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Decreased expression of hepatic glucokinase in type 2 diabetes.

Molecular metabolism

Haeusler RA, Camastra S, Astiarraga B, Nannipieri M, Anselmino M, Ferrannini E.
PMID: 25737948
Mol Metab. 2014 Dec 18;4(3):222-6. doi: 10.1016/j.molmet.2014.12.007. eCollection 2015 Mar.

BACKGROUND/OBJECTIVES: Increased endogenous glucose production is a hallmark of type 2 diabetes. Evidence from animal models has suggested that a likely cause of this is increased mRNA expression of glucose 6-phosphatase and phosphoenolpyruvate carboxykinase (encoded by G6PC, PCK1 and...

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Haeusler RA, Camastra S, Astiarraga B, et al. Decreased expression of hepatic glucokinase in type 2 diabetes. Mol Metab. 2014;4(3):222-6doi: 10.1016/j.molmet.2014.12.007.
Haeusler, R. A., Camastra, S., Astiarraga, B., Nannipieri, M., Anselmino, M., & Ferrannini, E. (2015). Decreased expression of hepatic glucokinase in type 2 diabetes. Molecular metabolism, 4(3), 222-6. https://doi.org/10.1016/j.molmet.2014.12.007
Haeusler, Rebecca A, et al. "Decreased expression of hepatic glucokinase in type 2 diabetes." Molecular metabolism vol. 4,3 (2015): 222-6. doi: https://doi.org/10.1016/j.molmet.2014.12.007
Haeusler RA, Camastra S, Astiarraga B, Nannipieri M, Anselmino M, Ferrannini E. Decreased expression of hepatic glucokinase in type 2 diabetes. Mol Metab. 2014 Dec 18;4(3):222-6. doi: 10.1016/j.molmet.2014.12.007. eCollection 2015 Mar. PMID: 25737948; PMCID: PMC4338311.
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Present status of clinical deployment of glucokinase activators.

Journal of diabetes investigation

Nakamura A, Terauchi Y.
PMID: 25802718
J Diabetes Investig. 2015 Mar;6(2):124-32. doi: 10.1111/jdi.12294. Epub 2014 Nov 10.

Glucokinase is one of four members of the hexokinase family of enzymes. Its expression is limited to the major organs (such as the pancreas, liver, brain and the gastrointestinal tract) that are thought to have an integrated role in...

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Nakamura A, Terauchi Y. Present status of clinical deployment of glucokinase activators. J Diabetes Investig. 2014;6(2):124-32doi: 10.1111/jdi.12294.
Nakamura, A., & Terauchi, Y. (2015). Present status of clinical deployment of glucokinase activators. Journal of diabetes investigation, 6(2), 124-32. https://doi.org/10.1111/jdi.12294
Nakamura, Akinobu, and Terauchi, Yasuo. "Present status of clinical deployment of glucokinase activators." Journal of diabetes investigation vol. 6,2 (2015): 124-32. doi: https://doi.org/10.1111/jdi.12294
Nakamura A, Terauchi Y. Present status of clinical deployment of glucokinase activators. J Diabetes Investig. 2015 Mar;6(2):124-32. doi: 10.1111/jdi.12294. Epub 2014 Nov 10. PMID: 25802718; PMCID: PMC4364845.
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Long-Term Efficacy and Safety of Insulin and Glucokinase Gene Therapy for Diabetes: 8-Year Follow-Up in Dogs.

Molecular therapy. Methods & clinical development

Jaén ML, Vilà L, Elias I, Jimenez V, Rodó J, Maggioni L, Ruiz-de Gopegui R, Garcia M, Muñoz S, Callejas D, Ayuso E, Ferré T, Grifoll I, Andaluz A, Ruberte J, Haurigot V, Bosch F.
PMID: 28626777
Mol Ther Methods Clin Dev. 2017 Apr 05;6:1-7. doi: 10.1016/j.omtm.2017.03.008. eCollection 2017 Sep 15.

Diabetes is a complex metabolic disease that exposes patients to the deleterious effects of hyperglycemia on various organs. Achievement of normoglycemia with exogenous insulin treatment requires the use of high doses of hormone, which increases the risk of life-threatening...

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Jaén ML, Vilà L, Elias I, et al. Long-Term Efficacy and Safety of Insulin and Glucokinase Gene Therapy for Diabetes: 8-Year Follow-Up in Dogs. Mol Ther Methods Clin Dev. 2017;6:1-7doi: 10.1016/j.omtm.2017.03.008.
Jaén, M. L., Vilà, L., Elias, I., Jimenez, V., Rodó, J., Maggioni, L., Ruiz-de Gopegui, R., Garcia, M., Muñoz, S., Callejas, D., Ayuso, E., Ferré, T., Grifoll, I., Andaluz, A., Ruberte, J., Haurigot, V., & Bosch, F. (2017). Long-Term Efficacy and Safety of Insulin and Glucokinase Gene Therapy for Diabetes: 8-Year Follow-Up in Dogs. Molecular therapy. Methods & clinical development, 61-7. https://doi.org/10.1016/j.omtm.2017.03.008
Jaén, Maria Luisa, et al. "Long-Term Efficacy and Safety of Insulin and Glucokinase Gene Therapy for Diabetes: 8-Year Follow-Up in Dogs." Molecular therapy. Methods & clinical development vol. 6 (2017): 1-7. doi: https://doi.org/10.1016/j.omtm.2017.03.008
Jaén ML, Vilà L, Elias I, Jimenez V, Rodó J, Maggioni L, Ruiz-de Gopegui R, Garcia M, Muñoz S, Callejas D, Ayuso E, Ferré T, Grifoll I, Andaluz A, Ruberte J, Haurigot V, Bosch F. Long-Term Efficacy and Safety of Insulin and Glucokinase Gene Therapy for Diabetes: 8-Year Follow-Up in Dogs. Mol Ther Methods Clin Dev. 2017 Apr 05;6:1-7. doi: 10.1016/j.omtm.2017.03.008. eCollection 2017 Sep 15. PMID: 28626777; PMCID: PMC5466581.
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Ingestion of a moderate high-sucrose diet results in glucose intolerance with reduced liver glucokinase activity and impaired glucagon-like peptide-1 secretion.

Journal of diabetes investigation

Sakamoto E, Seino Y, Fukami A, Mizutani N, Tsunekawa S, Ishikawa K, Ogata H, Uenishi E, Kamiya H, Hamada Y, Sato H, Harada N, Toyoda Y, Miwa I, Nakamura J, Inagaki N, Oiso Y, Ozaki N.
PMID: 24843603
J Diabetes Investig. 2012 Oct 18;3(5):432-40. doi: 10.1111/j.2040-1124.2012.00208.x.

UNLABELLED: Aims/Introduction:  Excessive intake of sucrose can cause severe health issues, such as diabetes mellitus. In animal studies, consumption of a high-sucrose diet (SUC) has been shown to cause obesity, insulin resistance and glucose intolerance. However, several in vivo...

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Sakamoto E, Seino Y, Fukami A, et al. Ingestion of a moderate high-sucrose diet results in glucose intolerance with reduced liver glucokinase activity and impaired glucagon-like peptide-1 secretion. J Diabetes Investig. 2012;3(5):432-40doi: 10.1111/j.2040-1124.2012.00208.x.
Sakamoto, E., Seino, Y., Fukami, A., Mizutani, N., Tsunekawa, S., Ishikawa, K., Ogata, H., Uenishi, E., Kamiya, H., Hamada, Y., Sato, H., Harada, N., Toyoda, Y., Miwa, I., Nakamura, J., Inagaki, N., Oiso, Y., & Ozaki, N. (2012). Ingestion of a moderate high-sucrose diet results in glucose intolerance with reduced liver glucokinase activity and impaired glucagon-like peptide-1 secretion. Journal of diabetes investigation, 3(5), 432-40. https://doi.org/10.1111/j.2040-1124.2012.00208.x
Sakamoto, Eriko, et al. "Ingestion of a moderate high-sucrose diet results in glucose intolerance with reduced liver glucokinase activity and impaired glucagon-like peptide-1 secretion." Journal of diabetes investigation vol. 3,5 (2012): 432-40. doi: https://doi.org/10.1111/j.2040-1124.2012.00208.x
Sakamoto E, Seino Y, Fukami A, Mizutani N, Tsunekawa S, Ishikawa K, Ogata H, Uenishi E, Kamiya H, Hamada Y, Sato H, Harada N, Toyoda Y, Miwa I, Nakamura J, Inagaki N, Oiso Y, Ozaki N. Ingestion of a moderate high-sucrose diet results in glucose intolerance with reduced liver glucokinase activity and impaired glucagon-like peptide-1 secretion. J Diabetes Investig. 2012 Oct 18;3(5):432-40. doi: 10.1111/j.2040-1124.2012.00208.x. PMID: 24843603; PMCID: PMC4019243.
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Polymorphisms in the GCKR are associated with serum lipid traits, the risk of coronary artery disease and ischemic stroke.

International journal of clinical and experimental medicine

Zhou YJ, Hong SC, Yin RX, Yang Q, Cao XL, Chen WX.
PMID: 26379859
Int J Clin Exp Med. 2015 Jul 15;8(7):10678-86. eCollection 2015.

The present study was to determine the association of two single nucleotide polymorphisms (SNPs) in the glucokinase regulator gene (GCKR) and serum lipid levels, and the risk of coronary artery disease (CAD) and ischemic stroke (IS). Genotypes of the...

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Zhou YJ, Hong SC, Yin RX, et al. Polymorphisms in the GCKR are associated with serum lipid traits, the risk of coronary artery disease and ischemic stroke. Int J Clin Exp Med. 2015;8(7):10678-86
Zhou, Y. J., Hong, S. C., Yin, R. X., Yang, Q., Cao, X. L., & Chen, W. X. (2015). Polymorphisms in the GCKR are associated with serum lipid traits, the risk of coronary artery disease and ischemic stroke. International journal of clinical and experimental medicine, 8(7), 10678-86.
Zhou, Yi-Jiang, et al. "Polymorphisms in the GCKR are associated with serum lipid traits, the risk of coronary artery disease and ischemic stroke." International journal of clinical and experimental medicine vol. 8,7 (2015): 10678-86.
Zhou YJ, Hong SC, Yin RX, Yang Q, Cao XL, Chen WX. Polymorphisms in the GCKR are associated with serum lipid traits, the risk of coronary artery disease and ischemic stroke. Int J Clin Exp Med. 2015 Jul 15;8(7):10678-86. eCollection 2015. PMID: 26379859; PMCID: PMC4565242.
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Do Genes Determine Our Health? Implications for Designing Lifestyle Interventions and Drug Trials.

Circulation. Cardiovascular genetics

Wessel J, Marrero D.
PMID: 26884607
Circ Cardiovasc Genet. 2016 Feb;9(1):2-3. doi: 10.1161/CIRCGENETICS.116.001367.

No abstract available.

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Wessel J, Marrero D. Do Genes Determine Our Health? Implications for Designing Lifestyle Interventions and Drug Trials. Circ Cardiovasc Genet. 2016;9(1):2-3doi: 10.1161/CIRCGENETICS.116.001367.
Wessel, J., & Marrero, D. (2016). Do Genes Determine Our Health? Implications for Designing Lifestyle Interventions and Drug Trials. Circulation. Cardiovascular genetics, 9(1), 2-3. https://doi.org/10.1161/CIRCGENETICS.116.001367
Wessel, Jennifer, and Marrero, David. "Do Genes Determine Our Health? Implications for Designing Lifestyle Interventions and Drug Trials." Circulation. Cardiovascular genetics vol. 9,1 (2016): 2-3. doi: https://doi.org/10.1161/CIRCGENETICS.116.001367
Wessel J, Marrero D. Do Genes Determine Our Health? Implications for Designing Lifestyle Interventions and Drug Trials. Circ Cardiovasc Genet. 2016 Feb;9(1):2-3. doi: 10.1161/CIRCGENETICS.116.001367. PMID: 26884607.
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Pediatric non-alcoholic fatty liver disease: New insights and future directions.

World journal of hepatology

Marzuillo P, Del Giudice EM, Santoro N.
PMID: 24799990
World J Hepatol. 2014 Apr 27;6(4):217-25. doi: 10.4254/wjh.v6.i4.217.

One of the most common complications of childhood obesity is the non-alcoholic fatty liver disease (NAFLD), which is the most common form of liver disease in children. NAFLD is defined by hepatic fat infiltration > 5% hepatocytes, as assessed...

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Marzuillo P, Del Giudice EM, Santoro N. Pediatric non-alcoholic fatty liver disease: New insights and future directions. World J Hepatol. 2014;6(4):217-25doi: 10.4254/wjh.v6.i4.217.
Marzuillo, P., Del Giudice, E. M., & Santoro, N. (2014). Pediatric non-alcoholic fatty liver disease: New insights and future directions. World journal of hepatology, 6(4), 217-25. https://doi.org/10.4254/wjh.v6.i4.217
Marzuillo, Pierluigi, et al. "Pediatric non-alcoholic fatty liver disease: New insights and future directions." World journal of hepatology vol. 6,4 (2014): 217-25. doi: https://doi.org/10.4254/wjh.v6.i4.217
Marzuillo P, Del Giudice EM, Santoro N. Pediatric non-alcoholic fatty liver disease: New insights and future directions. World J Hepatol. 2014 Apr 27;6(4):217-25. doi: 10.4254/wjh.v6.i4.217. PMID: 24799990; PMCID: PMC4009477.
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Lack of glibenclamide response in a case of permanent neonatal diabetes caused by incomplete inactivation of glucokinase.

JIMD reports

Oriola J, Moreno F, Gutiérrez-Nogués A, León S, García-Herrero CM, Vincent O, Navas MA.
PMID: 25665835
JIMD Rep. 2015;20:21-6. doi: 10.1007/8904_2014_383. Epub 2015 Feb 10.

BACKGROUND: Hypoglycaemic drugs that close the KATP channel have been tested in patients with permanent neonatal diabetes due to glucokinase mutations (PNDM-GCK). From the results obtained, it has been suggested that this treatment may be beneficial in patients carrying...

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Oriola J, Moreno F, Gutiérrez-Nogués A, et al. Lack of glibenclamide response in a case of permanent neonatal diabetes caused by incomplete inactivation of glucokinase. JIMD Rep. 2015;20:21-6doi: 10.1007/8904_2014_383.
Oriola, J., Moreno, F., Gutiérrez-Nogués, A., León, S., García-Herrero, C. M., Vincent, O., & Navas, M. A. (2015). Lack of glibenclamide response in a case of permanent neonatal diabetes caused by incomplete inactivation of glucokinase. JIMD reports, 2021-6. https://doi.org/10.1007/8904_2014_383
Oriola, Josep, et al. "Lack of glibenclamide response in a case of permanent neonatal diabetes caused by incomplete inactivation of glucokinase." JIMD reports vol. 20 (2015): 21-6. doi: https://doi.org/10.1007/8904_2014_383
Oriola J, Moreno F, Gutiérrez-Nogués A, León S, García-Herrero CM, Vincent O, Navas MA. Lack of glibenclamide response in a case of permanent neonatal diabetes caused by incomplete inactivation of glucokinase. JIMD Rep. 2015;20:21-6. doi: 10.1007/8904_2014_383. Epub 2015 Feb 10. PMID: 25665835; PMCID: PMC4375116.
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Respiration of Sugars in Spinach (Spinacia oleracea), Maize (Zea mays), and Chlamydomonas reinhardtii F-60 Chloroplasts with Emphasis on the Hexose Kinases.

Plant physiology

Singh KK, Chen C, Epstein DK, Gibbs M.
PMID: 12231848
Plant Physiol. 1993 Jun;102(2):587-593. doi: 10.1104/pp.102.2.587.

The role of hexokinase in carbohydrate degradation in isolated, intact chloroplasts was evaluated. This was accomplished by monitoring the evolution of 14CO2 from darkened spinach (Spinacia oleracea), maize (Zea mays) mesophyll, and Chlamydomonas reinhardtii chloroplasts externally supplied with 14C-labeled...

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Singh KK, Chen C, Epstein DK, et al. Respiration of Sugars in Spinach (Spinacia oleracea), Maize (Zea mays), and Chlamydomonas reinhardtii F-60 Chloroplasts with Emphasis on the Hexose Kinases. Plant Physiol. 1993;102(2):587-593doi: 10.1104/pp.102.2.587.
Singh, K. K., Chen, C., Epstein, D. K., & Gibbs, M. (1993). Respiration of Sugars in Spinach (Spinacia oleracea), Maize (Zea mays), and Chlamydomonas reinhardtii F-60 Chloroplasts with Emphasis on the Hexose Kinases. Plant physiology, 102(2), 587-593. https://doi.org/10.1104/pp.102.2.587
Singh, K. K., et al. "Respiration of Sugars in Spinach (Spinacia oleracea), Maize (Zea mays), and Chlamydomonas reinhardtii F-60 Chloroplasts with Emphasis on the Hexose Kinases." Plant physiology vol. 102,2 (1993): 587-593. doi: https://doi.org/10.1104/pp.102.2.587
Singh KK, Chen C, Epstein DK, Gibbs M. Respiration of Sugars in Spinach (Spinacia oleracea), Maize (Zea mays), and Chlamydomonas reinhardtii F-60 Chloroplasts with Emphasis on the Hexose Kinases. Plant Physiol. 1993 Jun;102(2):587-593. doi: 10.1104/pp.102.2.587. PMID: 12231848; PMCID: PMC158816.
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Truncated Glycolytic System in Veillonella.

Journal of bacteriology

Rogosa M, Krichevsky MI, Bishop FS.
PMID: 16562014
J Bacteriol. 1965 Jul;90(1):164-71. doi: 10.1128/jb.90.1.164-171.1965.

Rogosa, M., (National Institutes of Health, Bethesda, Md.), M. I. Krichevsky, and F. S. Bishop. Truncated glycolytic system in Veillonella. J. Bacteriol. 90:164-171. 1965.-Intact Veillonella cells do not utilize carbohydrates for growth, nor are carbohydrates fermented. In cell extracts,...

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Rogosa M, Krichevsky MI, Bishop FS. Truncated Glycolytic System in Veillonella. J Bacteriol. 1965;90(1):164-71doi: 10.1128/jb.90.1.164-171.1965.
Rogosa, M., Krichevsky, M. I., & Bishop, F. S. (1965). Truncated Glycolytic System in Veillonella. Journal of bacteriology, 90(1), 164-71. https://doi.org/10.1128/jb.90.1.164-171.1965
Rogosa, M, et al. "Truncated Glycolytic System in Veillonella." Journal of bacteriology vol. 90,1 (1965): 164-71. doi: https://doi.org/10.1128/jb.90.1.164-171.1965
Rogosa M, Krichevsky MI, Bishop FS. Truncated Glycolytic System in Veillonella. J Bacteriol. 1965 Jul;90(1):164-71. doi: 10.1128/jb.90.1.164-171.1965. PMID: 16562014; PMCID: PMC315610.
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Enzymes of sucrose and hexose metabolism in developing kernels of two inbreds of maize.

Plant physiology

Doehlert DC, Kuo TM, Felker FC.
PMID: 16666024
Plant Physiol. 1988 Apr;86(4):1013-9. doi: 10.1104/pp.86.4.1013.

Tissue distribution and activity of enzymes involved in sucrose and hexose metabolism were examined in kernels of two inbreds of maize (Zea mays L.) at progressive stages of development. Levels of sugars and starch were also quantitated throughout development....

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Doehlert DC, Kuo TM, Felker FC. Enzymes of sucrose and hexose metabolism in developing kernels of two inbreds of maize. Plant Physiol. 1988;86(4):1013-9doi: 10.1104/pp.86.4.1013.
Doehlert, D. C., Kuo, T. M., & Felker, F. C. (1988). Enzymes of sucrose and hexose metabolism in developing kernels of two inbreds of maize. Plant physiology, 86(4), 1013-9. https://doi.org/10.1104/pp.86.4.1013
Doehlert, D C, et al. "Enzymes of sucrose and hexose metabolism in developing kernels of two inbreds of maize." Plant physiology vol. 86,4 (1988): 1013-9. doi: https://doi.org/10.1104/pp.86.4.1013
Doehlert DC, Kuo TM, Felker FC. Enzymes of sucrose and hexose metabolism in developing kernels of two inbreds of maize. Plant Physiol. 1988 Apr;86(4):1013-9. doi: 10.1104/pp.86.4.1013. PMID: 16666024; PMCID: PMC1054620.
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Characterization of Sucrolysis via the Uridine Diphosphate and Pyrophosphate-Dependent Sucrose Synthase Pathway.

Plant physiology

Xu DP, Sung SJ, Loboda T, Kormanik PP, Black CC.
PMID: 16666820
Plant Physiol. 1989 Jun;90(2):635-42. doi: 10.1104/pp.90.2.635.

The breakdown of sucrose to feed both hexoses into glycolytic carbon flow can occur by the sucrose synthase pathway. This uridine diphosphate (UDP) and pyrophosphate (PPi)-dependent pathway was biochemically characterized using soluble extracts from several plants. The sucrolysis process...

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Xu DP, Sung SJ, Loboda T, et al. Characterization of Sucrolysis via the Uridine Diphosphate and Pyrophosphate-Dependent Sucrose Synthase Pathway. Plant Physiol. 1989;90(2):635-42doi: 10.1104/pp.90.2.635.
Xu, D. P., Sung, S. J., Loboda, T., Kormanik, P. P., & Black, C. C. (1989). Characterization of Sucrolysis via the Uridine Diphosphate and Pyrophosphate-Dependent Sucrose Synthase Pathway. Plant physiology, 90(2), 635-42. https://doi.org/10.1104/pp.90.2.635
Xu, D P, et al. "Characterization of Sucrolysis via the Uridine Diphosphate and Pyrophosphate-Dependent Sucrose Synthase Pathway." Plant physiology vol. 90,2 (1989): 635-42. doi: https://doi.org/10.1104/pp.90.2.635
Xu DP, Sung SJ, Loboda T, Kormanik PP, Black CC. Characterization of Sucrolysis via the Uridine Diphosphate and Pyrophosphate-Dependent Sucrose Synthase Pathway. Plant Physiol. 1989 Jun;90(2):635-42. doi: 10.1104/pp.90.2.635. PMID: 16666820; PMCID: PMC1061773.
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Showing 1 to 12 of 297 entries