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Journal articles on the topic 'Mitochondria Glucokinase'

Author: Grafiati

Published: 4 June 2021

Last updated: 18 February 2022

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1

LEE, J., W. KIM, J. LIM та ін. "Mitochondrial dysfunction: Glucokinase downregulation lowers interaction of glucokinase with mitochondria, resulting in apoptosis of pancreatic β-cells". Cellular Signalling 21, № 1 (2009): 69–78. http://dx.doi.org/10.1016/j.cellsig.2008.09.015.

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2

Bustamante, Ernesto, Peter Pediaditakis, Lihua He, and John J. Lemasters. "Isolated mouse liver mitochondria are devoid of glucokinase." Biochemical and Biophysical Research Communications 334, no. 3 (2005): 907–10. http://dx.doi.org/10.1016/j.bbrc.2005.06.174.

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3

Oka, Yoshitomo. "NIDDM — genetic marker; glucose transporter, glucokinase, and mitochondria gene." Diabetes Research and Clinical Practice 24 (October 1994): S117—S121. http://dx.doi.org/10.1016/0168-8227(94)90237-2.

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4

Arden, Catherine, Simone Baltrusch, and Loranne Agius. "Glucokinase regulatory protein is associated with mitochondria in hepatocytes." FEBS Letters 580, no. 8 (2006): 2065–70. http://dx.doi.org/10.1016/j.febslet.2006.03.009.

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5

Sweet, I. R., G. Li, H. Najafi, D. Berner, and F. M. Matschinsky. "Effect of a glucokinase inhibitor on energy production and insulin release in pancreatic islets." American Journal of Physiology-Endocrinology and Metabolism 271, no. 3 (1996): E606—E625. http://dx.doi.org/10.1152/ajpendo.1996.271.3.e606.

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Glucokinase has exclusively high control strength on glucose usage in the pancreatic beta-cell. However, glucokinase also has extraordinarily high control strength on insulin secretion, which is linked to the phosphate potential, [ATP]/([ADP][Pi]) (F.M. Matschinsky, Y.Liang, P. Kesavan, L. Wang, P. Froguel, G. Velho, D. Cohen, M.A. Permutt, Y. Tanizawa, T.L. Jetton, K. Niswender, and M.A. Magnuson. J. Clin. Invest. 92: 2092-2098, 1993). We propose that the ATP produced via the tricarboxylic acid cycle is approximately constant, irrespective of the glucose level. Furthermore, the component of A

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6

Kim, W. H., J. W. Lee, Y. H. Suh, et al. "Exposure to Chronic High Glucose Induces -Cell Apoptosis Through Decreased Interaction of Glucokinase With Mitochondria: Downregulation of Glucokinase in Pancreatic -Cells." Diabetes 54, no. 9 (2005): 2602–11. http://dx.doi.org/10.2337/diabetes.54.9.2602.

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7

Rutter, Guy A., Eleni Georgiadou, Aida Martinez-Sanchez, and Timothy J. Pullen. "Metabolic and functional specialisations of the pancreatic beta cell: gene disallowance, mitochondrial metabolism and intercellular connectivity." Diabetologia 63, no. 10 (2020): 1990–98. http://dx.doi.org/10.1007/s00125-020-05205-5.

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Abstract All forms of diabetes mellitus involve the loss or dysfunction of pancreatic beta cells, with the former predominating in type 1 diabetes and the latter in type 2 diabetes. Deeper understanding of the coupling mechanisms that link glucose metabolism in these cells to the control of insulin secretion is therefore likely to be essential to develop new therapies. Beta cells display a remarkable metabolic specialisation, expressing high levels of metabolic sensing enzymes, including the glucose transporter GLUT2 (encoded by SLC2A2) and glucokinase (encoded by GCK). Genetic evidence flowin

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8

Zhu, Liu-Luan, Yang Liu, An-Fang Cui та ін. "PGC-1α coactivates estrogen-related receptor-α to induce the expression of glucokinase". American Journal of Physiology-Endocrinology and Metabolism 298, № 6 (2010): E1210—E1218. http://dx.doi.org/10.1152/ajpendo.00633.2009.

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Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) is a key regulator of cellular energy metabolism and regulates processes such as adaptive thermogenesis, hepatic gluconeogenesis, fatty acid oxidation, and mitochondrial biogenesis by coactivating numerous nuclear receptors and transcription factors. Here, we demonstrate the presence of the ERRα binding site in the regulatory sequence of the glucokinase gene and that PGC-1α coactivates ERRα to stimulate the transcription of glucokinase. Simultaneous overexpression of PGC-1α and ERRα potently induced the glucokinase gene expre

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9

Sá-Nakanishi, Anacharis B., Jamil Soni-Neto, Lucas S. Moreira, et al. "Anti-Inflammatory and Antioxidant Actions of Methyl Jasmonate Are Associated with Metabolic Modifications in the Liver of Arthritic Rats." Oxidative Medicine and Cellular Longevity 2018 (August 23, 2018): 1–16. http://dx.doi.org/10.1155/2018/2056250.

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Methyl jasmonate (MeJA) is a fatty acid-derived cyclopentanone which shares structural similarities with prostaglandins and has been under study as a promising anti-inflammatory agent. This study investigated the actions of MeJA on systemic inflammation and oxidative status in rats with adjuvant-induced arthritis, a model for rheumatoid arthritis. MeJA (75 to 300 mg·kg−1) was administrated orally during 18 days after arthritis induction with Freund’s adjuvant. Articular and systemic inflammation was greatly increased in arthritic rats, likewise the oxidative stress in plasma and liver. The hep

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10

Eaton, S., I. Chatziandreou, S. Krywawych, S. Pen, P. T. Clayton, and K. Hussain. "Short-chain 3-hydroxyacyl-CoA dehydrogenase deficiency associated with hyperinsulinism: a novel glucose–fatty acid cycle?" Biochemical Society Transactions 31, no. 6 (2003): 1137–39. http://dx.doi.org/10.1042/bst0311137.

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Hyperinsulinism of infancy is caused by inappropriate insulin secretion in pancreatic β-cells, even when blood glucose is low. Several molecular defects are known to cause hyperinsulinism of infancy, such as KATP channelopathies and regulatory defects of glucokinase and glutamate dehydrogenase. Although defects of fatty acid oxidation have not previously been known to cause hyperinsulinism, patients with deficiency in SCHAD (short-chain 3-hydroxyacyl-CoA dehydrogenase; an enzyme of mitochondrial β-oxidation) have hyperinsulinism. A novel link between fatty acid oxidation and insulin secretion

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11

Danial, Nika N., Colette F. Gramm, Luca Scorrano, et al. "BAD and glucokinase reside in a mitochondrial complex that integrates glycolysis and apoptosis." Nature 424, no. 6951 (2003): 952–56. http://dx.doi.org/10.1038/nature01825.

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12

Martens, G. A., Q. Wang, K. Kerckhofs, G. Stangé, Z. Ling та D. Pipeleers. "Metabolic Activation of Glucose Low-Responsive β-Cells by Glyceraldehyde Correlates with Their Biosynthetic Activation in Lower Glucose Concentration Range But Not at High Glucose". Endocrinology 147, № 11 (2006): 5196–204. http://dx.doi.org/10.1210/en.2006-0580.

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Insulin synthesis and release activities of β-cells can be acutely regulated by glucose through its glycolytic and mitochondrial breakdown involving a glucokinase-dependent rate-limiting step. Isolated β-cell populations are composed of cells with intercellular differences in acute glucose responsiveness that have been attributed to differences in glucokinase (GK) expression and activity. This study first shows that glyceraldehyde can be used as GK-bypassing oxidative substrate and then examines whether the triose can metabolically activate β-cells with low glucose responsiveness. Glyceraldehy

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13

Riera, Alberto, Deifilia Ahuatzi, Pilar Herrero, Maria Adelaida Garcia-Gimeno, Pascual Sanz та Fernando Moreno. "Human pancreatic β-cell glucokinase: subcellular localization and glucose repression signalling function in the yeast cell". Biochemical Journal 415, № 2 (2008): 233–39. http://dx.doi.org/10.1042/bj20080797.

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Human GKβ (pancreatic β-cell glucokinase) is the main glucose-phosphorylating enzyme in pancreatic β-cells. It shares several structural, catalytic and regulatory properties with Hxk2 (hexokinase 2) from Saccharomyces cerevisiae. In fact, it has been previously described that expression of GKβ in yeast could replace Hxk2 in the glucose signalling pathway of S. cerevisiae. In the present study we report that GKβ exerts its regulatory role by association with the yeast transcriptional repressor Mig1 (multicopy inhibitor of GAL gene expression 1); the presence of Mig1 allows GKβ to bind to the SU

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14

Radu, Razvan Gheorghe, Shimpei Fujimoto, Eri Mukai, et al. "Tacrolimus suppresses glucose-induced insulin release from pancreatic islets by reducing glucokinase activity." American Journal of Physiology-Endocrinology and Metabolism 288, no. 2 (2005): E365—E371. http://dx.doi.org/10.1152/ajpendo.00390.2004.

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Tacrolimus is widely used for immunosuppressant therapy, including various organ transplantations. One of its main side effects is hyperglycemia due to reduced insulin secretion, but the mechanism remains unknown. We have investigated the metabolic effects of tacrolimus on insulin secretion at a concentration that does not influence insulin content. Twenty-four-hour exposure to 3 nM tacrolimus reduced high glucose (16.7 mM)-induced insulin secretion (control 2.14 ± 0.08 vs. tacrolimus 1.75 ± 0.02 ng·islet−1·30 min−1, P < 0.01) without affecting insulin content. In dynamic experiments, insul

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15

García-Flores, Marta, José Antonio Zueco, Joaquín Arenas, and Enrique Blázquez. "Expression of glucose transporter-2, glucokinase and mitochondrial glycerolphosphate dehydrogenase in pancreatic islets during rat ontogenesis." European Journal of Biochemistry 269, no. 1 (2002): 119–27. http://dx.doi.org/10.1046/j.0014-2956.2002.02625.x.

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16

OKA, YOSHITOMO. "Medicine disease and gene abnormality. 3. Gene abnormality and diabetes mellitus. Glucokinase gene and mitochondrial gene abnormality." Nihon Naika Gakkai Zasshi 85, no. 9 (1996): 1503–7. http://dx.doi.org/10.2169/naika.85.1503.

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17

ALCAZAR, Oscar, Markus TIEDGE, and Sigurd LENZEN. "Importance of lactate dehydrogenase for the regulation of glycolytic flux and insulin secretion in insulin-producing cells." Biochemical Journal 352, no. 2 (2000): 373–80. http://dx.doi.org/10.1042/bj3520373.

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The role of lactate dehydrogenase (LDH) in the generation of the metabolic signal for insulin secretion was studied after stable overexpression in INS-1 and RINm5F insulin-producing cells. INS-1 cells with a 25-fold overexpression of LDH-A, the highest level achieved, showed a 20–30% decrease in the glucose oxidation rate at glucose concentrations above 5mM when compared with control cells, whereas values were unchanged at lower glucose concentrations. Lactate release increased in parallel with a decrease in the glucose oxidation rate. However, the INS-1 cell glucose-induced insulin secretory

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18

Rafacho, Alex, Laura Marroquí, Sebastião R. Taboga, et al. "Glucocorticoids in Vivo Induce Both Insulin Hypersecretion and Enhanced Glucose Sensitivity of Stimulus-Secretion Coupling in Isolated Rat Islets." Endocrinology 151, no. 1 (2010): 85–95. http://dx.doi.org/10.1210/en.2009-0704.

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Abstract Although glucocorticoids are widely used as antiinflammatory agents in clinical therapies, they may cause serious side effects that include insulin resistance and hyperinsulinemia. To study the potential functional adaptations of the islet of Langerhans to in vivo glucocorticoid treatment, adult Wistar rats received dexamethasone (DEX) for 5 consecutive days, whereas controls (CTL) received only saline. The analysis of insulin release in freshly isolated islets showed an enhanced secretion in response to glucose in DEX-treated rats. The study of Ca2+ signals by fluorescence microscopy

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19

Chan, Catherine B. "β-Cell stimulus–secretion coupling defects in rodent models of obesity". Canadian Journal of Physiology and Pharmacology 73, № 10 (1995): 1414–24. http://dx.doi.org/10.1139/y95-197.

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Hyperinsulinemia accompanies obesity in human patients and experimental rodent models and exacerbates insulin resistance, but the causes of increased insulin secretion remain obscure. This review examines progress in defining biochemical and molecular β-cell defects that have been elucidated in the past 5 years. Some defects, such as decreased glucose transport, decreased mitochondrial FAD-linked glycerophosphate dehydrogenase activity, and altered anomeric specificity for glucose, become evident only after onset of non-insulin-dependent diabetes mellitus. Thus, these defects are unlikely to p

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20

da SILVA XAVIER, Gabriela, Qingwen QIAN, Peter J. CULLEN, and Guy A. RUTTER. "Distinct roles for insulin and insulin-like growth factor-1 receptors in pancreatic beta-cell glucose sensing revealed by RNA silencing." Biochemical Journal 377, no. 1 (2004): 149–58. http://dx.doi.org/10.1042/bj20031260.

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The importance of the insulin receptor (IR) and the insulin-like growth factor-1 receptor (IGF-1R) for glucose-regulated insulin secretion and gene expression in pancreatic islet β-cells is at present unresolved. Here, we have used small interfering RNAs (siRNAs) to silence the expression of each receptor selectively in clonal MIN6 β-cells. Reduction of IR levels by >90% completely inhibited glucose (30 mM compared with 3 mM)-induced insulin secretion, but had no effect on depolarization-stimulated secretion. IR depletion also blocked the accumulation of preproinsulin (PPI), pancreatic duod

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21

Schmitt, H., S. Lenzen, and S. Baltrusch. "Glucokinase mediates coupling of glycolysis to mitochondrial metabolism but not to beta cell damage at high glucose exposure levels." Diabetologia 54, no. 7 (2011): 1744–55. http://dx.doi.org/10.1007/s00125-011-2133-5.

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22

Kamiński, Marcin M., Sven W. Sauer, Marian Kamiński, et al. "T cell Activation Is Driven by an ADP-Dependent Glucokinase Linking Enhanced Glycolysis with Mitochondrial Reactive Oxygen Species Generation." Cell Reports 2, no. 5 (2012): 1300–1315. http://dx.doi.org/10.1016/j.celrep.2012.10.009.

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23

OKA, Yoshitomo. "Gene Abnormalities in Medical Diseases. Genetic Defects and Diabetes Mellitus-Defects of Glucokinase Gene and Mitochondrial Gene in Diabetic Patients." Internal Medicine 36, no. 2 (1997): 150–51. http://dx.doi.org/10.2169/internalmedicine.36.150.

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24

Wilson, David F., Abigail T. J. Cember та Franz M. Matschinsky. "Glutamate dehydrogenase: role in regulating metabolism and insulin release in pancreatic β-cells". Journal of Applied Physiology 125, № 2 (2018): 419–28. http://dx.doi.org/10.1152/japplphysiol.01077.2017.

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Regulation of insulin release and glucose homeostasis by pancreatic β-cells is dependent on the metabolism of glucose by glucokinase (GK) and the influence of that activity on oxidative phosphorylation. Genetic alterations that result in hyperactivity of mitochondrial glutamate dehydrogenase (GDH-1) can cause hypoglycemia-hyperammonemia following high protein meals, but the role of GDH-1 remains poorly understood. GDH-1 activity is strongly inhibited by GTP, to near zero in the absence of ADP, and cooperatively activated ( n = 2.3) by ADP. The dissociation constant for ADP is near 200 µM in vi

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25

Li, Longlong, Mengling Peng, Chongyang Ge, Lei Yu, and Haitian Ma. "(-)-Hydroxycitric Acid Reduced Lipid Droplets Accumulation Via Decreasing Acetyl-Coa Supply and Accelerating Energy Metabolism in Cultured Primary Chicken Hepatocytes." Cellular Physiology and Biochemistry 43, no. 2 (2017): 812–31. http://dx.doi.org/10.1159/000481564.

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Background/Aims: (-)-Hydroxycitric acid (HCA) had been shown to suppress fat accumulation in animals and humans, while the underlying biochemical mechanism is not fully understood, especially little information is available on whether (-)-HCA regulates energy metabolism and consequently affects fat deposition. Methods: Hepatocytes were cultured for 24 h and then exposed to (-)-HCA (0, 1, 10, 50 µM), enzyme protein content was determined by ELISA; lipid metabolism gene mRNA levels were detected by RT-PCR. Results: (-)-HCA significantly decreased the number and total area of lipid droplets. ATP-

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26

Liang, Y., G. Bai, N. Doliba, et al. "Glucose metabolism and insulin release in mouse beta HC9 cells, as model for wild-type pancreatic beta-cells." American Journal of Physiology-Endocrinology and Metabolism 270, no. 5 (1996): E846—E857. http://dx.doi.org/10.1152/ajpendo.1996.270.5.e846.

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Glucose metabolism and its relationship with glucose-induced insulin release were studied in beta HC9 and beta TC3 cells to identify and characterize key factors controlling the intermediary metabolism of glucose and glucose-induced insulin release. The beta HC9 cell line, derived from pancreatic islets with beta-cell hyperplasia, is characterized by a normal concentration-dependency curve for glucose-stimulated insulin release, whereas the beta TC3 cell line, derived from pancreatic beta-cell tumors, shows a marked leftward shift of this curve. Maximum velocity and the Michaelis-Menten consta

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27

Richter, Susan, Shona Morrison, Tim Connor, et al. "Zinc Finger Nuclease Mediated Knockout of ADP-Dependent Glucokinase in Cancer Cell Lines: Effects on Cell Survival and Mitochondrial Oxidative Metabolism." PLoS ONE 8, no. 6 (2013): e65267. http://dx.doi.org/10.1371/journal.pone.0065267.

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28

Park, Jae-Hyung, Sun-Joo Kim, Sung-Hee Park та ін. "Glucagon-Like Peptide-1 Enhances Glucokinase Activity in Pancreatic β-Cells through the Association of Epac2 with Rim2 and Rab3A". Endocrinology 153, № 2 (2012): 574–82. http://dx.doi.org/10.1210/en.2011-0259.

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Glucokinase (GK), which phosphorylates d-glucose, is a major glucose sensor in β-cells for glucose-stimulated insulin secretion (GSIS) and is a promising new drug target for type 2 diabetes (T2D). In T2D, pancreatic β-cells exhibit defective glucose sensitivity, which leads to impaired GSIS. Although glucagon-like peptide-1-(7–36)-amide (GLP-1) is known to enhance β-cell glucose sensitivity, the effect of GLP-1 on GK activity is still unknown. The present study demonstrated that GLP-1 pretreatment for 30 min significantly enhanced GK activity in a glucose-dependent manner, with a lower Michael

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29

Quintens, Roel, Nico Hendrickx, Katleen Lemaire та Frans Schuit. "Why expression of some genes is disallowed in β-cells". Biochemical Society Transactions 36, № 3 (2008): 300–305. http://dx.doi.org/10.1042/bst0360300.

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A differentiated β-cell results not only from cell-specific gene expression, but also from cell-selective repression of certain housekeeping genes. Indeed, to prevent insulin toxicity, β-cells should handle insulin stores carefully, preventing exocytosis under conditions when circulating insulin is unwanted. Some ubiquitously expressed proteins would significantly jeopardize this safeguard, when allowed to function in β-cells. This is illustrated by two studied examples. First, low-Km hexokinases are disallowed as their high affinity for glucose would, when expressed, significantly lower the t

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30

Hyatt, M. A., D. S. Gardner, S. Sebert, et al. "Suboptimal maternal nutrition, during early fetal liver development, promotes lipid accumulation in the liver of obese offspring." REPRODUCTION 141, no. 1 (2011): 119–26. http://dx.doi.org/10.1530/rep-10-0325.

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Maternal nutrition during the period of early organ development can modulate the offspring's ability to metabolise excess fat as young adults when exposed to an obesogenic environment. This study examined the hypothesis that exposing offspring to nutrient restriction coincident with early hepatogenesis would result in endocrine and metabolic adaptations that subsequently lead to increased ectopic lipid accumulation within the liver. Pregnant sheep were fed either 50 or 100% of total metabolisable energy requirements from 30 to 80 days gestation and 100% thereafter. At weaning, offspring were m

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31

Huang, Xiuting, Siqian Gong, Yumin Ma, et al. "Lower Circulating miR-122 Level in Patients with HNF1A Variant-Induced Diabetes Compared with Type 2 Diabetes." Journal of Diabetes Research 2018 (August 1, 2018): 1–6. http://dx.doi.org/10.1155/2018/7842064.

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miR-122, the expression of which is regulated by several transcription factors, such as HNF1A, was recently reported to be associated with type 2 diabetes (T2DM) and hepatocellular carcinoma. HNF1A variants can cause diabetes and might be involved in the development of primary liver neoplasm. Differences in miR-122 expression among different types of diabetes have not been studied. This study aimed to investigate differences in serum miR-122 levels in Chinese patients with different forms of diabetes, including T2DM, type 1 diabetes (T1DM), HNF1A variant-induced diabetes (HNF1A-DM), glucokinas

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32

Petrie, John L., Gillian L. Patman, Ishita Sinha, Thomas D. Alexander, Helen L. Reeves, and Loranne Agius. "The rate of production of uric acid by hepatocytes is a sensitive index of compromised cell ATP homeostasis." American Journal of Physiology-Endocrinology and Metabolism 305, no. 10 (2013): E1255—E1265. http://dx.doi.org/10.1152/ajpendo.00214.2013.

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Plasma levels of uric acid, the final product of purine degradation in humans, are elevated in metabolic syndrome and are strongly associated with insulin resistance and nonalcoholic fatty liver disease (NAFLD). Hepatic and blood levels of purine metabolites (inosine, hypoxanthine, and xanthine) are also altered in pathophysiological states. We optimized a rat hepatocyte model to test the hypothesis that the production of uric acid by hepatocytes is a potential marker of compromised homeostasis of hepatocellular inorganic phosphate (Pi) and/or ATP. The basal rate of uric acid production from e

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33

Iwasaki, N., H. Ohgawara, H. Nagahara, M. Kawamura, G. I. Bell, and Y. Omori. "Characterization of Japanese families with early-onset type 2 (non-insulin dependent) diabetes mellitus and screening for mutations in the glucokinase and mitochondrial tRNALeu(UUR) genes." Acta Diabetologica 32, no. 1 (1995): 17–22. http://dx.doi.org/10.1007/bf00581039.

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34

Fulgencio, Jean-Pierre, Claude Kohl, Jean Girard, and Jean-Paul Pégorier. "Effect of metformin on fatty acid and glucose metabolism in freshly isolated hepatocytes and on specific gene expression in cultured hepatocytes11Abbreviations: CPT I or II, carnitine palmitoyltransferase I or II; mtHMG-CoA synthase, mitochondrial hydroxymethylglutaryl-CoA synthase; Glc-6-Pase, glucose-6-phosphatase; PEPCK, phosphoenolpyruvate carboxykinase; GK, glucokinase; L-PK, liver-type pyruvate kinase; and ACS, acyl-CoA synthetase." Biochemical Pharmacology 62, no. 4 (2001): 439–46. http://dx.doi.org/10.1016/s0006-2952(01)00679-7.

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35

Lenzen, Sigurd. "The pancreatic beta cell: an intricate relation between anatomical structure, the signalling mechanism of glucose-induced insulin secretion, the low antioxidative defence, the high vulnerability and sensitivity to diabetic stress." ChemTexts 7, no. 2 (2021). http://dx.doi.org/10.1007/s40828-021-00140-3.

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AbstractThe biosynthesis of insulin takes place in the insulin-producing beta cells that are organized in the form of islets of Langerhans together with a few other islet cell types in the pancreas organ. The signal for glucose-induced insulin secretion is generated in two pathways in the mitochondrial metabolism of the pancreatic beta cells. These pathways are also known as the triggering pathway and the amplifying pathway. Glucokinase, the low-affinity glucose-phosphorylating enzyme in beta cell glycolysis acts as the signal-generating enzyme in this process. ATP ultimately generated is the

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36

Barry, William E., and Carl S. Thummel. "The Drosophila HNF4 nuclear receptor promotes glucose-stimulated insulin secretion and mitochondrial function in adults." eLife 5 (May 17, 2016). http://dx.doi.org/10.7554/elife.11183.

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Although mutations in HNF4A were identified as the cause of Maturity Onset Diabetes of the Young 1 (MODY1) two decades ago, the mechanisms by which this nuclear receptor regulates glucose homeostasis remain unclear. Here we report that loss of Drosophila HNF4 recapitulates hallmark symptoms of MODY1, including adult-onset hyperglycemia, glucose intolerance and impaired glucose-stimulated insulin secretion (GSIS). These defects are linked to a role for dHNF4 in promoting mitochondrial function as well as the expression of Hex-C, a homolog of the MODY2 gene Glucokinase. dHNF4 is required in the

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37

Samadder, Asmita, Sudatta Dey, Priyanka Sow, et al. "Phyto-chlorophyllin prevents food additive induced genotoxicity and mitochondrial dysfunction via cytochrome c mediated pathway in mice model." Combinatorial Chemistry & High Throughput Screening 23 (December 30, 2020). http://dx.doi.org/10.2174/1386207323666201230093510.

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Objectives: The issue of food-additive-toxicity causing several health hazards needs to be therapeutically managed in an immediate effect. Alloxan, a food additive, used for whitening and shining of flour, is capable of inducing genotoxicity, diabetes, and associated mitochondrial dysfunction. Therefore, to explore a non-toxic, phyto-based compound which could delay the onset of diabetes and prevent the multitude of damage associated therein, Chlorophyllin (CHL), was selected for our study having been reported to exhibit anti-cancer, anti-diabetes, anti-inflammatory responses. Therefore, the o

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38

Perrin-Cocon, Laure, Pierre-Olivier Vidalain, Clémence Jacquemin, et al. "A hexokinase isoenzyme switch in human liver cancer cells promotes lipogenesis and enhances innate immunity." Communications Biology 4, no. 1 (2021). http://dx.doi.org/10.1038/s42003-021-01749-3.

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AbstractDuring the cancerous transformation of normal hepatocytes into hepatocellular carcinoma (HCC), the enzyme catalyzing the first rate-limiting step of glycolysis, namely the glucokinase (GCK), is replaced by the higher affinity isoenzyme, hexokinase 2 (HK2). Here, we show that in HCC tumors the highest expression level of HK2 is inversely correlated to GCK expression, and is associated to poor prognosis for patient survival. To further explore functional consequences of the GCK-to-HK2 isoenzyme switch occurring during carcinogenesis, HK2 was knocked-out in the HCC cell line Huh7 and repl

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