Open AccessBeneficial effects of C-peptide on renal morphology in diabetic rats
Author(s) -
Wei Sun,
Xin Gao,
Xiaolong Zhao,
Dafu Cui,
Qi-Chang Xia
Publication year - 2010
Publication title -
acta biochimica et biophysica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.771
H-Index - 57
eISSN - 1745-7270
pISSN - 1672-9145
DOI - 10.1093/abbs/gmq100
Subject(s) - medicine , endocrinology , diabetes mellitus , streptozotocin , glycemic , insulin , c peptide , peptide , matrix metalloproteinase , chemistry , biochemistry
The study was undertaken to examine the effects of C-peptide on glomerular volume (V(GLOM)), mesangial matrix synthesis, and degradation in streptozotocin (STZ)-diabetic rats with poor or moderate glycemic control. Series 1 (poor glycemic control) included groups of healthy rats, hyperglycemic rats, diabetic insulin-treated rats and diabetic C-peptide-treated rats. Series 2 (moderate glycemic control) included groups of healthy rats, diabetic insulin-treated rats, diabetic insulin- and C-peptide-treated rats. After 8 weeks, the left kidney was excised for evaluation of V(GLOM) and mesangial matrix area via light microscopy. Mesangial cells were cultured for 48 h and type IV collagen expression and matrix metalloproteinase (MMP)-2 expression were measured by ELISA and RT-PCR. The results indicated that in Series 1, C-peptide administration suppressed the diabetes-induced increase in the V(GLOM) and the mesangial matrix area. In Series 2, C-peptide administration resulted in a similar decrease in the V(GLOM) and a greater decrease in the mesangial matrix area when compared with insulin therapy alone. Moreover, C-peptide (300 nM) completely inhibited the glucose-induced increase of the collagen IV mRNA expression and protein concentration in mesangial cells cultured in 30 mM glucose medium. MMP-2 mRNA expression was not influenced by C-peptide. In conclusion, C-peptide administration to STZ-diabetic rats for 8 weeks results in the inhibition of diabetes-induced expansion of the mesangial matrix. This effect is independent of the level of glycemic control and results from the inhibition of diabetes-induced excessive formation of mesangial type IV collagen.