FNS  Vol.3 No.11 , November 2012
Fe2+ Coupled with Vitamin c (Vc) Can Enhance Glucose Metabolism and Decrease Blood Glucose Levels of Alloxan-Induced Diabetic Mice
Abstract: That FeSO4 not FeCl3 can reduce the blood glucose levels of alloxan-induced diabetes mice has been reported in previous research. This study explained the cause of difference in activity of two different iron ions on diabetic mice based on glucose consumption (GC). FeSO4, FeCl3, Vitamine c (Vc), FeSO4 + Vc, metformin were administrated to the alloxan induced-diabetic mice, respectively. After administrated, serum glucose, fructosaminr, insulin, triglyceride, total cholesterol, total iron and Fe2+ levels and GC of liver in vivo were analyzed, respectively. In vitro, effect of different iron ions coupled with Vc or streptozotocin on GC of liver of diabetic mice of model group were analyzed. The body weights and serum insulin levels of Fe2+ and Fe2+ + Vc treated diabetic mice notably increased. The serum glucose, fructosamine, triglyceride and total cholesterol levels were significantly decreased, whereas serum total iron and Fe2+ levels and GC in liver were increased in the Fe2+, Vc and Fe2+ + Vc groups compared with in the model groups. In addition, hardly change of serum insulin level was caused by Fe2+, Vc and Fe2+ + Vc treatment. However, the similar resultst did not obtain a Fe3+ treated. Further, liver’s GC of untreated-diabetic mice was lower than of normal mice and significantly increased after Fe2+ not Fe3+ added to the reaction resolution in vitro, and further increased when Fe2+ and vitamin c (Vc) synchronously added to the reaction system, however, decreased when Fe2+ and Streptozotocin were added synchronously to the reaction resolution. It is suggested that iron coupled with reducer can enhance the glucose metabolism to eventually achieve to controlling blood glucose levels.
Cite this paper: H. Zhen, H. Chen, Z. Tian and Z. Zhang, "Fe2+ Coupled with Vitamin c (Vc) Can Enhance Glucose Metabolism and Decrease Blood Glucose Levels of Alloxan-Induced Diabetic Mice," Food and Nutrition Sciences, Vol. 3 No. 11, 2012, pp. 1586-1594. doi: 10.4236/fns.2012.311207.

[1]   V. B. Junqueira, S. B. Barros, S. S. Chan, L. Rodrigues, L. Giavarotti, R. L. Abud and G. P. Deucher, “Aging and Oxidative Stress,” Molecular Aspects of Medicine, Vol. 25, No. 1-2, 2004, pp. 5-16. doi:10.1016/j.mam.2004.02.003

[2]   J. Karolkiewicz, E. Michalak, B. Pospieszna, E. DeskurSmielecka, A. Nowak and L. Pilaczyńska-Szcze?niak, “Response of Oxidative Stress Markers and Antioxidant Parameters to an 8-Week Aerobic Physical Activity Program in Healthy, Postmenopausal Women,” Archives of Gerontology and Geriatrics, Vol. 49, No. 1, 2009, pp. e67-e71. doi:10.1016/j.archger.2008.09.001

[3]   P. Moller, H. Wallin and L. E. Knudsen, “Oxidative Stress Associated with Exercise, Psychological Stress and Life-Style Factors,” Chemico-Biology Interactions, Vol. 102, No. 1, 1996, pp. 17-36. doi:10.1016/0009-2797(96)03729-5

[4]   C. Nasuti, R. Gabbianelli, M. L. Falcioni, A. Di Stefano, P. Sozio and F. Cantalamessa, “Dopaminergic System Modulation, Behavioral Changes, and Oxidative Stress after Neonatal Administration of Pyrethroids,” Toxicology, Vol. 229, No. 3, 2007, pp. 194-205. doi:10.1016/j.tox.2006.10.015

[5]   A. Peter, “Bioenergentics and the Metabolism of Carbohydrates and Lipids,” In: K. Robert, K. Daryl and W. Victor, Eds., Harper’s Biochemistry, 25th Edition, Sicence Press, 2000, pp. 182-208.

[6]   S. Filiz, ?. Gülyüz, E. Deniz and H. Alev, “Antioxidant Effect of Vitamin E in the Treatment of Nutritional Iron Deficiency Anemia,” Turkish Journal of Hematology, Vol. 23, No. 1, 2006, pp. 15-24.

[7]   B. J. Clodfelder, B. M. Gullick, H. C. Lukaski, Y. Neggers and J. B. Vincent, “Oral Administration of the Biomimetic [Cr3O(O2CCH2CH3)6(H2O)3]+ Increases Insulin Sensitivity and Improves Blood Plasma Variables in Healthy and Type 2 Diabetic Rats,” Journal of Biological Inorganic Chemistry, Vol. 10, No. 2, 2005, pp. 119-130. doi:10.1007/s00775-004-0618-0

[8]   Y. Sun, K. Mallya, J. Ramirez and J. B. Vincent, “The Biomimetic [Cr3O(O2CCH2CH3)6(H2O)3]+ Decreases Plasma Cholesterol and Triglycerides in rats: Towards Chromium-Containing Therapeutics,” Journal of Biological Inorganic Chemistry, Vol. 4, No. 6, 1999, pp. 838-845. doi:10.1007/s007750050357

[9]   Z. C. Zhang, B. Lian and F. J. Cui, “Effect of FeSO4 Treatment on Glucose Metabolism in Diabetic Rats,” Biometals, Vol. 21, No. 6, 2008, pp. 685-691. doi:10.1007/s10534-008-9153-8

[10]   N. Aksoya, H. Vural, T. Sabuncub, O. Arslan and S. Aksoy, “Beneficial Effects of Vitamins C and E against Oxidative Stress in Diabetic Rats,” Nutrition Research, Vol. 25, No. 6, 2005, pp. 625-630. doi:10.1016/j.nutres.2005.05.005

[11]   Z. C. Zhang, X. Li, M. X. Chen and W. L. Shen, “Assay of the Glucose Consumption Rate in Liver with a Novel Colorimetric Method,” Current Pharmaceutical Analysis, Vol. 7, No. 3, 2011, pp. 195-201. doi:10.2174/157341211796353336

[12]   J. Lin and S. H. Ji, “The Determination of Dietary Fe (II) and (III),” Guangdong Microelement Science, Vol. 3, No. 8, 1996, pp. 148-152.

[13]   D. Duncan, “Multiple Range Tests for Correlated and Heteroscedastic Means,” Biometrics, Vol. 13, No. 2, 1957, pp. 164-176. doi:10.2307/2527799

[14]   M. Brownlee, “Biochemistry and Molecular Cell Biology of Diabetic Complications,” Nature, Vol. 414, No. 6865, 2001, pp. 813-820. doi:10.1038/414813a

[15]   M. Brownlee, “The Pathobiology of Diabetic Complications: A Unifying Mechanism,” Diabetes, Vol. 54, No. 6, 2005, pp.1615-1625. doi:10.2337/diabetes.54.6.1615

[16]   J. L. Evans, I. D. Goldfine, B. A. Maddux and G. M. Grodsky, “Oxidative Stress and Stress-Activated Signaling Pathways: A Unifying Hypothesis of Type 2 Diabetes,” Endocrine Reviews, Vol. 23, No. 5, 2002, pp. 599-622. doi:10.1210/er.2001-0039

[17]   D. Jay, H. Hitomi and K. K. Griendling, “Oxidative Stress and Diabetic Cardiovascular Complications,” Free Radical Biology & Medicine, Vol. 40, No .2, 2006, pp. 183-192. doi:10.1016/j.freeradbiomed.2005.06.018

[18]   P. Rosen, P. P. Nawroth, G. King, W. M?ller, H. J. Tritschler and L. Packer, “The Role of Oxidative Stress in the Onset and Progression of Diabetes and Its Complications: A Summary of a Congress Series Sponsored by UNESCO-MCBN, the American Diabetes Association and the German Diabetes Society,” Diabetes/Metabolism Research and Reviews, Vol. 17, No. 3, 2001, pp. 189-212. doi:10.1002/dmrr.196

[19]   J. A. Scott and G. L. King, “Oxidative Stress and Antioxidant Treatment in Diabetes,” Annal of the New York Academy Science, Vol. 1031, No. 12, 2004. pp. 204-213. doi:10.1196/annals.1331.020

[20]   I. C. West, “Radicals and Oxidative Stress in Diabetes,” Diabetic Medicine, Vol. 17, No. 3, 2000, pp. 171-180. doi:10.1046/j.1464-5491.2000.00259.x

[21]   P. Anabela and M. P. Carlos, “Diabetes and Mitochondrial Function: Role of Hyperglycemia and Oxidative Stress,” Toxicology and Applied Pharmacology, Vol. 212, No. 2, 2006, pp. 167-178. doi:10.1016/j.taap.2006.01.003

[22]   A. C. Maritim, R. A. Sanders and J. B. Watkins, “Diabetes, Oxidative Stress, and Antioxidants: A Review,” Journal of Biochemical and Molecular Toxicology, Vol. 17, No. 1, 2003, pp. 24-38. doi:10.1002/jbt.10058

[23]   Z. C. Feng, T. J. Sick, M. Rosenthal, “Oxygen Sensitivity of Mitochondrial Redox Status and Evoked Potential Recovery Early during Reperfusion in Post-Ischemic Rat Brain,” Resuscitation, Vol. 37, No. 1, 1998, pp. 33-41. doi:10.1016/S0300-9572(98)00031-8

[24]   M. A. Perez-Pinzon, P. L. Mumford, M. Rosenthal and T. J. Sick, “Antioxidants, Mitochondrial Hyperoxidation and Electrical Recovery after Anoxia in Hippocampal Slices,” Brain Research, Vol. 754, No. 1-2, 1997, pp. 163-170. doi:10.1016/S0006-8993(97)00066-8

[25]   M. Rosenthal, Z. C. Feng, C. N. Raffin, M. Harrison and T. J. Sick, “Mitochondrial Hyperoxidation Signals Residual Intracellular Dysfunction after Global Ischemi a in Rat Neocortex,” Journal of Cerebral Blood Flow & Metabolism, Vol. 15, No. 4, 1995, pp. 655-665. doi:10.1038/jcbfm.1995.81

[26]   T. Shen and J. Wang, “Biochemistry,” Higher Education Publisher, Beijing, 2000.

[27]   W. Ebel, “Carrier Facilitated Diffusion,” Journal of Mathematical Biology, Vol. 21, No. 3, 1985, pp. 243-271. doi:10.1007/BF00276225