PMID- 25816395 OWN - NLM STAT- MEDLINE DCOM- 20170404 LR - 20170404 IS - 0394-6320 (Print) IS - 0394-6320 (Linking) VI - 28 IP - 2 DP - 2015 Jun TI - Synthesis, characterization, and efficacy evaluation of a new anti-diabetic vanadyl(II) thiamine hydrochloride complex in streptozotocin-induced diabetic rats. PG - 227-39 LID - 10.1177/0394632015576036 [doi] AB - Diabetes mellitus (DM) is a chronic metabolic disorder characterized by hyperglycemia due to abnormalities in either insulin secretion or action. A range of vanadium complexes have been synthesized and demonstrated to be effective in lowering hyperglycemia. Thiamine administration was also reported to prevent deterioration in fasting glucose and insulin levels, and to improve glucose tolerance in hyperglycemic patients. This study has been conducted to evaluate the ionic vanadyl(II) thiamine hydrochloride complex (VC) as a new anti-diabetic candidate. The new complex was characterized by infrared spectroscopy (FT-IR), electronic spectra, magnetic susceptibility, electron spin resonance (ESR), scanning electron microscopy (SEM), and thermogravimetric analysis (TGA). The anti-diabetic effect of VC was investigated in comparison to vanadium sulfate in streptozotocin (STZ)-induced diabetic rats. Treatment of diabetic rats with VC versus vanadyl sulfate showed a more potent effect on reducing serum glucose and cholesterol close to normal levels. VC suppressed the diabetes-induced upregulation of hepatic glucose transporter (GLUT)-2, Phosphoenol pyruvate carboxykinase (PEPCK), and hormone-sensitive lipase (HSL) more significantly than vanadyl sulfate. Either vanadyl sulfate or VC restored hepatic sterol regulatory element-binding protein transcription factor-1c (SREBP-1c) and muscle hexokinase (HK) mRNA expression that was downregulated in diabetic group. Pyruvate kinase (PK) mRNA expression was restored more significantly in VC-treated than vanadyl sulfate-treated diabetic rats. These results indicate that the newly synthesized VC could be an effective anti-diabetic candidate as the anti-diabetic activity of the ionic vanadium was enhanced after being modified with the organic ligand, thiamin. The results also suggest that VC achieves its effect most likely through modulating the transcription of energy metabolizing enzymes. CI - (c) The Author(s) 2015. FAU - Ahmed El-Shazly, Samir AU - Ahmed El-Shazly S AD - Department of Biotechnology, College of Science, Taif University, Saudi Arabia Department of Biochemistry, Faculty of Veterinary Medicine, Kaferelsheikh University, Egypt. FAU - Ahmed, Mohamed Mohamed AU - Ahmed MM AD - Department of Biotechnology, College of Science, Taif University, Saudi Arabia Department of Biochemistry, Faculty of Veterinary Medicine, University of Sadat City, Egypt m_m_ahmed@yahoo.com. FAU - Ibrahim, Zein Shaban AU - Ibrahim ZS AD - Department of Physiology, Faculty of Veterinary Medicine, Kaferelsheikh University, Egypt Department of Physiology, Faculty of Medicine, Taif University, Saudi Arabia. FAU - Refat, Moamen S AU - Refat MS AD - Department of Chemistry, College of Science, Taif University, Saudi Arabia Department of Chemistry, Faculty of Science, Port Said University, Egypt. LA - eng PT - Journal Article DEP - 20150326 PL - England TA - Int J Immunopathol Pharmacol JT - International journal of immunopathology and pharmacology JID - 8911335 RN - 0 (Blood Glucose) RN - 0 (Hypoglycemic Agents) RN - 0 (Insulin) RN - 0 (Vanadium Compounds) RN - 5W494URQ81 (Streptozocin) RN - 6DU9Y533FA (vanadyl sulfate) RN - X66NSO3N35 (Thiamine) SB - IM MH - Animals MH - Blood Glucose/drug effects MH - Diabetes Mellitus, Experimental/*chemically induced/*drug therapy MH - Hypoglycemic Agents/*pharmacology MH - Insulin/metabolism MH - Liver/drug effects/metabolism MH - Male MH - Rats MH - Rats, Wistar MH - Streptozocin/*pharmacology MH - Thiamine/*pharmacology MH - Vanadium Compounds/*pharmacology OTO - NOTNLM OT - STZ-induced diabetes OT - gene expression OT - thiamine OT - vanadium EDAT- 2015/03/31 06:00 MHDA- 2017/04/05 06:00 CRDT- 2015/03/28 06:00 PHST- 2014/12/13 00:00 [received] PHST- 2015/02/13 00:00 [accepted] PHST- 2015/03/28 06:00 [entrez] PHST- 2015/03/31 06:00 [pubmed] PHST- 2017/04/05 06:00 [medline] AID - 0394632015576036 [pii] AID - 10.1177/0394632015576036 [doi] PST - ppublish SO - Int J Immunopathol Pharmacol. 2015 Jun;28(2):227-39. doi: 10.1177/0394632015576036. Epub 2015 Mar 26.