Showing 2 results for Stz Induced
Ali Mohammad Sharifi, Seyed Hadi Mousavi, Bagher Larijani,
Volume 3, Issue 2 (6-2004)
Abstract
Background: The precise mechanisms of vascular diseases in insulin dependent diabetes mellitus (IDDM) are not clearly understood. There are evidences of alteration in mechanisms involved in regulating vascular tone including increased ACE activity in some tissues. To investigate the effect of insulin treatment on these changes this study was performed.
Methods: Three groups of 8 male Sprauge Dawely rats including control (C) and two diabetic groups (D, IT) were used in this study. Diabetes was induced by injection of 60 mg/kg STZ ip. After induction of diabetes IT group were treated with insulin (10 units/kg/day s.c.) for four weeks. The control group and the untreated diabetic group were treated with the same amount of Saline and for the same time. ACE activity was determined by HPLC method.
Results: 4 weeks after induction of diabetes, SBP and ACE activity in serum, lung, heart and aorta increased in D group compared to control rats. Insulin treatment reversed these changes to normal values in IT group.
Conclusion: It is concluded that increased ACE activity could contribute to the development of diabetic vasculopathy and ACE reducing activity of insulin may be partially involved in decrease of cardiovascular complications in diabetes.
Ali Mohammad Sharifi, Seyed Hadi Mousavi, Bagher Larijani,
Volume 4, Issue 2 (8-2004)
Abstract
Background: Due to homeostatic and regulatory potentials of nitric oxide (NO) in vascular physiology, regulatory systems that determine NO bio-synthesis and bioavailability have been the subject of extensive research in molecular medicine. In the field of vascular system pathophysiology, endothelial nitric oxide synthase (eNOS) which is the major producer and regulator of NO in vascular tissues has received the most attention. Impairment of NO bioavailability (NO quenching) is a common feature in poorly controlled diabetics due to increased catabolism and decreased production of NO. Such impairment in severe forms could end to vasodilation breakdown in peripheral tissues (mainly in skeletal muscles) and defective regional blood flow, that in turn disturb insulin-dependent glucose uptake ensuing insulin resistance state.
Methods: The phenotypic impact of an eNOS gene polymorphism at position 786*C/T (that its functionality has been revealed already) on genetic propensity to diabetic retinopathy is evaluated in a British-Caucasian population with type 1 diabetes (T1DM).
Results: In contrast to genotypes, there was a significant difference in distribution of allele frequencies between T1DM patients (n= 249) and healthy controls (n= 104) (p= 0/036), that may imply eNOS and/or NO involvement in development of T1DM. Most notably a significant difference also was evident in allele frequency between retinopaths (n= 134) and healthy controls (p= 0/02). No significant difference was detected when the genotype/allele frequencies were compared between retinopaths (n= 134) and non-retinopaths diabetics (n= 115) (p=NS).
Conclusion: Our data is compatible with previous studies which demonstrated that allele C of eNOS 786*C/T polymorphism is associated with increased HbA1c levels. By emphasizing the phenotypic and prognostic value of the abovementioned polymorphism, our data calls for further investigations to find out whether this polymorphism can be employed as a genetic marker in clinical medicine to recognize high-risk diabetics at the time of diabetes onset/diagnosis.
