Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a previous study we demonstrated that the kidney content of somatomedin C was maximal one to two days after uninephrectomy or induction of diabetes, and that insulin treatment prevented an increase in kidney somatomedin C as well as kidney growth in diabetic animals. In the present study we have examined the effect of a somatostatin analogue on kidney somatomedin C and initial renal growth in the two experimental situations. The kidney hypertrophy in untreated diabetic animals amounted to 23% four days after streptozotocin injection and followed an increase in kidney somatomedin C content of 60% reaching the maximum after 48 h. In young and old uninephrectomized rats kidney growth was 19% and 16% after four days. In young animals a prompt increase of 50% in kidney somatomedin C was seen as reaching the maximum after 24 h, while the somatomedin C content in kidneys from old animals was maximal after 48 h (increase of 58%) in good accordance with the slightly slower kidney growth. The new findings of the present study are that administration of a long-acting somatostatin analogue (Sandostatin) effectively prevented the obligatory increase in kidney somatomedin C content as well as kidney growth both in experimental diabetes and after uninephrectomy. It is noteworthy that Sandostatin administration did not alter the metabolic state in diabetic animals indicating that the inhibition of kidney hypertrophy could not be attributed to improved metabolic control. The results thus support the concept that somatomedin C is involved in initial diabetic and post-nephrectomy renal growth.
 ...
PMID:Somatostatin analogue administration prevents increase in kidney somatomedin C and initial renal growth in diabetic and uninephrectomized rats. 275 63

IGF-I acts as a renotropic factor in early streptozotocin-induced diabetes. Somatostatin analogue (octreotide) treatment initiated at the onset of diabetes prevents kidney IGF-I accumulation and renal growth. Seven days of octreotide treatment initiated after 3, 5, 7 or 9 days of untreated diabetes was investigated. Diabetic renal hypertrophy was followed by renal hyperplasia. Compared with placebo-treated diabetic rats, the earliest octreotide intervention was followed by a greater reduction in renal growth compared with intervention later on (days 3 to 10, 12%; days 5 to 12, 10%; days 7 to 14, 9%; days 9 to 16, 6%; P < 0.05). Octreotide treatment was unable to reduce protein accumulation and kidney DNA increase consistently. No difference in glomerular volume fraction or total glomerular volume was observed between placebo- and octreotide-treated diabetic rats. Octreotide treatment was followed by reduced kidney and serum IGF-I especially following early intervention, while no effect over that of diabetes was observed in the later intervention periods. The results confirm the notion that initial renal IGF-I accumulation is a prerequisite for early diabetic kidney hypertrophy in rats and show that delayed octreotide treatment cannot reverse renal and glomerular growth which is already manifest.
 ...
PMID:Effect of octreotide on experimental diabetic renal and glomerular growth: importance of early intervention. 749 May 42

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 (IGF-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 (10 micrograms x 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 x 10(5) microns 3, 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 +/- 88.1 mg/day, P < 0.05) and estimated glomerular volume (7.69 +/- 0.16 vs. 9.72 +/- 0.15 x 10(5) microns 3, P < 0.001) significantly differed in insulin treated diabetic rats with vs. without octreotide.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Octreotide suppresses the kidney weight and glomerular hypertrophy in diabetic rats]. 850 54

Diabetic kidney disease (DKD), the leading cause of kidney failure, is characterized by albuminuria and renal hypertrophy. Metabolic alterations and mitochondrial dysfunction play critical roles in DKD initiation and progression. Artemether, a methyl ether derivative of artemisinin used for the treatment of malaria, has been identified as a putative candidate for treating diabetes, but its effect on DKD has not been studied. The goal of this study was to examine the effect of artemether on type 2 diabetic db/db mice. Our results show that artemether reduced urinary albumin excretion, prevented diabetic kidney hypertrophy, attenuated glomerular basement membrane and tubular basement membrane thickening, and ameliorated foot process effacement in type 2 diabetic db/db mice. Artemether also protected against hyperglycemia and improved diabetic symptoms. In addition, it increased serum insulin level and restored the normal ratio of insulin, glucagon, and somatostatin levels in islets. Specifically, artemether increased the respiratory exchange ratio and regulated mitochondrial function and the redox state in the kidney. In conclusion, this experiment confirmed the renal protection ability of artemether in DKD. The mechanisms of this effect might be associated with the ability of artemether to increase mitochondrial pyruvate carrier content.
 ...
PMID:Artemether ameliorates type 2 diabetic kidney disease by increasing mitochondrial pyruvate carrier content in db/db mice. 3097 69