Regulation of renal cortex cell membranes insulin receptor in diabetic rats by ACEI
Zhou Jianghu
Abstract
Zhou Jianghu
Abstract
Objective To investigate into the regulation of renal cortex cell membranes insulin receptor indiabeticratsbyangiotensinconvertingenzymeinhibitor(ACEI). Methods The rats were randomly divided into following groups: uninephrectomized rats (group C, n=6), streptozotocin induced diabetic rats (group D, n=7) and diabetic rats treated with benazepril (an ACEI), (group DB, n=7). Blood glucose, serum insulin, serum creatinine level as well as body weight, kidney weight and kidney weight/body weight were observed after 4 weeks of study. ACE activities in plasma, renal cortex and medulla were measured by fluorimetric assay. The expression of renal cortex cell membranes insulin receptor were determined by Western blot analysis. Results After 4 weeks of treatment, benazepril could ameliorate hyperglycemia, decrease serum insulin and increase serum creatinine level. It could also significantly supress kidney hypertrophy in diabetic state. ACE activities in plasma, renalcortexandmedulla were reduced by approximately 92.00%, 88.77% and 73.40%, respectively. Western blot analysis showed that the expression of renal cortex cell membranes insulin receptor was increased by about 2.10 folds in diabetic rats, however, benazepril might significantly down regulate its expression. Conclusion Benazepril may down regulate the increased expression of renal cortex cell membranes insulin receptor protein in diabetic rats, which may be one of the important mechanism of its nephroprotection.
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Objective To investigate into the regulation of renal cortex cell membranes insulin receptor indiabeticratsbyangiotensinconvertingenzymeinhibitor(ACEI). Methods The rats were randomly divided into following groups: uninephrectomized rats (group C, n=6), streptozotocin induced diabetic rats (group D, n=7) and diabetic rats treated with benazepril (an ACEI), (group DB, n=7). Blood glucose, serum insulin, serum creatinine level as well as body weight, kidney weight and kidney weight/body weight were observed after 4 weeks of study. ACE activities in plasma, renal cortex and medulla were measured by fluorimetric assay. The expression of renal cortex cell membranes insulin receptor were determined by Western blot analysis. Results After 4 weeks of treatment, benazepril could ameliorate hyperglycemia, decrease serum insulin and increase serum creatinine level. It could also significantly supress kidney hypertrophy in diabetic state. ACE activities in plasma, renalcortexandmedulla were reduced by approximately 92.00%, 88.77% and 73.40%, respectively. Western blot analysis showed that the expression of renal cortex cell membranes insulin receptor was increased by about 2.10 folds in diabetic rats, however, benazepril might significantly down regulate its expression. Conclusion Benazepril may down regulate the increased expression of renal cortex cell membranes insulin receptor protein in diabetic rats, which may be one of the important mechanism of its nephroprotection.
Key concepts: Benazepril, Endocrinology, Internal medicine, Streptozotocin, Renal cortex, Insulin, Kidney, Creatinine