6 years, registered with acromegaly between January and December 2013. In all the cases the values of blood glucose (fasting and during the oral glucose tolerance test), total cholesterol and triglycerides were analyzed. The glucose disorders were classified according to the current criteria of the American Diabetes Association. Regarding the lipid metabolism, the cases were classified as having normal cholesterol, normal triglycerides, high cholesterol and high triglycerides. Results. A number of 7 patients (50%) presented abnormalities of glucose metabolism. The prevalence of diabetes mellitus (14.3%) was lower compared to that reported by other studies (15.5%- 56%). Abnormalities of lipid metabolism were present in 8 patients (57.2%): high cholesterol was detected in 2 cases and 6 cases presented increased values for both cholesterol and triglycerides. Only 4/14 cases (28.6%) presented normal values for all glucose and lipid metabolisms parameters. Conclusions. Abnormalities of glucose and lipid metabolisms are very common in acromegalic patients.
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DEVARAKONDA, KAVYA, MITCHELL BAYNE, ALEXANDRA ALVARSSON, and SARAH STANLEY. "Amygdala Glucose-Sensing Neurons Regulate Glucose Metabolism." Diabetes 67, Supplement 1 (May 2018): 1807—P. http://dx.doi.org/10.2337/db18-1807-p.

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Lien, Yeoung-Hau, Mickey M. Tseng, and Robert Stern. "Glucose and glucose analogs modulate collagen metabolism." Experimental and Molecular Pathology 57, no. 3 (December 1992): 215–21. http://dx.doi.org/10.1016/0014-4800(92)90012-z.

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STEFANYSHYN, N. P. "STARVATION DURING DEVELOPMENT AFFECTS METABOLISM IN DROSOPHILA." Biotechnologia Acta 16, no. 2 (April 28, 2023): 44–46. http://dx.doi.org/10.15407/biotech16.02.044.

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Aim. To investigate how starvation during early stage of fly development affects carbohydrate metabolism in imago flies and their progeny of F1 generation. Methods. Wild-type Canton-S strain Drosophila melanogaster flies were used in all experiments. Flies of parental and offspring generations were used for the determination of glycogen and glucose content using the diagnostic kit Glucose-Mono-400-P according to the manufacturer's instructions. Results represent as the mean ± SEM of 3-4 replicates per group. According Student's t-test significant difference between groups was P<0.05. Graphing and statistical analysis were performed by using GraphPad Prism. Results. Starvation during development significantly influenced the level of hemolymph and body glucose in imago flies of parental generation. Hemolymph glucose concentration was lower by 34% (P=0.008) and 32% (P=0.033) in experimental females and males, respectively, as compared to control groups. Starvation during development led to lower level of body glucose in adult parental flies of both sexes. Adult males F1, generated by parents that were starved during development, showed 3-fold lower glycogen content, as compared to control. Conclusions. Starvation at early stage of development led to lower hemolymph glucose and body glucose level in imago flies. Moreover, parental starvation decreased glycogen pool in F1 males.
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Almeida Castro, Luis Henrique, Leandro Rachel Arguello, Nelson Thiago Andrade Ferreira, Geanlucas Mendes Monteiro, Jessica Alves Ribeiro, Juliana Vicente de Souza, Sarita Baltuilhe dos Santos, et al. "Energy metabolism." International Journal for Innovation Education and Research 8, no. 9 (September 1, 2020): 359–68. http://dx.doi.org/10.31686/ijier.vol8.iss9.2643.

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Most animal cells are able to meet their energy needs from the oxidation of various types of compounds: sugars, fatty acids, amino acids, but some tissues and cells of our body depend exclusively on glucose and the brain is the largest consumer of all. That is why the body has mechanisms in order to keep glucose levels stable. As it decreases, the degradation of hepatic glycogen occurs, which maintains the appropriate levels of blood glucose allowing its capture continues by those tissues, even in times of absence of food intake. But this reserve is limited, so another metabolic pathway is triggered for glucose production, which occurs in the kidneys and liver and is called gluconeogenesis, which means the synthesis of glucose from non-glucose compounds such as amino acids, lactate, and glycerol. Most stages of glycolysis use the same enzymes as glycolysis, but it makes the opposite sense and differs in three stages or also called deviations: the first is the conversion of pyruvate to oxaloacetate and oxaloacetate to phosphoenolpyruvate. The second deviation is the conversion of fructose 1,6 biphosphate to fructose 6 phosphate and the third and last deviation is the conversion of glucose 6 phosphate to glucose.
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Dissertations / Theses on the topic "Glucose metabolism"

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Pennant, Mary Elizabeth. "Measuring glucose metabolism." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611215.

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Roberts, Justin D. "Post exercise glucose metabolism." Thesis, Brunel University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249789.

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Thiên. "Glucose metabolism in falciparum Malaria." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2004. http://dare.uva.nl/document/74040.

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Williams, Andrew C. "Glucose metabolism in human spermatozoa." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302101.

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Rotondo, Floriana. "Glucose and white adipose tissue metabolism. Effects of site and sex on the fate of glucose." Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/482142.

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The current theories about endothelial inflammation in the adipose tissue in metabolic syndrome point to hypoxia as one of its main causes. Nevertheless, our group has found that both 3T3L1 adipocytes, under normoxic conditions, and WAT, in vivo, consume large amount of glucose, with high production of lactate and glycerol irrespective of oxygen availability. This thesis is based on the hypothesis that adipocytes act essentially as glycolytic cells impervious to hypoxia, and their metabolism may help reduce the blood glucose levels. We assumed that hypoxia, could affect the cells of the stromal fraction, eliciting an inflammatory response. To this purpose, we have studied ex vivo the glycolytic and anaerobic capacity of adult adipocytes and stromal vascular cells of both sex and obtained from different WAT sites, developing the methodology needed for a quantitative comparative analysis of data obtained from the same cultured cells well. We found that adipocytes, despite being the cells present in WAT in lower numbers, occupied almost the whole volume of the tissue, a consequence of their huge size due to their inert fat vacuole. The overall “live cell" volume represented only about 1.5% of the tissue, thus showing a very high metabolic activity of WAT in relative terms. Adipocytes ex vivo incubated with glucose, also took large amounts of the sugar, irrespective of its concentration, releasing instead 3C metabolites, such as lactate and glycerol to the medium. Lactate was fully derived from glucose and was produced at a steady pace, irrespective the presence of oxygen, to form the ATP needed for cell functions. Glycerol efflux increased over time and its origin shifted from glycolitic to glycolytic-lipolytic: new-formed glycerol was incorporated into TAG, by esterification with acyl-CoA, derived from the same TAG lipolisis. The coexistence of these processes appears as a “futile cycle”, with the probable function further to waste excess energy. Lipogenesis was limited because the size of cells limits the access to oxidative mitochondrial pathways. The release of 3C metabolites seems to be a mechanism to lower glycemia, defend WAT against excess of substrate, and provide 3C fragments as more accessible substrates for other tissues. Mesenteric WAT adipocytes presented the highest metabolic activity, probably to help the hepatic handling of NEFA and reduce the flow of intestinal glucose to the liver. While in almost all WAT sites, excess mitochondrial pyruvate is returned to the cytoplasm to keep forming lactate; in female mesenteric adipocytes it is in part oxidized to acetyl-CoA to fuel lipogenesis. Stromal vascular cells also released lactate, even more than adipocytes per unit of tissue weight, but not glycerol nor NEFA. Red blood cells produced lactate, but its contribution was quantitatively minimal. Thus, stromal cells, acted in consonance with adipocytes, in all sites and sexes examined, wasting glucose in an anaerobic way, producing high amounts of 3C units. Thus, reinforcing the idea that WAT may be an active protagonist both in energy handling and in the body control of glycemia.
Las teorías actuales sobre la inflamación endotelial en el tejido adiposo en el síndrome metabólico apuntan a la hipoxia como una de sus causas. Nuestro grupo ha encontrado que adipocitos 3T3L1, bajo condiciones normóxicas, consumen grandes cantidades de glucosa, con elevada producción de lactato y glicerol. La hipótesis de esta tesis es que los adipocitos actuan como células glucolíticas y su metabolismo ayuda a reducir la glucemia, mientre la hipoxia podría afectar las células estromales. Hemos estudiado ex vivo la capacidad glucolítica de adipocitos adultos y células estromales de ambos sexos y de diferentes ubicaciones del TAB, desarrollando la metodología para un análisis cuantitativo. Hallamos que los adipocitos eran las células menos númerosas del tejido y la parte "viva" representaba solo el 1,5% del total, mostrando así el TAB una actividad metabólica muy elevada. Los adipocitos ex vivo captaban grandes cantidades de glucosa, independientemente de su concentración; liberando metabolitos de 3C. El lactato, liberado a ritmo constante y independientemente de la presencia de oxígeno, procedía totalmente de la glucosa. El eflujo de glicerol aumentó con el tiempo y su origen cambió de glucolítico a glucolítico-lipolítico. El glicerol neoformado se incorporaba a los TAG, reciclado acil-CoA de la misma lipolisis. Este"ciclo fútil", probablemente sirve para desperdiciar e energía, disminuir la glucemia, y proporcionar sustratos energéticos para otros tejidos. Los adipocitos del TAB presentaban la más alta actividad metabólica; probablemente para ayudar al manejo hepático de ácidos grasos y reducir el flujo de glucosa intestinal. Mientras que en todas las localizaciones, el exceso de piruvato mitocondrial regresaba al citoplasma y seguía formando lactato; en los adipocitos de las hembras de mesentérico, parte se oxidaba a acetil-CoA para sostener la lipogénesis. Las células estromales, por unidad de tejido, liberaban más lactato que los adipocitos, pero no glicerol ni ácidos grasos. Los eritrocitos produjeron mínimas cantidades de lactato.Así las células estromales, actúan en consonancia con los adipocitos, en todas las localizaciones estudiadas y en ambos sexos. Estos resultados refuerzan la idea de que el TAB puede ser un protagonista activo en el manejo de la energía y en el control de la glucemia.
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Fraser, Bernadine Heather. "Glycogen and glucose metabolism in cardioprotection." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0028/NQ34764.pdf.

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Butler, Mark Henry. "Information processing in liver glucose metabolism." Thesis, University of Liverpool, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367289.

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Vo, Annie Phuong. "Glucose Metabolism in Cancer-Associated Fibroblasts." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:11025.

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Under normal conditions, non-transformed cells rely on glycolysis followed by oxidative phosphorylation to generate ATPs. When oxygen is scarce or when cells are actively proliferating, cellular ATPs come mainly from glycolysis. Pyruvate is converted into lactate to allow glycolysis to continue. Interestingly, cancer cells have adapted to favor lactate production even at normal oxygen tensions, exhibiting a metabolic shift known as the Warburg effect. However, the metabolic state of other cellular constituents within the tumor remains mostly unknown. Cancer-associated fibroblasts (CAFs) are the most abundant stromal cells. They aid tumor growth and metastasis by providing growth factors, cytokine, ECM remodeling proteins and interacting with other tumor stromal cells. Here I show that the Warburg effect also operates in stromal fibroblasts of the tumor microenvironment. Using mass spectrometry, genetic mouse models, gene expression and methylation studies, I demonstrate that CAFs from human and mouse mammary tumors exhibit hyperactive glycolysis and a metabolic shift towards lactate production. Furthermore, this phenotype may be sustained through epigenetic modifications of endogenous hypoxia-inducible factor 1α, key regulatory enzymes fructose-bisphosphatase 1 and pyruvate kinase M2. Depletion of stromal fibroblasts or suppression of lactate production specifically in these cells alters the metabolic profile of not only the tumors but also the cancer cells and results in impeded tumor growth. These results collectively suggest that tumor growth is dependent on metabolic state and metabolic support of stromal fibroblasts, highlighting these cells as attractive therapeutic targets in controlling cancer progression.
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Karki, Rabindra. "Regulation of glucose metabolism by Alox8." OpenSIUC, 2014. https://opensiuc.lib.siu.edu/theses/1507.

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Type II diabetes is one of the leading cause of morbidity in the U.S. and other parts of the world. Insulin resistance which precedes Type II diabetes is a complex state of the body where the body fails to respond to insulin. Its complexity lies in its multifactorial origin that is to say various environmental and polygenic components come into play. Here we try to dissect one of these components - `Alox8' in transgenic mice and try to see if it affects blood glucose homeostasis. Comparison of glucose tolerance and insulin sensitivity among sixteen mice comprising of six wild type, five heterozygous and five knockout mice with respect to Alox8 gene showed that wild type mice had relatively more glucose tolerance than knockout mice and this corresponded with relatively more insulin sensitiveness of wild type mice with respect to the knock out. However, these findings were not significant statistically at p=0.05. In search of any relevant biological significance, periodic acid schiff staining of the liver sections from these mice in three independent repeated experiments revealed that the knockout phenotype led to accumulation of glycogen deposits as compared to the wild type mice, an indication of insulin resistance. Taken together, our data suggests that these findings when extrapolated to human which carries ALOX15B instead of mice orthologue Alox8, could lead to a benefit of administration of lower doses of insulin in the wild type phenotype as compared to its polymorphic alleles carrying individuals.
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Segarra, Mondéjar Marc. "Estudio de la regulación del metabolismo de la glucosa por la actividad sináptica." Doctoral thesis, Universitat de Barcelona, 2019. http://hdl.handle.net/10803/668643.

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La actividad sináptica regula una larga lista de procesos esenciales para el desarrollo y la supervivencia neuronal mediante cambios en los niveles de Ca2+ citoplasmático. Modula desde la morfología del árbol dendrítico neuronal hasta la plasticidad neuronal o los mecanismos de protección contra el daño oxidativo. La entrada de Ca2+ a través de los receptores sinápticos promueve diferentes cambios a nivel celular que van desde la remodelación del citoesqueleto a la estimulación de diferentes cascadas de señalización que finalmente activan diferentes factores de transcripción implicados en la regulación de toda una serie de programas de transcripción. Durante las primeras semanas tras el nacimiento tiene lugar el período, enmarcado dentro del desarrollo del sistema nervioso, en que se da una mayor tasa de crecimiento de dendritas y axones. El crecimiento neuronal debe ir acompañado de la síntesis de nuevos lípidos, necesarios para la generación de nuevas membranas. A pesar de que los mecanismos implicados en la regulación del crecimiento de dendritas y axones han sido ampliamente estudiados, se conoce muy poco con respecto a los cambios a nivel metabólico destinados a la síntesis de las biomoléculas necesarias para abastecer la generación de nuevas membranas. El principal objetivo de este trabajo ha sido estudiar el mecanismo por el que la actividad sináptica es capaz de regular el metabolismo neuronal para promover la síntesis de diferentes metabolitos precursores para la síntesis de los lípidos necesarios para el crecimiento neurítico. El principal modelo utilizado en este estudio ha sido los cultivos primarios de neuronas corticales de embriones de rata. La actividad sináptica se ha estimulado mediante un protocolo basado en la desinhibición de la red neuronal, que consiste en el tratamiento combinado con Bicuculina y 4-aminopiridina. Los resultados de esta tesis demuestran que la actividad sináptica estimula la captación y el metabolismo de la glucosa incrementando la transcripción del principal transportador de glucosa en neuronas (Glut3) y de diferentes enzimas implicadas en la glucólisis (HK2, PKM1/2 y PFKFB3). Todo el proceso está regulado por un mecanismo caracterizado por la activación de dos factores de transcripción: CREB y HIF-1α. La activación de CREB, uno de los principales factores de transcripción regulados por la actividad sináptica, promueve la expresión de Glut3 y de la enzima ubiquitina ligasa, Siah2. La actividad de esta última es necesaria para promover la estabilización y, en consecuencia, la activación de HIF-1α, que finalmente promueve la expresión de las enzimas implicadas en la glucólisis. La inhibición de la glucólisis o el bloqueo de la actividad de HIF-1α son suficientes para inhibir la estimulación del crecimiento neuronal por la actividad sináptica. De acuerdo con estos resultados en cultivos celulares, la inhibición de esta vía o la eliminación de este factor de transcripción durante las primeras semanas de desarrollo postnatal en roedores tiene como consecuencia una reducción de la complejidad del árbol dendrítico. Tal como se muestra en el presente trabajo, la actividad sináptica también podría estar implicada en la regulación de diferentes orgánulos como son los peroxisomas y las mitocondrias. En el primer caso se ha observado que la actividad sináptica promueve la síntesis de diferentes implicados tanto el desarrollo y el mantenimiento de los peroxisomas (Pex5, Pex11b y Pex13) como en el metabolismo lipídico peroxisomal (ABCD2 y ACOT8). Cuanto a las mitocondrias se ha comprobado que las neuronas estimuladas sinápticamente activas presentan un incremento en el transporte anterógrado mitocondrial a lo largo del axón que depende de la actividad de HIF-1α.
During the first weeks after birth occurs the period of the nervous system development in which takes place the highest dendritic and axonal growth ratio. Neuronal growth must be accompanied by the synthesis of new lipids, which are necessary for the formation of new membranes. Although the mechanisms involved in the regulation of dendrites and axons growth have been widely studied, there is very little known about the changes at the metabolic level involved in the synthesis of the biomolecules necessary to supply the formation of new membranes. The main goal of this doctoral thesis has been studying the mechanism by which synaptic activity, one of the most important inducers of neurite growth, regulates neuronal metabolism to promote the synthesis of different precursor metabolites involved in the synthesis of lipids required for neuritic growth. The results of this thesis show that synaptic activity stimulates glucose uptake and metabolism by increasing the transcription of the main glucose transporter in neurons, Glut3 and different enzymes involved in glycolysis. The whole process is regulated by a mechanism characterized by the activation of two transcription factors: CREB and HIF-1α. The activation of CREB, one of the main transcription factors regulated by synaptic activity, promotes the expression of Glut3 and the ubiquitin-protein ligase, Siah2. The activity of the latter is necessary to promote the stabilization and, consequently, the activation of HIF-1α, which finally promotes the expression of enzymes involved in glycolysis. Glycolysis inhibition or blocking of HIF-1α activity are sufficient to inhibit stimulation of neuronal growth by synaptic activity. A shown in this thesis, synaptic activity may also be involved in the regulation of peroxisomes and mitochondria. In the first case, it has been observed that synaptic activity promotes the synthesis of different agents involved in the development and maintenance of peroxisomes and in peroxisomal lipid metabolism. In regard to mitochondria, it has been proven that synaptically active neurons exhibit an increase in mitochondrial anterograde transport along the axon which requires HIF-1α activity.
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Books on the topic "Glucose metabolism"

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Donard, Dwyer, ed. Glucose metabolism in the brain. Amsterdam: Academic Press, 2002.

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Permert, Johan. Glucose metabolism in patients with exocrine pancreatic adenocarcinoma. Linköping: Univ., 1993.

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Polakof, Sergio. Brain glucosensing: Physiological implications. Hauppauge, N.Y: Nova Science Publishers, 2010.

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W, Gould Gwyn, ed. Facilitative glucose transporters. Austin: R.G. Landes, 1997.

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Whetstone, Heather Catherine. Role of quinoprotein glucose dehydrogenase in metabolism of glucose and gluconate in agrobacterium tumefaciens. Sudbury, Ont: Laurentian University, Chemistry and Biochemistry Department, 1997.

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Trumbach, Sabine. Glukose-Toleranz und Insulin-Sekretion unter simulierter Schwerelosigkeit. Koln: DFLVR, 1988.

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1952-, Brand Miller Janette, Foster-Powell Kaye, Lintner Lisa, and Burani Johanna C, eds. The new glucose revolution: The authoritative guide to the glycemic index : the dietary solution for lifelong health. New York: Marlowe & Co., 2003.

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Jennie, Brand-Miller, ed. The new glucose revolution: The authoritative guide to the glycemic index -- the dietary solution for lifelong health. New York: Marlowe & Co, 2003.

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Czyżewska, Krystyna. Przezotrzewnowy transport glukozy: Studium funkcji i efektów. Poznań: Akademia Medyczna im. Karola Marcinkowskiego w Poznaniu, 2001.

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Perus̆ic̆ová, Jindra. Glucose tolerance and secretion of insulin in chronic pancreatitis. Praha: Univerzita Karlova, 1990.

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Book chapters on the topic "Glucose metabolism"

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Greene, Michael. "Glucose Metabolism." In Encyclopedia of Cancer, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_7118-3.

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Greene, Michael. "Glucose Metabolism." In Encyclopedia of Cancer, 1917–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_7118.

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McDonald, Matthew. "Glucose Metabolism." In Encyclopedia of Personality and Individual Differences, 1818–20. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-24612-3_756.

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McDonald, Matthew. "Glucose Metabolism." In Encyclopedia of Personality and Individual Differences, 1–3. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-28099-8_756-1.

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Heller, S. R., and R. T. C. Robinson. "Glucose Metabolism." In Frontiers of Hormone Research, 4–26. Basel: KARGER, 1999. http://dx.doi.org/10.1159/000061008.

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Kwon, Obin. "Glucose Metabolism." In Stroke Revisited, 3–13. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-5123-6_1.

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Cowett, Richard M., and Hussien M. Farrag. "Neonatal Glucose Metabolism." In Principles of Perinatal—Neonatal Metabolism, 683–722. New York, NY: Springer New York, 1998. http://dx.doi.org/10.1007/978-1-4612-1642-1_32.

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Heiss, Wolf-Dieter. "Cerebral Glucose Metabolism." In PET and SPECT of Neurobiological Systems, 85–101. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-42014-6_3.

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Gjedde, Albert, William R. Bauer, and Dean F. Wong. "Metabolism of Glucose." In Neurokinetics, 211–39. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-7409-9_7.

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Cowett, Richard M. "Neonatal Glucose Metabolism." In Principles of Perinatal-Neonatal Metabolism, 356–89. New York, NY: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-0400-5_20.

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Conference papers on the topic "Glucose metabolism"

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El-fadl, Rihab, Nasser Rizk, Amena Fadel, and Abdelrahman El Gamal. "The Profile of Hepatic Gene Expression of Glucose Metabolism in Mice on High Fat Diet." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0213.

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Obesity is a growing problem worldwide, and recent data indicated that 20% of the populations would be obese. Obesity arises as a multifactorial disease caused by inherited traits that interact with lifestyle factors such as diet and physical activity. The liver plays an essential role in the gluco-regulation via regulating glucose, lipid and protein metabolism. The process of glucose metabolism is controlled by a range of molecular mechanisms and genes which affect the metabolism of the liver during intake of high fat diet (HFD). The objective of this research is to investigate the profile of hepatic gene expression of glucose metabolism in mice on HFD treated with leptin (5 mg/kg BW Ip injection). Ten wild type CD1 mice fed on HFD is used for this study, where groups are control (vehicle - leptin) and test group (vehicle + leptin). Body weight (BW) was measured, and blood chemistry, insulin and leptin were measured at the end of the experiments. Total RNA was isolated from the liver tissue, and RTPCR profiler array technology was used to evaluate the mRNA expression of 84 essential genes of hepatic glucose metabolism. The data of the BW and blood chemistry are not significantly different between the two groups. Leptin treatment enhanced the metabolic pathways and the candidate genes of the different metabolic pathway; glycogen metabolism such as Gys1, Gys2 and Pygm, pentose phosphate shunt such as Rpia and suppressed the glycolysis such as Aldob, and TCA cycle such as Mdh1b. In conclusion, this study has shown that leptin could affect the profile of the hepatic mouse genes of glucose metabolism in the early stages of HFD to induce obesity
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Machado, Luiza, Camila Santos, Bianca Leonardi, Andréia Rocha, Igor Fontana, Bruna Bellaver, Gianina Venturin, et al. "ACUTE PERIPHERAL INFLAMMATION IMPACT ON CEREBRAL GLUCOSE METABOLISM." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda072.

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Background: Neuroinflammation is a phenomenon already described in Alzheimer’s disease (AD). However, the effect of peripheral inflammation in AD is less understood. We recently demonstrated that severe sepsis causes acute brain metabolic disturbances. Nevertheless, whether mild acute peripheral inflammation affects brain metabolism remains unclear. Objective: We aimed at investigating the impact of mild acute peritonitis on glucose brain metabolism. Methods: Adult male wistar rats (n=6, per group) received a single intraperitoneal injection of 500 ml of carrageenan (CG, 500 µg of carrageenan i.p.) or saline (CO). Brain glucose metabolism was assessed using (18F) FDG-PET 4h after i.p. injections, which represents the first peak of inflammation. The peripheral inflammatory process was evaluated by analyzing the peritoneal lavage in a flow cytometer 48h after the injections, during the second peak of inflammation. Results: The CG animals presented a 5-fold increase in macrophages numbers (p0,05). However, carrageenan-induced inflammation did not cause acute changes in brain glucose metabolism (p>0,05). Conclusion: Mild acute peripheral inflammation does not change brain glucose metabolism. Further evaluations aiming to investigate long-term consequences of sustained mild inflammation are needed.
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Shirakashi, Ryo, Tomomi Yoshida, Christophe Provin, Kiyoshi Takano, Yasuyuki Sakai, and Teruo Fujii. "Steady Measurement of Glucose Metabolism of Hepatocyte." In ASME/JSME 2007 Thermal Engineering Heat Transfer Summer Conference collocated with the ASME 2007 InterPACK Conference. ASMEDC, 2007. http://dx.doi.org/10.1115/ht2007-32750.

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Production of hybrid artificial organs for implantation is one of the main topics of tissue engineering. A large organ consisting of soft tissues requires a high cell density, c.a. 108 cells/mL, to satisfy the same physiological metabolic rate per organ-volume as an organ in vivo. Therefore, the supply of oxygen and nutrition to all the cells composing the soft tissue is always critical problem for the in vitro artificial organ production. Energy metabolic rates, such as oxygen and glucose metabolism rate, of single cell at various temperatures are the basic data for designing the oxygen and nutrition transport in an artificial organ. It is reported that several conditions including pH, temperature, oxygen or glucose concentration have effects on energy metabolism, although these interactions are not clearly quantitatively measured mainly because of the problems of measuring systems. In this study, convenient method to measure glucose consumption rate of hepatocyte (HepG2 cell line) at different temperature and glucose concentration is proposed. A device for the measurement was developed which consists of a small closed chamber with an inlet and an outlet of culture medium at the both ends of the chamber. On the one side of the walls in the chamber, confluent HepG2 on a coverslip was installed. Culture medium supplemented with various concentration of glucose was supplied to the open flow chamber in a constant flow rate. The whole chamber was in a thermostatic bath to keep the temperature in the chamber constant. Glucose consumption rate can be calculated by measuring the difference between glucose concentration of inlet culture medium and outlet culture medium, the flow rate and the number of cells in the chamber. Enzymatic analysis using D-Glucose-HK allows quantification of the sample glucose concentration. The advantages of the proposed method include; 1) small number of cells is required for the measurement, c. a. 105cells, 2) the flow pattern and the glucose supply are in steady state. Especially the latter advantage made it possible to evaluate the effects of different conditions on the glucose consumption rate. Since the most of the metabolic rate were measured under unsteady state, conditions, such as pH, oxygen concentration and glucose concentration, were changed sometime drastically during the measurement. The results provided the several parameters of Michaelis-Menten kinetics at various temperatures.
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Casey, Daniel E. "TARDIVE DYSKINESIA MECHANISMS AND ABNORMAL GLUCOSE METABOLISM." In IX World Congress of Psychiatry. WORLD SCIENTIFIC, 1994. http://dx.doi.org/10.1142/9789814440912_0008.

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Meiman, Evan, Bryana Braxton, John Trent, Jason Chesney, and Sucheta Telang. "Abstract 5992: Targeting glucose metabolism in cancer." 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.am2020-5992.

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Xiong, Wangping, Xian Zhou, Bin Nie, and Jianqiang Du. "Computer-Based Kinetic Model of Glucose Metabolism." In 2010 International Conference on Intelligent Computation Technology and Automation (ICICTA). IEEE, 2010. http://dx.doi.org/10.1109/icicta.2010.690.

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Huang, Chun-Yuh, and Wei Yong Gu. "Effects of Compression on Glucose Consumption in Intervertebral Disc." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192812.

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Nutrition supply is a concern for the health of avascular cartilaginous tissues such as intervertebral disc (IVD). Maintaining tissue integrity relies on cellular biosynthesis of extracellular matrix, which is an energy demanding process [1]. In the IVD, energy is mainly generated through glycolysis (i.e., glucose consumption). Metabolism of nutrients (e.g., oxygen and glucose) within the IVD depends on local concentrations of nutrients, and coupling effects between nutrient level and metabolic rate [2,3]. Our previous theoretical study had developed a new theoretical formulation by incorporating the metabolic rates of solutes into the mechano-electrochemical mixture theory [4,5]. By using this new theoretical model, the distribution of oxygen and lactate can be predicted within the IVD under static and dynamics compressions [4]. However, the effect of compression on glucose consumption in the IVD has not been studied. The objective of this study was to examine the effects of compression on glucose consumption in the IVD under static and dynamic unconfined compression numerically.
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Huang, Chun-Yuh, and Wei Yong Gu. "Distribution of Oxygen, Glucose and Lactate in Degenerated Intervertebral Disc." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206557.

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Poor nutritional supply has been a major concern for the health of intervertebral disc (IVD) since the IVD is the largest avascular tissue in the human body. The transport of vital nutrients to cells relies on diffusion and convection through the extracellular matrix (ECM) in the IVD. Transport and metabolism of nutrients (e.g., oxygen and glucose) within the IVD depend on many factors, including the material properties of ECM (e.g., permeability, elastic modulus, and solute diffusivity), cellular metabolic rates, nutritional supply at the edge of the IVD, and mechanical loading [1–6]. Tissue degeneration alters the material properties of the IVD, such as an increase in elastic modulus and a decrease in water content, fixed charge density, permeability and solute diffusivity [6]. However, the effect of tissue degeneration on transport and metabolism of nutrients in the IVD under mechanical loading has not been elucidated. The objective of this study was to numerically investigate the distribution of glucose, oxygen and lactate in the degenerated IVD under static unconfined compression using the mechano-electrochemical mixture theory [7].
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Cescon, Marzia, Rolf Johansson, and Eric Renard. "Low-complexity MISO models of T1DM glucose metabolism." In 2013 9th Asian Control Conference (ASCC). IEEE, 2013. http://dx.doi.org/10.1109/ascc.2013.6606387.

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Wysocki, Beata J., Emalie J. Clement, Paul H. Davis, and Tadeusz A. Wysocki. "Simulation of central glucose metabolism using queueing network." In 2017 IEEE International Conference on Electro Information Technology (EIT). IEEE, 2017. http://dx.doi.org/10.1109/eit.2017.8053358.

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Reports on the topic "Glucose metabolism"

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Corscadden, Louise, and Anjali Singh. Metabolism And Measurable Metabolic Parameters. ConductScience, December 2022. http://dx.doi.org/10.55157/me20221213.

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Metabolism is the sum of chemical reactions involved in sustaining the life of organisms.[1] It constantly provides your body with the energy to perform essential functions. The process is categorized into two groups:[2] Catabolism: It’s the process of breaking down molecules to obtain energy. For example, converting glucose to pyruvate by cellular respiration. Anabolism: It’s the process of synthesis of compounds required to run the metabolic process of the organisms. For example, carbohydrates, proteins, lipids, and nucleic acids.[2] Metabolism is affected by a range of factors, such as age, sex, muscle mass, body size, and physical activity affect metabolism or BMR (the basal metabolic rate). By definition, BMR is the minimum amount of calories your body requires to function at rest.[2] Now, you have a rough idea about the concept. But, you might wonder why you need to study it. What and how metabolic parameters are measured to determine the metabolism of the organism? Find the answer to all these questions in this article.
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Harmon, David L., Israel Bruckental, Gerald B. Huntington, Yoav Aharoni, and Amichai Arieli. Influence of Small Intestinal Protein on Carbohydrate Assimilation in Beef and Dairy Cattle. United States Department of Agriculture, August 1995. http://dx.doi.org/10.32747/1995.7570572.bard.

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The long term goal of the proposed research, "Influence of small intestinal protein on carbohydrate assimilation and metabolism in beef and dairy cattle" was to define the limits of small intestinal starch digestion and clarify regulatory mechanisms involved in starch assimilation in cattle. It was hypothesized that dietary protein plays a critical role in the regulation of intestinal digestion; however, studies clearly identifying this role were lacking. The first two experiments quantified starch digestion (disappearance from the small intestine) in response to known increments in duodenal protein supply and found that the quantity of DM, OM and starch disappearing from the small intestine increased linearly (P <.01) with protein infusion. A follow-up experiment also demonstrated that casein infusion linearly increased pancreatic a-amylase concentration and secretion rate. The final experiment provided critical data on metabolic fates of glucose derived from intestinal starch digestion. These data demonstrated that increasing postruminal starch supply does increase the metabolism of glucose by visceral tissues: however, this increase is minor (20%) compared with the increase in portal production (70%). These changes can have a dramatic impact on the glucose economy of the animal and result in large increases in the amount of glucose reaching peripheral tissues.
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Research, Gratis. Brown Fat Activation: A Future Treatment for Obesity & Diabetes. Gratis Research, November 2020. http://dx.doi.org/10.47496/gr.blog.01.

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Brown fat holds a promising therapeutic approach to prevent obesity and type 2 diabetes by its profound effects on body weight reduction, heat generation, increased insulin sensitivity and glucose metabolism regulation
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Cohen, Jerry D., and Ephraim Epstein. Metabolism of Auxins during Fruit Development and Ripening. United States Department of Agriculture, August 1995. http://dx.doi.org/10.32747/1995.7573064.bard.

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We had proposed to look at several aspects of auxin metabolism in fruit tissues: 1) IAA biosynthesis from tryptophan and IAA biosynthesis via the non-tryptophan pathway; 2) changes in the capacity to form conjugates and catabolites of auxin at different times during fruit development and; 3) the effects of modifying auxin metabolism in fruit tissues. The latter work focused primarily on the maize iaglu gene, with initial studies also using a bacterial gene for hydrolysis of IAA-aspartate. These metabolic and molecular studies were necessary to define potential benefits of auxin metabolism modification and will direct future efforts for crop improvement by genetic methods. An in vitro system was developed for the production of tomato fruit in culture starting from immature flowers in order to ascertain the effect of auxin modification on fruit ripening. IAA supplied to the fruit culture media prior to breaker stage resulted in an increase in the time period between breaker and red-ripe stages from 7 days without additional IAA to 12 days when 10-5 M IAA was added. These results suggest that significant changes in the ripening period could be obtained by alteration of auxin relationships in tomato fruit. We generated transgenic tomato plants that express either the maize iaglu gene or reduced levels of the gene that encodes the enzyme IAA-glucose synthetase. A modified shuttle vector pBI 121 expressing the maize iaglu gene in both sense and antisense orientations under a 35S promoter was used for the study. The sense plants showed total lack of root initiation and development. The antisense transgenic plants, on the other hand, had unusually well developed root systems at early stages in development. Analysis showed that the amount and activity of the endogenous 75 kDa IAGLU protein was reduced in these plants and consequently these plants had reduced levels of IAA-glucose and lower overall esterified IAA.
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Gao, Hui, Chen Gong, Shi-chun Shen, Jia-ying Zhao, Dou-dou Xu, Fang-biao Tao, Yang Wang, and Xiao-chen Fan. A systematic review on the associations between prenatal phthalate exposure and childhood glycolipid metabolism and blood pressure: evidence from epidemiological studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0111.

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Review question / Objective: The present systematic review was performed to obtain a summary of epidemiological evidence on the relationships of in utero exposure to phthalates with childhood glycolipid metabolism and blood pressure. Condition being studied: Childhood cardiovascular risk factors including blood pressure, lipid profile (e.g., triglycerides, total cholesterol, HDL−C, LDL−C) and glucose metabolism (e.g., insulin, insulin resistance, insulin sensitivity, glucose) were the interested outcomes. Eligibility criteria: In brief, epidemiological studies including cohort study, case-control study and cross-sectional survey were screened. Studies regarding relationships between human exposure to organophosphate esters and neurotoxicity were possible eligible for the present systematic review. The adverse neurodevelopmental outcomes included development of cognition, behavior, motor, brain change, emotion, etc. Studies that did not meet the above criteria were not included in this systematic review.
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Lekhanya, Portia Keabetswe, and Kabelo Mokgalaboni. Exploring the effectiveness of vitamin B12 complex and alpha-lipoic acid as a treatment for diabetic neuropathy. Protocol for systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0167.

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Review question / Objective: Does Alpha-Lipoic acid increase the uptake of glucose for better glycaemic control? Does vitamin B12 and Alpha-Lipoic acid improve inflammation? The aim of the study is to explore the effectiveness of Vitamin B12 and Alpha-Lipoic Acid as a possible treatment for diabetic neuropathy with major emphasis on markers of inflammation and glucose metabolism. Condition being studied: Diabetic Neuropathy (DN) is a heterogeneous type of nerve damage associated with diabetes mellitus, the condition most often damages nerves in the legs and feet. It presents both clinically and sub-clinically affecting the peripheral nervous system as a result of an increase in glucose concentration which interferes with nerve signalling. After the discovery of insulin as a treatment for Diabetes Mellitus (DM), the prevalence of DN has since increased significantly due to DM patients having a longer life expectancy. It has been estimated that atleast 50% of DM patients will develop DN in their life, with approximately 20% of these patients experiencing neuropathic pain. Nerves are susceptible to changes in glucose concentrations and insulin makes it impossible for neurons to continue regulating glucose uptake.
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Cicero, Arrigo F. G. Effects of a combined nutraceutical on glucose and lipid metabolism in women with post-menopausal incident metabolic syndrome: a double-blind, placebocontrolled, randomized clinical trial. Science Repository, June 2019. http://dx.doi.org/10.31487/j.jfnm.2019.02.01.

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Han, Yiran, Zeyuan Lu, Meng Meng, Heran Wang, Pan Ting, Gao Tianjiao, and Mingjun Liu. Effect of Acupuncture on Glucose and Lipid Metabolism in Obese Type 2 Diabetes: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2021. http://dx.doi.org/10.37766/inplasy2021.3.0087.

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Han, Yiran, Zeyuan Lu, Meng Meng, Heran Wang, Pan Ting, Tianjiao Gao, and Mingjun Liu. Effect of Electroacupuncture on Glucose and Lipid Metabolism in Type 2 Diabetes: A protocol for Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0008.

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Bennett, Alan B., Arthur Schaffer, and David Granot. Genetic and Biochemical Characterization of Fructose Accumulation: A Strategy to Improve Fruit Quality. United States Department of Agriculture, June 2000. http://dx.doi.org/10.32747/2000.7571353.bard.

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The goal of the research project was to evaluate the potential to genetically modify or engineer carbohydrate metabolism in tomato fruit to enhance levels of fructose, a sugar with nearly twice the sweetness value of other sugars. The specific research objectives to achieve that goal were to: 1. Establish the inheritance of a fructose-accumulating trait identified in F1 hybrids of an inferspecific cross between L. hirsutum XL. esculentum and identify linked molecular markers to facilitate its introgression into tomato cultivars. This objective was completed with the genetic data indicating a single major gene, termed Fgr (Fructose glucose ratio), that controlled the partitioning of hexose in the mature fruit. Molecular markers for the gene, were developed to aid introgression of this gene into cultivated tomato. In addition, a second major gene encoding fructokinase 2 (FK2) was found to be a determinant of the fructose to glucose ratio in fruit. The relationship between FK2 and Fgr is epistatic with a combined synergistic effect of the two hirsutum-derived genes on fructose/glucose ratios. 2. Characterize the metabolic and transport properties responsible for high fructose/glucose ratios in fructose-accumulating genotypes. The effect of both the Fgr and FK2 genes on the developmental accumulation of hexoses was studied in a wide range of genetic backgrounds. In all backgrounds the trait is a developmental one and that the increase in fructose to glucose ratio occurs at the breaker stage of fruit development. The following enzymes were assayed, none of which showed differences between genotypes, at either the breaker or ripe stage: invertase, sucrose synthase, FK1, FK2, hexokinase, PGI and PGM. The lack of effect of the FK2 gene on fructokinase activity is surprising and at present we have no explanation for the phenomenon. However, the hirsutum derived Fgr allele was associated with significantly lower levels of phosphorylated glucose, G1c-1-P and G1c-6-P and concomitantly higher levels of the phosphorylated fructose, Fru-6-P, in both the breaker and ripe stage. This suggests a significant role for the isomerase reaction. 3. Develop and implement molecular genetic strategies for the production of transgenic plants with altered levels of enzymes that potentially control fructose/glucose ratios in fruit. This objective focused on manipulating hexokinase and fructokinase expression in transgenic plants. Two highly divergent cDNA clones (Frk1 and Frk2), encoding fructokinase (EC 2.7.1.4), were isolated from tomato (Lycopersicon esculentum) and a potato fructokinase cDNA clone was obtained from Dr. Howard Davies. Following expression in yeast, each fructokinase was identified to code for one of the tomato or potato fructokinase isoforms Transgenic tomato plants were generated with the fructokinase cDNA clone in both sense and antisense orientations and the effect of the gene on tomato plants is currently being studied.
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