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Relevant bibliographies by topics / Mitochondria Glucokinase

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Journal articles

Academic literature on the topic 'Mitochondria Glucokinase'

Author: Grafiati

Published: 4 June 2021

Last updated: 18 February 2022

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Journal articles on the topic "Mitochondria Glucokinase"

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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