Advanced glycosylation end products, protein kinase C and renal alterations in diabetic rats
- Author:
Jian RONG
1
;
Hongxin QIU
;
Shuping WANO
Author Information
1. Daping IIospltal of Thinl Military Medical University
- Keywords:
dtabetic nephropathy . nonenzvmatic g1ycosylation;
protein kinase C;
insulin;
aminoguanidine advanced glycosylation end products;
glomerular basement membrane
- From:
Chinese Medical Journal
2000;113(12):1087-1091
- CountryChina
- Language:Chinese
-
Abstract:
Objective To sludy the relationship between advanced glycosylation end products (AGE) and protein kinase C (PKC), and their effects on ranal alteration in diabetic rats. Methods Insulin or anlinoguanidine was administered to diabetic rats. Blood glucose, hermoglobin A1c (HbA1c ), glomemlar tissue extracts AGE ( GTE AGE ), PKC, glomerular basement membrane thickness ( GBMT ) and udne protein/creatinine (Pr/Cr) ratio in diabetic rats were measured and analysed. Results LeveLs of blood glucose, HbA1C and AGE, PKC activity, the Pr/Or ratio and GBMT were all significantly increased ( p values all less than 0.01 ) in diabetic rats. Insulin could decrease the formation of kbAlc and AGE, and improve PKC activity. Aminoguanidine had no influecce on PKC activity (P>O.05) although it decreased the formation of AGE. Botah drugs could de4ay the increase of urine Pr/Cr ratio and GBMT ( P<0.05 or P< 0.01). Conclusions Chronic hyperglycemia may lead to an increase of PKC activity. HbAlc and AGE may not directly coritribute to alterations of PKC activity, but the increase of PKC activity could promote the action of AGE on GEM thickening. It is important to inhibit the formanion of AGE and reduce the PKC activity so as to pceveat or delay the development of diabetic nephropathy.
