Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2016
Insulin Prevents Hyperfiltration and Proteinuria but Not Glomerular Hypertrophy and Increases Mesangial Matrix Expansion in Diabetic Rats.
Сравнительное исследованиеСтатьяНазвание и аннотация: Перевод в очереди
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Malatiali Slava, Francis Issam, Barac-Nieto Mario
Аннотация
OBJECTIVE: The aim of this work was to study the effect of 7 days of strict glycemic control with insulin on glomerular function and structure in streptozotocin (STZ)-diabetic rats.
MATERIALS AND METHODS: Three groups of adult male Fischer rats were studied: controls (n = 15), diabetics (n = 15), and insulin-treated diabetics (n = 15). Diabetes was induced by treating the rats with STZ (55 mg/kg i.p.). One week after the induction of diabetes, blood glucose, protein excretion rate (PER), glomerular filtration rate (GFR), and renal plasma flow (RPF) were estimated in each group. Furthermore, morphometric analysis was performed to estimate the tuft volume and changes in mesangial matrix area. The results are expressed as the mean ± SEM.
RESULTS: STZ diabetes caused significant increases in GFR (0.89 ± 0.1 to 1.21 ± 0.1 mL/min/100 g; p < 0.01) and RPF (1.78 ± 0.37 to 3.32 ± 0.6 mL/min/100 g; p < 0.05). Furthermore, the diabetic rats had higher glomerular volumes but mesangial matrix areas similar to controls. Insulin treatment prevented the increases in blood glucose (4.5 ± 0.2 mM), PER (66.1 ± 7.8 mg/day), GFR (0.6 ± 0.07 mL/min/100 g), and RPF (1.72 ± 0.36 mL/min/100 g), but did not prevent glomerular hypertrophy (21.7% increase), but induced mesangial matrix expansion (25% increase).
CONCLUSIONS: Insulin prevented the diabetes-induced hyperfiltration and proteinuria, but did not prevent glomerular growth, and induced mesangial expansion. Hyperglycemic episodes could be partly responsible for persistent glomerular growth and accelerated mesangial growth.
MATERIALS AND METHODS: Three groups of adult male Fischer rats were studied: controls (n = 15), diabetics (n = 15), and insulin-treated diabetics (n = 15). Diabetes was induced by treating the rats with STZ (55 mg/kg i.p.). One week after the induction of diabetes, blood glucose, protein excretion rate (PER), glomerular filtration rate (GFR), and renal plasma flow (RPF) were estimated in each group. Furthermore, morphometric analysis was performed to estimate the tuft volume and changes in mesangial matrix area. The results are expressed as the mean ± SEM.
RESULTS: STZ diabetes caused significant increases in GFR (0.89 ± 0.1 to 1.21 ± 0.1 mL/min/100 g; p < 0.01) and RPF (1.78 ± 0.37 to 3.32 ± 0.6 mL/min/100 g; p < 0.05). Furthermore, the diabetic rats had higher glomerular volumes but mesangial matrix areas similar to controls. Insulin treatment prevented the increases in blood glucose (4.5 ± 0.2 mM), PER (66.1 ± 7.8 mg/day), GFR (0.6 ± 0.07 mL/min/100 g), and RPF (1.72 ± 0.36 mL/min/100 g), but did not prevent glomerular hypertrophy (21.7% increase), but induced mesangial matrix expansion (25% increase).
CONCLUSIONS: Insulin prevented the diabetes-induced hyperfiltration and proteinuria, but did not prevent glomerular growth, and induced mesangial expansion. Hyperglycemic episodes could be partly responsible for persistent glomerular growth and accelerated mesangial growth.