Park S K, Meyer T W
Department of Medicine, Palo Alto Veterans Administration Medical Center, CA 94304, USA.
J Lab Clin Med. 1995 Apr;125(4):501-7.
Studies were carried out in two groups of obese male Zucker rats with hereditary insulin resistance. Group 1 rats were made hyperglycemic by reducing beta-cell reserve with streptozotocin. Group 2 rats served as controls. Group 1 rats exhibited hyperglycemia (blood glucose concentration, 263 +/- 14 mg/dl) whereas insulin levels remained greater than those observed in lean rats (plasma insulin concentrations: group 1,508 +/- 89 mU/ml; lean rats, 91 +/- 23 mU/ml). In group 2 rats more marked hyperinsulinemia (plasma insulin concentration, 1096 +/- 234 mU/ml) maintained normoglycemia (blood glucose concentration, 75 +/- 4 mg/dl). Studies at 5 weeks showed that hyperglycemic group 1 rats exhibited increases in kidney weight (group 1, 2.78 +/- 0.11 gm; group 2, 2.16 +/- 0.07 gm; p < 0.05) and glomerular filtration rate (GFR) (group 1, 1.83 +/- 0.08 ml/min; group 2, 1.55 +/- 0.10 ml/min; p < 0.05). Micropuncture revealed that the increase in GFR in hyperglycemic rats was attributable to increases in the single-nephron plasma flow rate (group 1, 225 +/- 16 nl/min; group 2, 172 +/- 14 nl/min; p < 0.05) and the glomerular ultrafiltration coefficient (group 1, 2.49 +/- 0.17 nl/min/mm Hg; group 2, 2.02 +/- 0.14 nl/min/mm Hg; p < 0.05), which were not accompanied by an increase in glomerular transcapillary hydraulic pressure (group 1, 49 +/- 1 mm Hg; group 2, 48 +/- 1 mm Hg). Morphologic studies revealed that the increase in GFR in group 1 was associated with an increase in glomerular volume (group 1, 3.46 +/- 0.15 x 10(6) m3; group 2, 2.99 +/- 0.14 x 10(6) m3; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
