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Journal articles on the topic 'Glucose metabolism'

To see the other types of publications on this topic, follow the link: Glucose metabolism.

Author: Grafiati

Published: 4 June 2021

Last updated: 28 July 2024

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Navarro, Francisco, Aline V. N. Bacurau, Andréa Vanzelli, Marcela Meneguello-Coutinho, Marco C. Uchida, Milton R. Moraes, Sandro S. Almeida, et al. "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%), aerobic glucose metabolism (55%), maximal activity of glucose-6-phosphate dehydrogenase (49%), citrate synthase activity (34%), total glutamine consumption (30%), aerobic glutamine consumption (20.3%) and glutaminase activity (56%). In LY isolated from spleen, IFNα also reduced the proliferation and impaired metabolism. These data demonstrate that in LY, the antiproliferative effects of IFNα are associated with a reduction in glucose and glutamine metabolisms.

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12

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 (March 31, 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. muciniphila cell-free supernatant significantly improved the movement ability, prolonged the lifespan, reduced the level of ROS, and alleviated oxidative damage in Caenorhabditis elegans. A. muciniphila cell-free supernatant supported resistance to increases in glucose and triglyceride induced by a high-glucose diet and downregulated the expression of key genes of glucose metabolism, such as gsy-1, pygl-1, pfk-1.1, and pyk-1, while upregulating the expression of key genes of lipid metabolism, such as acs-2, cpt-4, sbp-1, and tph-1, as well as down-regulating the expression of the fat-7 gene to inhibit fatty acid biosynthesis. These findings indicated that A. muciniphila cell-free supernatant, as a postbiotic, has the potential to prevent obesity and improve glucose metabolism disorders and other diseases.

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13

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 (September 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 metabolism) and lactic acid (anaerobic metabolism) were used to decide whether aerobic or anaerobic metabolism predominated at a given atmosphere composition. The boundary conditions between dominantly anaerobic and aerobic metabolisms were determined by logistic regression. The metabolism of glucose by B. thermosphacta was influenced not only by the oxygen content of the atmosphere but also by the carbon dioxide content. At high CO2 percentages, glucose metabolism remained anaerobic under greater oxygen contents.

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14

Wong, Wei. "Forced into glucose metabolism." Science Signaling 14, no. 684 (May 25, 2021): eabj5683. http://dx.doi.org/10.1126/scisignal.abj5683.

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15

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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16

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

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17

Goel, Ashish, Saroj P. Mathupala, and Peter L. Pedersen. "Glucose Metabolism in Cancer." Journal of Biological Chemistry 278, no. 17 (February 3, 2003): 15333–40. http://dx.doi.org/10.1074/jbc.m300608200.

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18

Barth, Eberhard, Gerd Albuszies, Katja Baumgart, Martin Matejovic, Ulrich Wachter, Josef Vogt, Peter Radermacher, and Enrico Calzia. "Glucose metabolism and catecholamines." Critical Care Medicine 35, Suppl (September 2007): S508—S518. http://dx.doi.org/10.1097/01.ccm.0000278047.06965.20.

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19

Makhmudov, E. S., and V. A. Khodzhimatov. "Glucose metabolism and conception." Problems of Endocrinology 39, no. 2 (April 15, 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 the mother's body can inhibit the development and even cause early death of the offspring. Therefore, given the importance of glucose for a developing organism, this review discusses issues related to its metabolism and regulation during pregnancy.

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20

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

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21

Lee, Min Gyu, and Peter L. Pedersen. "Glucose Metabolism in Cancer." Journal of Biological Chemistry 278, no. 42 (July 31, 2003): 41047–58. http://dx.doi.org/10.1074/jbc.m307031200.

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22

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

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23

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

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24

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

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25

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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26

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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27

Andrianantoandro, E. "Hedgehog Drives Glucose Metabolism." Science Signaling 5, no. 247 (October 23, 2012): ec275-ec275. http://dx.doi.org/10.1126/scisignal.2003715.

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28

Zierler, Kenneth. "Whole body glucose metabolism." American Journal of Physiology-Endocrinology and Metabolism 276, no. 3 (March 1, 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 transporters to the cell membrane accounts completely, or even mainly, for insulin-stimulated glucose uptake, whether exercise stimulates release of a circulating insulinomimetic factor, and the relation between muscle glucose uptake and muscle blood flow. The review points out that there is no compartment of glucose in the body at which all glucose is at the same concentration, and that models of glucose metabolism, including effects of insulin on glucose metabolism based on assumptions of concentration homogeneity, cannot be entirely correct. A fresh approach to modeling is needed.

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29

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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30

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

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31

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

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32

Rajas, Fabienne, Amandine Gautier-Stein, and Gilles Mithieux. "Glucose-6 Phosphate, a Central Hub for Liver Carbohydrate Metabolism." Metabolites 9, no. 12 (November 20, 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 reprogramming occurring in two pathologies characterized by a deregulation of glucose homeostasis, namely type 2 diabetes, which is characterized by fasting hyperglycemia; and glycogen storage disease type I, where patients develop severe hypoglycemia during short fasting periods. In these two conditions, dysfunction of glucose metabolism results in non-alcoholic fatty liver disease, which may possibly lead to the development of hepatic tumors. Moreover, we also emphasize the role of the transcription factor carbohydrate response element-binding protein (ChREBP), known to link glucose and lipid metabolisms. In this regard, comparing these two metabolic diseases is a fruitful approach to better understand the key role of glucose-6 phosphate in liver metabolism in health and disease.

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33

Kagotho, Elizabeth. "Insulin-Mediated Glucose Metabolism: An Atherogenic Lipid Profile of Fructose Consumption." Endocrinology and Disorders 2, no. 2 (February 27, 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 diets could lead to increased caloric intake or decreased energy expenditure, thereby contributing to weight gain and obesity. Results from a study conducted in rhesus monkeys produced equivocal results. Carefully controlled and adequately powered long-term studies are needed to address these hypotheses. In both short- and long-term studies we demonstrated that consumption of fructose-sweetened beverages substantially increases postprandial triacylglycerol concentrations compared with glucose-sweetened beverages. In the long-term studies, apolipoproteinB concentrations were also increased in subjects consuming fructose, but not those consuming glucose. Data from a short-term study comparing consumption of beverages sweetened with fructose, glucose, high fructose corn syrup (HFCS) and sucrose, suggest that HFCS and sucrose increase postprandial triacylglycerol to an extent comparable to that induced by 100% fructose alone. Increased consumption of fructose-sweetened beverages along with increased prevalence of obesity, metabolic syndrome, and type 2 diabetes underscore the importance of investigating the metabolic consequences fructose consumption in carefully controlled experiments.

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34

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 (July 16, 2015): 715–57. http://dx.doi.org/10.1111/obr.12298.

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35

Kagotho, Elizabeth. "Insulin-Mediated Glucose Metabolism: An Atherogenic Lipid Profile of Fructose Consumption." Endocrinology and Disorders 2, no. 2 (February 15, 2018): 01–02. http://dx.doi.org/10.31579/2640-1045/021.

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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 relation between high-density lipoprotein cholesterol (HDL-C) and variations in HbA1c was analyzed in 158 patients. We also constructed a state space model consisting of an observation model (HDL-C and HbA1c) and an internal model (disorders of lipid metabolism and glucose metabolism) and applied this model to 116 cases. Results: The root mean square error between the observed HbA1c and predicted HbA1c was 0.25. Conclusions: In the observation model, HDL-C levels were useful for prediction of increases in HbA1c. Even with numerous missing values over time, as occurs in clinical practice, clinically valid predictions can be made using this state space model.

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37

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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38

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 (July 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 as a true endocrine organ. Further studies are required to elucidate the role of osteocalcin in the regulation of glucose and energy metabolism in humans and its potential therapeutic implications in diabetes, obesity and metabolic syndrome.

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39

Ha, Eunyoung. "Glucose Metabolism in the Intestine." Journal of Metabolic and Bariatric Surgery 5, no. 1 (June 30, 2016): 1–3. http://dx.doi.org/10.17476/jmbs.2016.5.1.1.

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40

Millichap, J. Gordon. "Friedreich's Ataxia and Glucose Metabolism." Pediatric Neurology Briefs 2, no. 8 (August 1, 1988): 58. http://dx.doi.org/10.15844/pedneurbriefs-2-8-3.

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41

Millichap, J. Gordon. "Cerebral Glucose Metabolism and ADHD." Pediatric Neurology Briefs 4, no. 11 (November 1, 1990): 83. http://dx.doi.org/10.15844/pedneurbriefs-4-11-4.

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42

SARUC, Murat, Mehmet KARAARSLAN, Kemal RASA, Ozlem SAYGILI, Umit INCE, Caglar BAYSAL, Parviz M. POUR, Metin CAKMAKCI, and Nurdan TOZUN. "Pancreatic cancer and glucose metabolism." Turkish Journal of Gastroenterology 20, no. 4 (December 1, 2009): 257–60. http://dx.doi.org/10.4318/tjg.2009.0022.

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43

Hecking, Manfred, Alexander Kainz, Johannes Werzowa, Michael Haidinger, Dominik Döller, Andrea Tura, Angelo Karaboyas, et al. "Glucose Metabolism After Renal Transplantation." Diabetes Care 36, no. 9 (May 8, 2013): 2763–71. http://dx.doi.org/10.2337/dc12-2441.

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44

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

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45

&NA;. "Gemfibrozil, hypertriglyceridaemia and glucose metabolism." Inpharma Weekly &NA;, no. 986 (May 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 (October 1, 2014): R461—R471. http://dx.doi.org/10.1530/erc-14-0284.

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Abstract:

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 reduces cellular energy availability and glucose entrapment by inhibiting hexokinase-II, which catalyses the glucose phosphorylation reaction. In this review, we discuss recent findings on molecular mechanisms that sustain the anticancer effect of metformin through regulation of glucose metabolism. In particular, we have focused on the emerging action of metformin on glycolysis in normal and cancer cells, with a drug discovery perspective.

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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 (May 1, 1992): 195S. http://dx.doi.org/10.1042/bst020195s.

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Remde, H., G. Hanslik, N. Rayes, and M. Quinkler. "Glucose Metabolism in Primary Aldosteronism." Hormone and Metabolic Research 47, no. 13 (December 14, 2015): 987–93. http://dx.doi.org/10.1055/s-0035-1565208.

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Sharma, Sapna, Jennifer Kriebel, and Harald Grallert. "Epigenetic regulation of glucose metabolism." Current Opinion in Clinical Nutrition & Metabolic Care 20, no. 4 (July 2017): 266–71. http://dx.doi.org/10.1097/mco.0000000000000375.

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Franzini, Laura, Diego Ardigò, and Ivana Zavaroni. "Dietary antioxidants and glucose metabolism." Current Opinion in Clinical Nutrition and Metabolic Care 11, no. 4 (July 2008): 471–76. http://dx.doi.org/10.1097/mco.0b013e328303be79.

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