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Molecular Endocrinology Laboratory, Soroka Medical Center and Ben-Gurion
University of the Negev, Beer-Sheva, Israel
Department of Pediatrics, Soroka Medical Center and Ben-Gurion University
of the Negev, Beer-Sheva, Israel
Department of Cell Biology, Institute of Anatomy, University of Aarhus,
Aarhus, Denmark
§
Medical Department M, Medical Research Laboratory M, Institute of
Experimental Clinical Research, Aarhus Kommunehospital, Aarhus,
Denmark
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Felsenstein Medical Research Center, Institute for Endocrinology and
Diabetes, Schneider Children's Medical Center, Petah Tikva and Tel Aviv
University, Tel Aviv, Israel.
Correspondence to Dr. Moshe Phillip, Institute for Endocrinology and Diabetes, Schneider Children's Medical Center, 14 Kaplan Street, Petah Tikva 49202, Israel. Phone: 972-3-9253731; Fax: 972-3-9253836; E-mail: phillip{at}bgumail.bgu.ac.il
Abstract. The growth hormone (GH)/insulin-like growth factor (IGF) axis is involved in diabetic renal disease. The role of a specific GH receptor (GHR) antagonist in the development of early renal changes in nonobese diabetic (NOD) mice was investigated. Female diabetic (nonketotic) NOD mice treated with a polyethylene glycol-treated GHR antagonist (2 mg/kg, every other day) (DA group) or saline (D group) and their nonhyperglycemic age-matched littermates (control animals) were euthanized 3 wk after the onset of diabetes. Body weights at euthanasia were similar among the groups. Serum GH levels were markedly elevated, and serum IGF-I levels were significantly decreased in D and DA animals, compared with controls. The increases in kidney weights and glomerular volumes observed for the D group were absent in the DA group. Albuminuria was increased in the D group but was normalized in the DA group. Extractable renal IGF-I protein levels were increased in the D group but were partially normalized in the DA group. Renal IGF-binding protein 1 mRNA levels were increased in the D group but returned to almost normal levels in the DA animals. Kidney IGF-I and GHR mRNA levels were decreased in both the D and DA groups. Renal GH-binding protein mRNA levels remained unchanged in both diabetic groups. GHR antagonism had a blunting effect on renal/glomerular hypertrophy and albuminuria in diabetic NOD mice. These salutary effects were associated with concomitant inhibition of increased renal IGF-I protein levels and were obtained without affecting either somatic growth or circulating GH and IGF-I levels. Therefore, modulation of GH effects may have beneficial therapeutic implications in diabetic nephropathy.
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