Relevant bibliographies by topics / Gluconeogenese

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Gluconeogenese'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 July 2024

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Journal articles on the topic "Gluconeogenese"

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Slahor, Lea. "CME: Metformin – Dos und Don’ts CME-Fragen." Praxis 110, no. 16 (2021): 939–45. http://dx.doi.org/10.1024/1661-8157/a003774.

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Zusammenfassung. Obwohl sich die Diabetestherapie im Wandel befindet, stellt Metformin weiterhin die Standardtherapie bei Diabetes mellitus Typ 2 dar, fehlende Kontraindikationen vorausgesetzt. Metformin wird sowohl als Monotherapie als auch in Kombination mit allen anderen Präparaten in der Diabetestherapie eingesetzt. Als Biguanid wirkt Metformin über eine Hemmung der hepatischen Gluconeogenese und verbessert die Insulinsensitivät im peripheren Gewebe. Metformin führt zu einer moderaten Gewichtsabnahme und weist weitere Vorteile auf: Fehlendes Hypoglykämierisiko, gute Verträglichkeit, Langzeiterfahrungen in der Anwendung, geringe Therapiekosten. Die häufigsten gastrointestinalen Nebenwirkungen sind meist mild und passager, doch kann ein Vitamin-B12-Mangel auftreten. Auch wenn die Metformin-assoziierte Laktatazidose (MALA) selten auftritt, stellt diese eine relevante Komplikation dar, die mit einer hohen Mortalität assoziiert ist. Das Risiko steigt mit eingeschränkter Nierenfunktion, sodass die Metformindosis an die eGFR angepasst werden muss und Metformin bei einer eGFR <30 ml/min/1,73 m2 nicht eingesetzt werden darf. Als weitere Kontraindikationen gelten: aktive oder progrediente Lebererkrankung, Alkoholabusus, instabile oder akute Herzinsuffizienz, Situationen mit Hypoperfusion oder hämodynamische Instabilität, sowie eine Laktatazidose in der Vorgeschichte. Metformin bleibt eine moderne Therapie, deren Indikationen und Kontraindikationen es zu kennen gilt.
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Slahor, Lea. "CME/Antworten: Metformin – Dos und Don’ts." Praxis 111, no. 1 (2022): 5–7. http://dx.doi.org/10.1024/1661-8157/a003775.

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Zusammenfassung. Obwohl sich die Diabetestherapie im Wandel befindet, stellt Metformin weiterhin die Standardtherapie bei Diabetes mellitus Typ 2 dar, fehlende Kontraindikationen vorausgesetzt. Metformin wird sowohl als Monotherapie als auch in Kombination mit allen anderen Präparaten in der Diabetestherapie eingesetzt. Als Biguanid wirkt Metformin über eine Hemmung der hepatischen Gluconeogenese und verbessert die Insulinsensitivät im peripheren Gewebe. Metformin führt zu einer moderaten Gewichtsabnahme und weist weitere Vorteile auf: Fehlendes Hypoglykämierisiko, gute Verträglichkeit, Langzeiterfahrungen in der Anwendung, geringe Therapiekosten. Die häufigsten gastrointestinalen Nebenwirkungen sind meist mild und passager, doch kann ein Vitamin-B12-Mangel auftreten. Auch wenn die Metformin-assoziierte Laktatazidose (MALA) selten auftritt, stellt diese eine relevante Komplikation dar, die mit einer hohen Mortalität assoziiert ist. Das Risiko steigt mit eingeschränkter Nierenfunktion, sodass die Metformindosis an die eGFR angepasst werden muss und Metformin bei einer eGFR <30 ml/min/1,73 m2 nicht eingesetzt werden darf. Als weitere Kontraindikationen gelten: aktive oder progrediente Lebererkrankung, Alkoholabusus, instabile oder akute Herzinsuffizienz, Situationen mit Hypoperfusion oder hämodynamische Instabilität, sowie eine Laktatazidose in der Vorgeschichte. Metformin bleibt eine moderne Therapie, deren Indikationen und Kontraindikationen es zu kennen gilt.
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Tian, Xiaoting, Zhou Xu, Pei Hu, et al. "Determination of the antidiabetic chemical basis of Phellodendri Chinensis Cortex by integrating hepatic disposition in vivo and hepatic gluconeogenese inhibition in vitro." Journal of Ethnopharmacology 263 (December 2020): 113215. http://dx.doi.org/10.1016/j.jep.2020.113215.

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ESCHRICH, D., P. KOTTER, and K. ENTIAN. "Gluconeogenesis in." FEMS Yeast Research 2, no. 3 (2002): 315–25. http://dx.doi.org/10.1016/s1567-1356(02)00087-9.

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Eschrich, D., P. Kötter, and K. D. Entian. "Gluconeogenesis inCandida albicans." FEMS Yeast Research 2, no. 3 (2002): 315–25. http://dx.doi.org/10.1111/j.1567-1364.2002.tb00100.x.

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Rodriguez-Contreras, Dayana, and Nicklas Hamilton. "Gluconeogenesis inLeishmania mexicana." Journal of Biological Chemistry 289, no. 47 (2014): 32989–3000. http://dx.doi.org/10.1074/jbc.m114.569434.

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Minton, Kirsty. "CDK4 suppresses gluconeogenesis." Nature Reviews Molecular Cell Biology 15, no. 7 (2014): 429. http://dx.doi.org/10.1038/nrm3831.

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van den Berghe, G. "Disorders of gluconeogenesis." Journal of Inherited Metabolic Disease 19, no. 4 (1996): 470–77. http://dx.doi.org/10.1007/bf01799108.

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Hetenyi, G. "Gluconeogenesis in vivo." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 249, no. 6 (1985): R792—R793. http://dx.doi.org/10.1152/ajpregu.1985.249.6.r792.

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Frizzell, R. Tyler, Peter J. Campbell, and Alan D. Cherrington. "Gluconeogenesis and hypoglycemia." Diabetes / Metabolism Reviews 4, no. 1 (1988): 51–70. http://dx.doi.org/10.1002/dmr.5610040107.

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Dissertations / Theses on the topic "Gluconeogenese"

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Regelmann, Jochen. "Katabolitinaktivierung der Fructose-1,6-bisphosphatase: Identifizierung und Charakterisierung neuer, für ihren Ubiquitin-Proteasom-katalysierten Abbau benötigter Proteine." [S.l. : s.n.], 2005. http://nbn-resolving.de/urn:nbn:de:bsz:93-opus-25854.

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BahaaAldeen, Al-Trad. "Effects of Increasing Intravenous Glucose Infusions on Lactation Performance, Metabolic Profiles, and Metabolic Gene Expression in Dairy Cows." Doctoral thesis, Universitätsbibliothek Leipzig, 2010. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-38233.

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Knowledge on the precise effects of surplus glucose supply in dairy cows is limited by the lack of information on how intermediary metabolism adapts at different levels of glucose availability. Therefore, a gradual increase of glucose supply via intravenous glucose infusion was used in the present study to test the dose effect of surplus provision of glucose on the metabolic status and milk production of dairy cows. Furthermore, the effects of increasing levels of surplus glucose on mRNA expressions and activities of rate-limiting enzymes involved in hepatic gluconeogenesis were investigated. Based on a previous finding that a positive energy balance may decrease hepatic carnitine palmitoyltransferase (CPT) enzyme activity, it was also of interest whether skeletal muscle CPT activity is downregulated in a similar manner during positive energy balance. Twelve midlactating Holstein-Friesian dairy cows were continuously infused over a 28-d experimental period with either saline (SI group, six cows) or 40% glucose solutions (GI group, six cows). The infusion dose was calculated as a percentage of the daily energy (NEL) requirements by the animal, starting at 0% on d 0 and increasing gradually by 1.25%/d until a maximum dose of 30% was reached by d 24. Dose was then maintained at 30% NEL requirement for 5 d. No infusions were made between d 29-32. Liver and skeletal muscle biopsies were taken on d 0, 8, 16, 24, and 32. Body weight (BW) and back fat thickness (BFT) were recorded on biopsies days. Blood samples were taken every 2 d. In addition, blood samples over 24 h (6-h intervals) were taken the days before each biopsy. Milk and urine samples were taken on biopsies days. BW and BFT increased linearly with increasing glucose dose for GI cows. No differences were observed in the dry matter intake, milk energy output, and energy corrected milk yield between groups. However, milk protein percentage and yield increased linearly in the GI group. Only occasional increases in blood glucose and insulin concentrations were observed in blood samples taken at 1000 h every 2 d. However, during infusion dose of 30% NEL requirements on d 24, GI cows developed postprandial hyperglycemia associated with hyperinsulinemia, coinciding with glucosuria. The revised quantitative insulin sensitivity check index (RQUIKI) indicated linear development of insulin resistance for the GI treatment. GI decreased serum concentrations of beta-hydroxybutyrate (BHBA) and blood urea nitrogen and tended to decrease the serum concentration of non-esterified fatty acids (NEFA). Liver glycogen content increased, while glycogen content in skeletal muscle only tended to increase by GI. No significant changes were observed in the activities and relative mRNA expression levels of hepatic phosphoenolpyruvate carboxykinase and glucose 6-phospatase. The activity of fructose 1,6-bisphosphatase (FBPase) and relative mRNA expression levels of pyruvate carboxylase (PC) were decreased in the GI group but only during the high dose of glucose infusion. Hepatic CPT activity decreased with GI and remained decreased on d 32. The hepatic expression levels of CPT-1A and CPT-2 mRNA were not significantly altered but tended to reflect the changes in enzyme activity. No effect of glucose infusion was observed on skeletal muscle CPT activity. The aforementioned adaptations were reversed four days after the end of glucose infusions except for those of BW, BFT, and lipid metabolism (i.e. serum BHBA and NEFA concentrations, hepatic CPT activity). It is concluded that mid-lactation dairy cows on an energy-balanced diet direct intravenously infused glucose predominantly to body fat reserves but not to increased lactation performance. Cows rapidly adapted to increasing glucose supply but experienced dose-dependent development of insulin resistance corresponding with postprandial hyperglycemia/hyperinsulinemia and glucosuria at dosages equivalent to 30% NEL requirements. The catalytic capacity of key hepatic gluconeogenesis enzymes in mid-lactating dairy cows is not significantly affected by nutritionally relevant increases of glucose supply. Only very high dosages selectively suppress PC transcription and FBPase activity. Finally, it can be concluded that suppression of CPT activity by positive energy balance appears to be specific for the liver in midlactating dairy cows.
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Leverve, Xavier. "Périfusion d'hépatocytes et analyse du contrôle : description et application à l'étude de la protéolyse et de la gluconéogénèse." Lyon 1, 1989. http://www.theses.fr/1989LYO1H078.

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Filippi, Céline. "Conséquences métaboliques d'une hypoxie modérée : étude sur hépatocytes périfusés." Université Joseph Fourier (Grenoble), 1999. http://www.theses.fr/1999GRE10175.

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Le but de ce travail etait d'etudier les consequences d'une hypoxie moderee sur la glycolyse et la neoglucogenese hepatocytaires. Notre modele consiste en une hypoxie transitoire en perifusion, d'une duree de 30 minutes qui permet de maintenir une consommation d'oxygene relativement importante par les cellules, de l'ordre de 6 micromol. Min - 1. Gps - 1, alors que la pression partielle en oxygene est proche de zero. La premiere partie presente les resultats obtenus avec divers substrats : alanine, lactate et pyruvate, pyruvate seul, glycerol, dihydroxyacetone ou fructose. Au cours de l'hypoxie, la glycolyse est stimulee quel que soit le substrat utilise. Au bout des 30 minutes d'hypoxie, la gluconeogenese est effondree a partir de tous les substrats sauf a partir du fructose qui permet de maintenir 70% de la production de glucose hepatocytaire. La seconde partie de ce travail tente donc d'expliquer le maintien de la neoglucogenese hepatocytaire lorsque les cellules sont perifusees en presence de fructose. Pour ceci, nous avons compare son metabolisme a celui de la dihydroxyacetone, un autre hydrate de carbone qui, comme le fructose, entre dans la voie de la glycolyse/neoglucogenese au niveau des trioses phosphate. La preservation du flux de glucose a partir du fructose au cours de l'hypoxie n'est pas due a une accumulation de composes phosphoryles ou de glycogene pendant la preincubation precedant l'hypoxie. Elle ne semble pas non plus due a une action sur le pore de transition de permeabilite mitochondriale. Une augmentation de la phosphorylation directe du fructose par l'hexokinase au cours de l'hypoxie n'a pas pu etre ni confirmee ni infirmee. En revanche, un flux glycolytique eleve et le maintien d'un rapport nadh/nad bas, caracteristiques du metabolisme du fructose, semblent necessaires pour maintenir le flux glucogenique en hypoxie.
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MacDonald, Donald John. "Gluconeogenesis in pregnancy." Thesis, Glasgow Caledonian University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382733.

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Nedelec, Jean-François. "Modifications du metabolisme hepatique chez la souris : effets d'une leucemie (mplv) : effets de la conservation a basse temperature : application de la resonnance magnetique nucleaire." Paris 6, 1988. http://www.theses.fr/1988PA066436.

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Ekberg, Karin. "Quantitation of gluconeogenesis in humans /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-2810-x.

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Magnoni, Leonardo J. "Antarctic Notothenioid Fishes Do Not Display Metabolic Cold Adaptation in Hepatic Gluconeogenesis." Fogler Library, University of Maine, 2002. http://www.library.umaine.edu/theses/pdf/MagnoniLJ2002.pdf.

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chalhoub, Elie R. "An In silico Liver: Model of gluconeogenesis." Cleveland State University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=csu1363603404.

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Leclercq, Pascale. "Etat infectieux et métabolisme des hydrates de carbone : études in vitro sur hépatocytes isolés et in vivo chez des patients infectés par le VIH." Université Joseph Fourier (Grenoble ; 1971-2015), 1997. http://www.theses.fr/1997GRE10122.

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Le sepsis induit une inhibition de la neoglucogenese (ngg). Modele experimental : sepsis de gravite moderee chez des rats traites par endotoxine avec preparation d'hepatocytes isoles et technique de perfusion. Localisation du niveau et des mecanismes de l'inhibition. Inhibition au niveau du cycle pyruvatephosphoenolpyruvate sans modification de la pyruvate kinase (role de la pepck). Pas d'alteration du cycle des fructoses par le sepsis ; possible inhibition du cycle des glucoses (inhibition de la glucose-6-phosphatase). Etude de la ngg a partir du glycerol (independante de la pepck et fonction du potentiel redox cellulaire) : inhibition avec accumulation de glycerol-3-phosphate (g3p) d'ou activation de la voie de la glycerol-3-phosphate deshydrogenase mitochondriale (navette g3p/dhap) et modification du potentiel redox. Sepsis : augmentation du volume cellulaire independante des substrats qui agit comme second messager sur le metabolisme hepatocytaire. Pas de modification de l'etat energetique cellulaire dans ce sepsis de gravite moderee. Resume des modifications induites par le sepsis : par le biais des cytokines et du no comme messager intracellulaire, induction d'un gonflement cellulaire (modification des transporteurs ?) puis modifications enzymatiques : inhibition de la pepck. Dans le cas du glycerol, c'est l'accumulation du glycerol-3-phosphate qui est responsable de l'inhibition de la ngg. 2eme partie : modifications metaboliques chez le patient infecte par le vih protocole experimental associant une etude du metabolisme du lactate et une mesure par calorimetrie indirecte de la depense energetique de repos (der) et celle induite par le test d'hyperlactatemie (patients vih et controles). Mesures de der : les patients vih en phase stable ne sont pas hypermetaboliques. Pas de modification du metabolisme du lactate (demi-vie, clairance, production endogene) chez les vih. Insulino-sensibilite avec moindre elevation de la glycemie chez les malades.
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Books on the topic "Gluconeogenese"

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Naomi, Kraus-Friedmann, ed. Hormonal control of gluconeogenesis. CRC Press, 1986.

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S, Milʹman L., ed. Reguli͡a︡t͡s︡ii͡a︡ gli͡u︡koneogeneza v ontogeneze. "Nauka", 1987.

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Pennington, Anne June. Glycogenolysis and gluconeogenesis in the segmental ganglia of the leech Haemopis Sanguisuga. University of Salford, 1988.

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Zhang, Weizhen, ed. Gluconeogenesis. InTech, 2017. http://dx.doi.org/10.5772/63700.

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Hormonal control of gluconeogenesis. CRS Press, 1986.

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Kraus-Friedmann. Hormonal Control of Gluconeogenesis: Signal Transmission. CRC, 1986.

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Kraus-Friedmann, Naomi. Hormonal Control of Gluconeogenesis: Function and Experimental Approaches. Crc Pr I Llc, 1986.

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Glucoregulation and work performance in gluconeogenesis-inhibited iron deficient rats. 1992.

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Glucoregulation and work performance in gluconeogenesis-inhibited iron deficient rats. 1991.

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Glucose kinetics at rest and during exercise in gluconeogenesis-inhibited rats. 1988.

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Book chapters on the topic "Gluconeogenese"

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Berg, Jeremy M., John L. Tymoczko, Gregory J. Gatto, and Lubert Stryer. "Glykolyse und Gluconeogenese." In Stryer Biochemie. Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-54620-8_16.

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Berg, Jeremy M., John L. Tymoczko, and Lubert Stryer. "Glykolyse und Gluconeogenese." In Stryer Biochemie. Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-8274-2989-6_16.

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Schuit, F. C. "Glycogeenmetabolisme, gluconeogenese en ketogenese." In Leerboek metabolisme en voeding. Bohn Stafleu van Loghum, 2019. http://dx.doi.org/10.1007/978-90-368-2358-6_6.

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Müller-Esterl, Werner. "Gluconeogenese und Cori-Zyklus." In Biochemie. Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-54851-6_43.

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Müller-Esterl, Werner. "Gluconeogenese und Cori-Zyklus." In Biochemie. Spektrum Akademischer Verlag, 2011. http://dx.doi.org/10.1007/978-3-8274-2227-9_43.

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Schuit, Frans C. "Glycogeenmetabolisme, gluconeogenese en pentosefosfaatweg." In Leerboek metabolisme. Bohn Stafleu van Loghum, 2015. http://dx.doi.org/10.1007/978-90-368-0620-6_6.

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Christen, Philipp, Rolf Jaussi, and Roger Benoit. "Gluconeogenese, Glykogen, Disaccharide und Pentosephosphatweg." In Biochemie und Molekularbiologie. Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46430-4_16.

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Nelson, David L., and Michael M. Cox. "Glycolyse, Gluconeogenese und der Pentosephosphatweg." In Springer-Lehrbuch. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-540-68638-5_14.

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Stryer, Lubert. "Der Pentosephosphatweg und die Gluconeogenese." In Biochemie. Vieweg+Teubner Verlag, 1987. http://dx.doi.org/10.1007/978-3-322-83526-0_15.

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Schuit, Frans C. "6 Glycogeenmetabolisme, gluconeogenese en pentosefosfaatweg." In Metabolisme. Bohn Stafleu van Loghum, 2010. http://dx.doi.org/10.1007/978-90-313-8225-5_6.

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Conference papers on the topic "Gluconeogenese"

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Andrade-Cetto, A., G. Mata-Torres Valle, A. Espinoza-Hernández, and J. Cárdenas-Vázquez René de. "Hepatic gluconeogenesis inhibition by four traditional used, hypoglycemic plants." In GA 2017 – Book of Abstracts. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1608562.

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Berilli, Ana Luiza de Jesus, and Maria Luiza Ferreira Stringhini. "Type 2 diabetes mellitus and depression." In V Seven International Multidisciplinary Congress. Seven Congress, 2024. http://dx.doi.org/10.56238/sevenvmulti2024-072.

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Type 2 diabetes mellitus (DM2) is a chronic non-communicable disease characterized by persistent hyperglycemia resulting from a deficiency in the synthesis and/or secretion of insulin by pancreatic b-cells, associated with other factors such as insulin resistance in peripheral tissues, hyperglucagonemia , increased hepatic gluconeogenesis, among others (American Diabetes Association, 2023; WHO, 2019). According to the International Diabetes Federation 2021, approximately 8.8% of the world's adult population has diabetes, of which 79% live in developing countries. Following this projection, it is estimated that by 2045 around 628.6 million individuals will have the disease.
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Paudel, Iru, Ramlogan Sowamber, Leah Dodds, et al. "Abstract B15: BRCA haploinsufficiency promotes gluconeogenesis in fallopian tube epithelial cells." In Abstracts: AACR Special Conference on Advances in Ovarian Cancer Research; September 13-16, 2019; Atlanta, GA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3265.ovca19-b15.

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Wang, Li, Yongqian Zhang, Hong Qing, et al. "Retention Time Prediction Based Proteomic Analysis on Proteins from Glycolysis/Gluconeogenesis Pathway of E. coli." In 2012 International Conference on Biomedical Engineering and Biotechnology (iCBEB). IEEE, 2012. http://dx.doi.org/10.1109/icbeb.2012.344.

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Hsu, Wei-Hsiang, Hong-Jhih Jhuang та Chi-Ying Huang. "Abstract 1132: Gluconeogenesis, lipogenesis, and HBV replication are commonly regulated by PGC-1α-dependent pathway". У Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1132.

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Wang, Bo, Shuhao Hsu, Wendy Frankel, Kalpana Ghoshal та Samson T. Jacob. "Abstract 5155: Suppression of gluconeogenesis in hepatocellular carcinoma by miR-23 directed downregulation of key gluconeogenic enzymes and the transcription factorPGC-1α". У Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5155.

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Luiza Figueiredo Vieira, Ana, Caroline Capitani, Isabela Micheletti Lorizola, Josiane Érica Miyamoto, and Marciane Milanski. "Evaluation of the weight gain of hepatic gluconeogenesis markers in animals submitted to a hyperlipid diet supplemented with beet stems and leaves (​Beta vulgaris​ L.)." In XXV Congresso de Iniciação Cientifica da Unicamp. Galoa, 2017. http://dx.doi.org/10.19146/pibic-2017-78993.

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Reports on the topic "Gluconeogenese"

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Cuervo Vivas, Wilmer Alfonso. Factores limitantes de la Gluconeogenesis en el periodo de transición de la vaca lechera. Universidad Nacional Abierta y a Distancia, 2017. http://dx.doi.org/10.22490/ecapma.1823.

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Butler, Walter R., Uzi Moallem, Amichai Arieli, Robert O. Gilbert, and David Sklan. Peripartum dietary supplementation to enhance fertility in high yielding dairy cows. United States Department of Agriculture, 2007. http://dx.doi.org/10.32747/2007.7587723.bard.

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Objectives of the project: To evaluate the effects of a glucogenic supplement during the peripartum transition period on insulin, hepatic triglyceride accumulation, interval to first ovulation, and progesterone profile in dairy cows. To compare benefits of supplemental fats differing in fatty acid composition and fed prepartum on hepatic triglyceride accumulation, interval to first ovulation, progesterone profile, and uterine prostaglandin production in lactating dairy cows. To assess the differential and carry-over effects of glucogenic and fat supplements fed to peripartum dairy cows on steroidogenesis and fatty acids in ovarian follicles. To determine the carry-over effects of peripartum glucogenic or fat supplements on fertility in high producing dairy cows (modified in year 3 to Israel only). Added during year 3 of project: To assess the activity of genes related to hepatic lipid oxidation and gluconeogenesis following dietary supplementation (USA only). Background: High milk yields in dairy cattle are generally associated with poor reproductive performance. Low fertility results from negative energy balance (NEBAL) of early lactation that delays resumption of ovarian cycles and exerts other carryover effects. During NEBAL, ovulation of ovarian follicles is compromised by low availability of insulin and insulin-like growth factor-I (IGF-I), but fatty acid mobilization from body stores is augmented. Liver function during NEBAL is linked to the resumption of ovulation and fertility: 1) Accumulation of fatty acids by the liver and ketone production are associated with delayed first ovulation; 2) The liver is the main source of IGF-I. NEBAL will continue as a consequence of high milk yield, but dietary supplements are currently available to circumvent the effects on liver function. For this project, supplementation was begun prepartum prior to NEBAL in an effort to reduce detrimental effects on liver and ovarian function. Fats either high or low in unsaturated fatty acids were compared for their ability to reduce liver triglyceride accumulation. Secondarily, feeding specific fats during a period of high lipid turnover caused by NEBAL provides a novel approach for manipulating phospholipid pools in tissues including ovary and uterus. Increased insulin from propylene glycol (glucogenic) was anticipated to reduce lipolysis and increase IGF-I. The same supplements were utilized in both the USA and Israel, to compare effects across different diets and environments. Conclusions: High milk production and very good postpartum health was achieved by dietary supplementation. Peripartum PGLY supplementation had no significant effects on reproductive variables. Prepartum fat supplementation either did not improve metabolic profile and ovarian and uterine responses in early lactation (USA) or decreased intake when added to dry cow diets (Israel). Steroid production in ovarian follicles was greater in lactating dairy cows receiving supplemental fat (unsaturated), although in a field trail fertility to insemination was not improved.
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3

Uni, Zehava, and Peter Ferket. Enhancement of development of broilers and poults by in ovo feeding. United States Department of Agriculture, 2006. http://dx.doi.org/10.32747/2006.7695878.bard.

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The specific objectives of this research were the study of the physical and nutritional properties of the In Ovo Feeding (IOF) solution (i.e. theosmostic properties and the carbohydrate: protein ratio composition). Then, using the optimal solution for determining its effect on hatchability, early nutritional status and intestinal development of broilers and turkey during the last quarter of incubation through to 7 days post-hatch (i.e. pre-post hatch period) by using molecular, biochemical and histological tools. The objective for the last research phase was the determination of the effect of in ovo feeding on growth performance and economically valuable production traits of broiler and turkey flocks reared under practical commercial conditions. The few days before- and- after hatch is a critical period for the development and survival of commercial broilers and turkeys. During this period chicks make the metabolic and physiological transition from egg nutriture (i.e. yolk) to exogenous feed. Late-term embryos and hatchlings may suffer a low glycogen status, especially when oxygen availability to the embryo is limited by low egg conductance or poor incubator ventilation. Much of the glycogen reserve in the late-term chicken embryo is utilized for hatching. Subsequently, the chick must rebuild that glycogen reserve by gluconeogenesis from body protein (mostly from the breast muscle) to support post-hatch thermoregulation and survival until the chicks are able to consume and utilize dietary nutrients. Immediately post-hatch, the chick draws from its limited body reserves and undergoes rapid physical and functional development of the gastrointestinal tract (GIT) in order to digest feed and assimilate nutrients. Because the intestine is the nutrient primary supply organ, the sooner it achieves this functional capacity, the sooner the young bird can utilize dietary nutrients and efficiently grow at its genetic potential and resist infectious and metabolic disease. Feeding the embryo when they consume the amniotic fluid (IOF idea and method) showed accelerated enteric development and elevated capacity to digest nutrients. By injecting a feeding solution into the embryonic amnion, the embryo naturally consume supplemental nutrients orally before hatching. This stimulates intestinal development to start earlier as was exhibited by elevated gene expression of several functional genes (brush border enzymes an transporters , elvated surface area, elevated mucin production . Moreover, supplying supplemental nutrients at a critical developmental stage by this in ovo feeding technology improves the hatchling’s nutritional status. In comparison to controls, administration of 1 ml of in ovo feeding solution, containing dextrin, maltose, sucrose and amino acids, into the amnion of the broiler embryo increased dramatically total liver glycogen in broilers and in turkeys in the pre-hatch period. In addition, an elevated relative breast muscle size (% of broiler BW) was observed in IOF chicks to be 6.5% greater at hatch and 7 days post-hatch in comparison to controls. Experiment have shown that IOF broilers and turkeys increased hatchling weights by 3% to 7% (P<0.05) over non injected controls. These responses depend upon the strain, the breeder hen age and in ovo feed composition. The weight advantage observed during the first week after hatch was found to be sustained at least through 35 days of age. Currently, research is done in order to adopt the knowledge for commercial practice.
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