Metabolic fate of excessive glucose in fibroblast cells in a diabetic setting
Author:
Affiliation:
1. Laboratory of Pharmacotherapy, Osaka University of Pharmaceutical Sciences
Publisher
Japanese Society of Toxicology
Link
https://www.jstage.jst.go.jp/article/fts/2/2/2_55/_pdf
Reference17 articles.
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2. Brownlee, M. (2005): The pathobiology of diabetic complications: a unifying mechanism. Diabetes, 54, 1615-1625.
3. Curto, M., Novi, R.F., Rabbone, I., Maurino, M., Piccinini, M., Mioletti, S., Mostert, M., Bruno, R. and Rinaudo, M.T. (1997): Insulin resistance in obese subjects and newly diagnosed NIDDM patients and derangements of pyruvate dehydrogenase in their circulating lymphocytes. Int. J. Obes. Relat. Metab. Disord., 21, 1137-1142.
4. Hammes, H.P., Du, X., Edelstein, D., Taguchi, T., Matsumura, T., Ju, Q., Lin, J., Bierhaus, A., Nawroth, P., Hannak, D., Neumaier, M., Bergfeld, R., Giardino, I. and Brownlee, M. (2003): Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat. Med., 9, 294-299.
5. Heimberg, H., De Vos, A., Vandercammen, A., Van Schaftingen, E., Pipeleers, D. and Schuit, F. (1993): Heterogeneity in glucose sensitivity among pancreatic beta-cells is correlated to differences in glucose phosphorylation rather than glucose transport. EMBO J., 12, 2873-2879.
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