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2017 ; 26
(1
): 78-83
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Insulin Prevents Hyperfiltration and Proteinuria but Not Glomerular Hypertrophy
and Increases Mesangial Matrix Expansion in Diabetic Rats
#MMPMID27643698
Malatiali S
; Francis I
; Barac-Nieto M
Med Princ Pract
2017[]; 26
(1
): 78-83
PMID27643698
show ga
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.