The Japanese Journal of Nephrology
Online ISSN : 1884-0728
Print ISSN : 0385-2385
ISSN-L : 0385-2385
Octreotide suppresses the kidney weight and glomerular hypertrophy in diabetic rats
SHIGEKI IWASAKI
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JOURNAL FREE ACCESS

1993 Volume 35 Issue 3 Pages 247-255

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Abstract

It was previously demonstrated that initial kidney hypertrophy has been seen in diabetic animals and somatostatin infusion suppresses GFR and serum insulin like growth factor (1GF-1) in diabetic patients. I studied the effects of somatostatin analogue (octreotide) on glomerular hypertrophy in diabetic rats. The animals were randomized into six groups: two groups of streptozocin (STZ) induced diabetic, insulin-treated diabetic and non-diabetic rat groups. One of these three groups were treated with two daily subcutaneous injections of octreotide (10μg × 2) for a period of five weeks. In diabetic rats, body weight, blood sugar, glucose excretion, serum insulin, urinary volume, urinary protein, serum creatinine or creatinine clearance did not differ in diabetic rats with vs. without octreotide injection, but kidney weight (2.97 ± 0.12 vs. 3.28 ± 0.08 mg, P < 0.05; mean ± SEM) and estimated glomerular volume (9.13±0.22 vs. 12.77±0.34×105μm3. P<0.001) were all reduced in diabetic rats with octreotide when compared with untreated diabetic rats. In non-diabetic rats, octreotide reduced body weight (340.3±6.5 vs. 367.1±3.8g, P<0.01) and kidney weight (2.29 ± 0.08 vs. 2.51 ± 0.04 g, P < 0.05) when compared with non-diabetic rats without octreotide. Urinary protein excretion (8, 57±1.39 vs. 14.29±1.53 mg/day, P<0. 05), serum 1GF-1 concentration (956.3 ± 180.7 vs. 1546.1 ± 88.1mg/day, P < 0.05) and estimated glomerular volume (7.69±0.16vs.9, 72±0.15×105 μm3, P<0. 001) significantly differed in insulin treated diabetic rats with vs. without octreotide. In conclusion, subcutaneous infusion of octreotide for five weeks prevents renal hypertrophy or glomerular hypertrophy in diabetic rats with and without insulin treatment. The suppressive effects of octreotide on glomerular hypertrophy may be in part due to reduction of 1GF-1.

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