Showing 2 results for Type I Diabetes.
Majid Tavafi , Abdolahman Dezfulian, Mohammad Hadi Kochek , Hayat Mombeini , Asadollah Tavakoli , Mohammad Javad Tarahi ,
Volume 6, Issue 4 (2-2005)
Abstract
Background: Diabetic nephropathy is one of the cause of the end stage of renal disease (ESRD). Hyperglicemia activate intrarenal Renin-Angiotensin system and highly AngiotensinII is produced locally in glomeruli. In this research AT1(Angiotensin type 1) receptors blocked by Losartan and effects of this drug in inhibition of renal structural lesions were assessed quantitatively.
Materials & methods: 24 male rats (2 month ages) were uninephrectomised from left flank and then randomly divided in 3 groups (8 per group), then Diabetes were induced in second and third groups by injection of alloxan tetrahydrate (120 mg/kg) subcutaneously. Five days after diabetes induction third group received losartan (5 mg/kg/day) orally for 8 weeks. After 8 weeks kidneys from all groups were sampled, fixed and each kidney sliced in 1 mm thickness (systematic random sampling) for stereological study. After tissue processing section pairs were made with 5 micron thickness from each slice and stained by PAS method. Kidney volume, glomerular volume and glomerular number estimated by cavalieri and physical disector methods.
Results: Significancy test between means variables in groups were analyzed with Mann Withney statistical test in P<0.05 by SPSS12 software. For three variables (kidney volume,glomerular volume and glomerular number) losartan treated group showed significant difference to in comparison nontreated diabetic group.
Conclusion: Chronic low dose usage of losartan in uninephrectomized diabetic rats can prevent kidney volume increasing (84%), inhibit increase glomerular volume (67%) and prevent glomerular number decreasing (68%) significantly. Combined drug therapy is recommended for better results.
Abdolrahman Haj-Dezfulian , Majid Tavafi , Asadollah Tavakoli , Mohammad Javad Tarahi ,
Volume 8, Issue 2 (1-2007)
Abstract
Background: Diabetic nephropathy is one of the causes of end stage renal diseases (ESRD). Increase of IGF-1(insulin like growth factor) and GH (growth hormone) in diabetes induce kidney lesions especially Intraglomerular mesangial expansion, glomerular sclerosis and finally nephron dysfunction. In this research, IGF-1 and GH production inhibition by octreotide and sclerosis inhibition assessed quantitatively.
Materials and methods: 21 male rats (2-month ages) were uninephrectomized from left flank and then randomly divided in 3 groups (7 per group). Diabetes was induced in second and third groups by injection of alloxan tetrahydrate (120 mg/kg) subcutaneously. Five days after diabetes induction, third group received octreotide (10 μg/day) subcutaneously for 8 weeks. After 8 weeks, kidneys from all groups were removed, fixed and sliced in 1 mm thickness for stereological study. After tissue processing, sections with 5 micron thickness were prepared from each slice and stained by PAS method. Cortex volume, glomerular volume and glomerular mesangium volume were estimated by Cavalieri and point counting methods. Mean difference of variables was analyzed by Mann-Whitney statistical test at P<0.05 level using SPSS V.12.0.
Results: Chronic low dose usage of octreotide in diabetic rats can prevent increase of cortex volume (67%) and glomerular mesangial expansion (53%) significantly. This treatment inhibits increase of glomerular volume by 26% which is not significant.
Conclusion: Inhibition of cortex volume and mesangial expansion in octreotide treated group showed significant effects in comparison to the non-treated diabetic group. But this treatment has no significant effect on glomerular hypertrophy in diabetic rats.
