EFFECT OF CHRONIC GROWTH-HORMONE ADMINISTRATION ON DIABETIC NEPHROPATHY IN THE RAT

Indirect data exist which implicate elevated growth hormone (GH) as a factor in the development of diabetic nephropathy. The administration of somatostatin (SRIH) has been shown to reverse many of the changes f ound in early diabetic nephropathy; however, it is unknown whether SRI H causes these effects by the suppression of GH or by other unspecifie d factors. To study directly the possible effect of excess GH in the d evelopment of diabetic nephropathy, either ovine growth hormone (0.2 m g oGH) or diluent buffer was administered IM daily for 19 weeks to dia betic rats and to controls. Severity of nephropathy was assessed by 24 hour urine albumin excretion (UAE), relative kidney weight, and kidne y histology. Results showed that diabetic rats overall had elevated UA E and kidney weight vs non-diabetic rats (46.2 +/- 8.6 vs 5.4 +/- 1.3 mg per day and 5.7 +/- 0.2 vs 2.7 +/- 0.1 mg per g of body weight, res pectively, p < 0.001). However, no differences were detected between d iabetic rats treated with GH compared to control diabetic rats. Additi onally, diabetic rats had histopathologic changes consistent with earl y diabetic nephropathy, but no difference in severity scores was found between diabetic groups. These data provide evidence against GH as an etiologic factor in the development of diabetic nephropathy and it is speculated by the authors that SRIH exerts its protective renal effec ts in diabetes by mechanisms other than GH suppression.