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1

Kumar, B. Hemanth. "Regulation of Glucose Metabolism by Glucagon: A Review." Indian Journal of Applied Research 3, no. 9 (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 (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 (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 (2011): 628–35. http://dx.doi.org/10.1097/coc.0b013e3181e84dec.

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Vlad, Mihaela, Daniela Amzar, Diana Bănică, et al. "Glucose and Lipid Abnormalities in Newly Diagnosed Acromegalic Patients." Romanian Journal of Diabetes Nutrition and Metabolic Diseases 22, no. 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
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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 (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 indexa
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Navarro, Francisco, Aline V. N. Bacurau, Andréa Vanzelli та ін. "Changes in Glucose and Glutamine Lymphocyte Metabolisms Induced by Type I Interferon α". Mediators of Inflammation 2010 (2010): 1–6. http://dx.doi.org/10.1155/2010/364290.

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In lymphocytes (LY), the well-documented antiproliferative effects of IFN-α are associated with inhibition of protein synthesis, decreased amino acid incorporation, and cell cycle arrest. However, the effects of this cytokine on the metabolism of glucose and glutamine in these cells have not been well investigated. Thus, mesenteric and spleen LY of male Wistar rats were cultured in the presence or absence of IFN-α, and the changes on glucose and glutamine metabolisms were investigated. The reduced proliferation of mesenteric LY was accompanied by a reduction in glucose total consumption (35%),
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8

Pin, Carmen, Gonzalo D. García de Fernando, and Juan A. Ordóñez. "Effect of Modified Atmosphere Composition on the Metabolism of Glucose by Brochothrix thermosphacta." Applied and Environmental Microbiology 68, no. 9 (2002): 4441–47. http://dx.doi.org/10.1128/aem.68.9.4441-4447.2002.

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ABSTRACT The influence of atmosphere composition on the metabolism of Brochothrix thermosphacta was studied by analyzing the consumption of glucose and the production of ethanol, acetic and lactic acids, acetaldehyde, and diacetyl-acetoin under atmospheres containing different combinations of carbon dioxide and oxygen. When glucose was metabolized under oxygen-free atmospheres, lactic acid was one of the main end products, while under atmospheres rich in oxygen mainly acetoin-diacetyl was produced. The proportions of the total consumed glucose used for the production of acetoin (aerobic metabo
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Wu, Zhong-Qin, Xin-Ming Chen, Hui-Qin Ma, Ke Li, Yuan-Liang Wang, and Zong-Jun Li. "Akkermansia muciniphila Cell-Free Supernatant Improves Glucose and Lipid Metabolisms in Caenorhabditis elegans." Nutrients 15, no. 7 (2023): 1725. http://dx.doi.org/10.3390/nu15071725.

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To explore the mechanism by which Akkermansia muciniphila cell-free supernatant improves glucose and lipid metabolisms in Caenorhabditis elegans, the present study used different dilution concentrations of Akkermansia muciniphila cell-free supernatant as an intervention for with Caenorhabditis elegans under a high-glucose diet. The changes in lifespan, exercise ability, level of free radicals, and characteristic indexes of glucose and lipid metabolisms were studied. Furthermore, the expression of key genes of glucose and lipid metabolisms was detected by qRT-PCR. The results showed that A. muc
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10

Almeida Castro, Luis Henrique, Leandro Rachel Arguello, Nelson Thiago Andrade Ferreira, et al. "Energy metabolism." International Journal for Innovation Education and Research 8, no. 9 (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 tri
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11

STEFANYSHYN, N. P. "STARVATION DURING DEVELOPMENT AFFECTS METABOLISM IN DROSOPHILA." Biotechnologia Acta 16, no. 2 (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. Graphi
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12

DEVARAKONDA, KAVYA, MITCHELL BAYNE, ALEXANDRA ALVARSSON, and SARAH STANLEY. "Amygdala Glucose-Sensing Neurons Regulate Glucose Metabolism." Diabetes 67, Supplement 1 (2018): 1807—P. http://dx.doi.org/10.2337/db18-1807-p.

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13

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

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Rajas, Fabienne, Amandine Gautier-Stein, and Gilles Mithieux. "Glucose-6 Phosphate, a Central Hub for Liver Carbohydrate Metabolism." Metabolites 9, no. 12 (2019): 282. http://dx.doi.org/10.3390/metabo9120282.

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Cells efficiently adjust their metabolism according to the abundance of nutrients and energy. The ability to switch cellular metabolism between anabolic and catabolic processes is critical for cell growth. Glucose-6 phosphate is the first intermediate of glucose metabolism and plays a central role in the energy metabolism of the liver. It acts as a hub to metabolically connect glycolysis, the pentose phosphate pathway, glycogen synthesis, de novo lipogenesis, and the hexosamine pathway. In this review, we describe the metabolic fate of glucose-6 phosphate in a healthy liver and the metabolic r
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15

Wong, Wei. "Forced into glucose metabolism." Science Signaling 14, no. 684 (2021): eabj5683. http://dx.doi.org/10.1126/scisignal.abj5683.

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Tanabe, Akiyo. "Glucose metabolism in pheochromocytoma." Nihon Shuchu Chiryo Igakukai zasshi 16, no. 3 (2009): 248–50. http://dx.doi.org/10.3918/jsicm.16.248.

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17

Fraenkel, D. G. "Mutants in Glucose Metabolism." Annual Review of Biochemistry 55, no. 1 (1986): 317–37. http://dx.doi.org/10.1146/annurev.bi.55.070186.001533.

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Goel, Ashish, Saroj P. Mathupala, and Peter L. Pedersen. "Glucose Metabolism in Cancer." Journal of Biological Chemistry 278, no. 17 (2003): 15333–40. http://dx.doi.org/10.1074/jbc.m300608200.

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19

Barth, Eberhard, Gerd Albuszies, Katja Baumgart, et al. "Glucose metabolism and catecholamines." Critical Care Medicine 35, Suppl (2007): S508—S518. http://dx.doi.org/10.1097/01.ccm.0000278047.06965.20.

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Makhmudov, E. S., and V. A. Khodzhimatov. "Glucose metabolism and conception." Problems of Endocrinology 39, no. 2 (1993): 60–62. http://dx.doi.org/10.14341/probl11980.

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The birth of a full-fledged viable offspring is directly dependent on the state of the mother's body. Since the earliest periods of pregnancy, many factors of the external and internal environment have an effect on the intrauterine development of the fetus. Successful completion of pregnancy and the birth of healthy offspring are possible with a balanced metabolism and the satisfaction of all the needs of the mother's body. In this process, a large role is played by carbohydrates, and in particular glucose, which is intensively used by the intrauterine developing embryo. Glucose deficiency in
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21

Giugliano, Dario, Antonio Ceriello, and Katherine Esposito. "Glucose metabolism and hyperglycemia." American Journal of Clinical Nutrition 87, no. 1 (2008): 217S—222S. http://dx.doi.org/10.1093/ajcn/87.1.217s.

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22

Lee, Min Gyu, and Peter L. Pedersen. "Glucose Metabolism in Cancer." Journal of Biological Chemistry 278, no. 42 (2003): 41047–58. http://dx.doi.org/10.1074/jbc.m307031200.

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23

van Hooff, J. P., E. M. van Duijnhoven, and M. H. L. Christiaans. "Tacrolimus and glucose metabolism." Transplantation Proceedings 31, no. 7 (1999): 49–50. http://dx.doi.org/10.1016/s0041-1345(99)00795-2.

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24

Shaw, Reuben J. "Glucose metabolism and cancer." Current Opinion in Cell Biology 18, no. 6 (2006): 598–608. http://dx.doi.org/10.1016/j.ceb.2006.10.005.

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Ladds, Brian, and David Trachtenberg. "Glucose metabolism in murderers." Biological Psychiatry 38, no. 5 (1995): 342–43. http://dx.doi.org/10.1016/0006-3223(95)00216-4.

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26

Shmueli, E., and KGMM Alberti. "Glucose metabolism in cirrhosis." Journal of Hepatology 13 (January 1991): S171. http://dx.doi.org/10.1016/0168-8278(91)91658-4.

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Karner, Courtney M., and Fanxin Long. "Glucose metabolism in bone." Bone 115 (October 2018): 2–7. http://dx.doi.org/10.1016/j.bone.2017.08.008.

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28

Andrianantoandro, E. "Hedgehog Drives Glucose Metabolism." Science Signaling 5, no. 247 (2012): ec275-ec275. http://dx.doi.org/10.1126/scisignal.2003715.

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Zierler, Kenneth. "Whole body glucose metabolism." American Journal of Physiology-Endocrinology and Metabolism 276, no. 3 (1999): E409—E426. http://dx.doi.org/10.1152/ajpendo.1999.276.3.e409.

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This review describes major factors that, singly or together, influence the concentration and distribution ofd-glucose in mammals, particularly in humans, with emphasis on rest, physical activity, and alimentation. It identifies areas of uncertainty: distribution and concentrations of glucose in interstitial fluid, kinetics and mechanism of transcapillary glucose transport, kinetics and mechanism of glucose transport via its transporters into cells, detailed mechanisms by which hormones, exercise, and hypoxia affect glucose movement across cell membranes, whether translocation of glucose trans
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30

Leturque, A., S. Hauguel, P. Ferré, and J. Girard. "Glucose Metabolism in Pregnancy." Neonatology 51, no. 2 (1987): 64–69. http://dx.doi.org/10.1159/000242634.

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31

Mithieux, Gilles, and Amandine Gautier-Stein. "Intestinal glucose metabolism revisited." Diabetes Research and Clinical Practice 105, no. 3 (2014): 295–301. http://dx.doi.org/10.1016/j.diabres.2014.04.008.

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Vranic, Mladen. "Glucose metabolism in acromegaly." Diabetologia 30, no. 6 (1987): 442. http://dx.doi.org/10.1007/bf00292551.

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Yajurvedi, HN. "Stress and Glucose metabolism: A Review." Imaging Journal of Clinical and Medical Sciences 5, no. 1 (2018): 008–12. https://doi.org/10.17352/2455-8702.000037.

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Stress is an inescapable fact of life. The perceived stress induces endocrine alterations characterized by the activation of hypothalamo-pituitary-adrenal axis and sympathetic adreno-medullary axis. The glucocorticoids and catecholamines which are secreted in response to stress induce variations in the physiology and behavior that help the individual to adapt to changing demands of the body. Glucocorticoids are known to play a central role in inducing the stress related pathophysiology. These hormones induce hypermetabolism in order to cope up with the increasing energy demands of the body. Ho
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Agung, Biworo, Rezki Amalia Dwi, Rizky Amalia Lisda, Halim Valentina, and Suhartono Eko. "In Vitro Diabetogenic Effect of Cadmium on Liver." International Journal of Current Pharmaceutical Review and Research 8, no. 1 (2017): 68–73. https://doi.org/10.5281/zenodo.12678459.

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The objectives of this study were to determine the effect of cadmium (Cd) on glucose metabolism disruption in liver cellshomogenate in vitro. The glucose metabolism disruption was analyzed by measuring the level of liver glucose, glycogenand methylglyoxal (MG), and the activity of glucokinase activity. In this experiment, a liver sample was taken from malerats (Rattus novergicus). Samples then homogenized and divided into four groups with; C served as control which containsliver homogenate only; T1 which contains liver homogenate + 0.03 mg/l of cadmium sulphate (CdSO4); T2 which containsliver
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35

Kagotho, Elizabeth. "Insulin-Mediated Glucose Metabolism: An Atherogenic Lipid Profile of Fructose Consumption." Endocrinology and Disorders 2, no. 2 (2018): 01–02. http://dx.doi.org/10.31579/2640-1045/096.

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Our laboratory has investigated two hypotheses regarding the effects of fructose consumption: 1) The endocrine effects of fructose consumption favor a positive energy balance, and 2) Fructose consumption promotes the development of an atherogenic lipid profile. In previous short- and long-term studies, we demonstrated that consumption of fructose-sweetened beverages with 3 meals results in lower 24-hour plasma concentrations of glucose, insulin, and leptin in humans compared with consumption of glucose-sweetened beverages. We have also tested whether prolonged consumption of high-fructose diet
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36

Kataoka, H., N. Nakajima, T. Watabe, S. Fujimoto, Y. Okuhara, and Y. Hatakeyama. "Prediction Model for Glucose Metabolism Based on Lipid Metabolism." Methods of Information in Medicine 53, no. 05 (2014): 357–63. http://dx.doi.org/10.3414/me14-01-0034.

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Summary Objectives: We developed a robust, long-term clinical prediction model to predict conditions leading to early diabetes using laboratory values other than blood glucose and insulin levels. Our model protects against missing data and noise that occur during long-term analysis. Methods: Results of a 75-g oral glucose tolerance test (OGTT) were divided into three groups: diabetes, impaired glucose tolerance (IGT), and normal (n = 114, 235, and 325, respectively). For glucose metabolic and lipid metabolic parameters, near 30-day mean values and 10-year integrated values were compared. The r
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Fransisca, Diana Alexandra, Mutiasari Dian, Lestaris Trilianty, and Suhartono Eko. "The Protective Efficacy of Ethanolic Leaves Extract of Citronella Gras (Cymbopogon nardus) on Glucose Metabolism Alteration Induced By Mercury in Rats." International Journal of Toxicological and Pharmacological Research 9, no. 3 (2017): 215–20. https://doi.org/10.5281/zenodo.12700722.

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The present study was undertaken to investigate the protective effect of ethanolic citronella grass (C. nardus) leaves extract against mercury (Hg) induced glucose metabolism alteration in rats. Four groups of rats were selected, with 6 rats for each group. Animals of group I  was received a 1 ppm of Hg only. Animals of groups II, III, and IV received a combination of 1 ppm Hg and plant extract in different dose (1650, 2520, and 3360 mg/ml). The experiment lasted for 4 weeks. The various parameters studied included liver weight, liver glucose, glycogen, and malondialdehyde (MDA) level in
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38

Stinkens, R., G. H. Goossens, J. W. E. Jocken, and E. E. Blaak. "Targeting fatty acid metabolism to improve glucose metabolism." Obesity Reviews 16, no. 9 (2015): 715–57. http://dx.doi.org/10.1111/obr.12298.

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Zhang, Yi, Qiong Li, Zhao Huang, et al. "Targeting Glucose Metabolism Enzymes in Cancer Treatment: Current and Emerging Strategies." Cancers 14, no. 19 (2022): 4568. http://dx.doi.org/10.3390/cancers14194568.

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Reprogramming of glucose metabolism provides sufficient energy and raw materials for the proliferation, metastasis, and immune escape of cancer cells, which is enabled by glucose metabolism-related enzymes that are abundantly expressed in a broad range of cancers. Therefore, targeting glucose metabolism enzymes has emerged as a promising strategy for anticancer drug development. Although several glucose metabolism modulators have been approved for cancer treatment in recent years, some limitations exist, such as a short half-life, poor solubility, and numerous adverse effects. With the rapid d
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40

Itagaki, Teruyuki, Yoshinori Itoh, Yuichi Sugai, Naomi Suematsu, Eiichi Ohtomo, and Masahito Yamada. "Glucose Metabolism and Alzheimer's Dementia." Nippon Ronen Igakkai Zasshi. Japanese Journal of Geriatrics 33, no. 8 (1996): 569–72. http://dx.doi.org/10.3143/geriatrics.33.569.

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Zanatta, Leila C. B., Cesar L. Boguszewski, Victoria Z. C. Borba, and Carolina A. M. Kulak. "Osteocalcin, energy and glucose metabolism." Arquivos Brasileiros de Endocrinologia & Metabologia 58, no. 5 (2014): 444–51. http://dx.doi.org/10.1590/0004-2730000003333.

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Osteocalcin is a bone matrix protein that has been associated with several hormonal actions on energy and glucose metabolism. Animal and experimental models have shown that osteocalcin is released into the bloodstream and exerts biological effects on pancreatic beta cells and adipose tissue. Undercarboxylated osteocalcin is the hormonally active isoform and stimulates insulin secretion and enhances insulin sensitivity in adipose tissue and muscle. Insulin and leptin, in turn, act on bone tissue, modulating the osteocalcin secretion, in a traditional feedback mechanism that places the skeleton
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42

Ha, Eunyoung. "Glucose Metabolism in the Intestine." Journal of Metabolic and Bariatric Surgery 5, no. 1 (2016): 1–3. http://dx.doi.org/10.17476/jmbs.2016.5.1.1.

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Millichap, J. Gordon. "Friedreich's Ataxia and Glucose Metabolism." Pediatric Neurology Briefs 2, no. 8 (1988): 58. http://dx.doi.org/10.15844/pedneurbriefs-2-8-3.

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Millichap, J. Gordon. "Cerebral Glucose Metabolism and ADHD." Pediatric Neurology Briefs 4, no. 11 (1990): 83. http://dx.doi.org/10.15844/pedneurbriefs-4-11-4.

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SARUC, Murat, Mehmet KARAARSLAN, Kemal RASA, et al. "Pancreatic cancer and glucose metabolism." Turkish Journal of Gastroenterology 20, no. 4 (2009): 257–60. http://dx.doi.org/10.4318/tjg.2009.0022.

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Hecking, Manfred, Alexander Kainz, Johannes Werzowa, et al. "Glucose Metabolism After Renal Transplantation." Diabetes Care 36, no. 9 (2013): 2763–71. http://dx.doi.org/10.2337/dc12-2441.

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Rutkowski, Joseph M. "Fixing lymphatics improves glucose metabolism." Nature Metabolism 3, no. 9 (2021): 1139–41. http://dx.doi.org/10.1038/s42255-021-00442-3.

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&NA;. "Gemfibrozil, hypertriglyceridaemia and glucose metabolism." Inpharma Weekly &NA;, no. 986 (1995): 19. http://dx.doi.org/10.2165/00128413-199509860-00037.

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Salani, Barbara, Alberto Del Rio, Cecilia Marini, Gianmario Sambuceti, Renzo Cordera, and Davide Maggi. "Metformin, cancer and glucose metabolism." Endocrine-Related Cancer 21, no. 6 (2014): R461—R471. http://dx.doi.org/10.1530/erc-14-0284.

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Metformin is the first-line treatment for type 2 diabetes. Results from several clinical studies have indicated that type 2 diabetic patients treated with metformin might have a lower cancer risk. One of the primary metabolic changes observed in malignant cell transformation is an increased catabolic glucose metabolism. In this context, once it has entered the cell through organic cation transporters, metformin decreases mitochondrial respiration chain activity and ATP production that, in turn, activates AMP-activated protein kinase, which regulates energy homeostasis. In addition, metformin r
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SUGDEN, M. C., K. K. CHANGANI, J. BENTLEY, and M. J. HOLNESS. "Cardiac glucose metabolism during pregnancy." Biochemical Society Transactions 20, no. 2 (1992): 195S. http://dx.doi.org/10.1042/bst020195s.

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