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      Somatostatin Analogue Attenuates Estrogen-Induced Augmentation of Glomerular Injury in Spontaneous Hypercholesterolemic Female Imai Rats

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          Background: Aggravating effect of estrogen replacement therapy on glomerular injury associated with an elevation of growth hormone (GH) levels has been reported. Therefore, in the present study, to clarify an association between GH elevation and the aggravating effect of estrogen on glomerular injury, we investigated the effect of somatostatin, an inhibitor of GH secretion, on glomerular injury in estrogen-treated hypercholesterolemic female Imai rats. Method: Control female rats were assigned to group 1 (Cont, n = 10). Group 2 (Cont-E, n = 10) received estrogen, and groups 3 (Cont-E-LS, n = 10) and 4 (Cont-E-HS) received estrogen and either a low dose of somatostatin analogue or a high dose of somatostatin analogue. Body weight, urinary protein, serum albumin, total cholesterol, triglycerides, blood urea nitrogen and serum creatinine were investigated every 4 weeks from 10 weeks through 30 weeks of age. At 30 weeks of age, rats were studied morphologically. Results: Estrogen administration resulted in an increase in urinary protein excretion rates and serum total cholesterol levels, and aggravated glomerular injury associated with an increase in GH. In contrast, somatostatin treatment reduced both urinary protein excretion rates and total cholesterol levels and attenuated glomerular injury to levels close to those of controls associated with a reduction of GH levels. Conclusion: The results suggest that increased GH levels may contribute to an enhancing effect of estrogen administration on glomerular injury.

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          Estrogen accelerates the development of renal disease in female obese Zucker rats.

          Renal failure is the primary cause of death in obese Zucker rats (OZR). We previously found that renal injury occurred earlier and with greater severity in female OZR; also, prevention of hyperphagia decreased renal damage in females more than males. To examine the relationship between estrogen (E), hyperphagia, hyperlipidemia, and renal injury in female OZR, we studied four groups from 5 to 10 or 21 weeks of age: Sham-operated (Sham), ovariectomized (Ovx), Ovx with estrogen treatment (Ovx + E), and since Ovx increases food intake, Ovx pair-fed to sham (Ovx-PF). By only six weeks of age, albumin excretion (UAE) increased significantly in Ovx + E (9.9 +/- 4.1 mg/day). Ovx + E also ate least and gained the least weight, but had the highest plasma lipid levels. In contrast, UAE in Ovx did not increase by 10 weeks of age, despite a significantly greater food consumption. The hyperlipidemia of Ovx + E was due primarily to triglycerides. Both plasma triglycerides and renal injury, judged from either histology or UAE, were greatest in the Ovx + E group Fasting plasma glucose was lower and insulin was higher in Ovx + E compared to Ovx rats at 15 weeks of age. Estrogen may promote renal injury in female OZR by increasing the plasma concentration of triglyceride-rich lipoproteins.
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            Estrogen Replacement Therapy with Its Physiological Dose Does Not Eliminate the Aggravating Effect of Ovariectomy on Glomerular Injury in Hypercholesterolemic Female Imai Rats

            Hypercholesterolemic Imai rats spontaneously develop proteinuria and glomerulosclerosis, especially in males. Estrogen administration attenuated glomerular injury in male Imai rats, and the aggravating effect of ovariectomy in female rats is found. To clarify whether this aggravating effect of ovariectomy is due to a lack of estrogen, we administered estrogen to ovariectomized female Imai rats. At 6 weeks of age, group 1 (control) was sham-operated and group 2 was ovariectomized. Groups 3 and 4 were ovariectomized and received estrogen replacement therapy (0.1 mg in group 3 and 0.2 mg in group 4 once a month subcutaneously). Body weight, urinary protein and serum constituents were investigated every month from 3 to 6 months of age. At 6 months of age, rats were studied morphologically. Estrogen replacement therapy increased serum estrogen to levels close to those of controls when 0.1 mg was used, or higher when 0.2 mg was used. Estrogen replacement therapy with 0.1 mg did not eliminate the aggravating effect of ovariectomy on glomerular injury and rather aggravated it, but conversely therapy with 0.2 mg attenuated glomerular injury and abolished the aggravating effect of ovariectomy. Estrogen replacement therapy markedly elevated serum GH levels dose-dependently. These results suggested that other hormones as well as estrogen may play a protective role of the ovary for the development of glomerular injury, and that estrogen seems to exert a dual effect on glomerular injury.

              Author and article information

              S. Karger AG
              22 November 2001
              : 89
              : 4
              : 448-454
              Department of Internal Medicine, Saga Medical School, Saga, Japan
              46118 Nephron 2001;89:448–454
              © 2001 S. Karger AG, Basel

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              Page count
              Figures: 6, Tables: 2, References: 36, Pages: 7
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              Original Paper

              Cardiovascular Medicine, Nephrology

              Somatostatin, Growth hormone, Glomerulosclerosis, Estrogen, Female rats


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