Treatment of hyperlipidemia reduces glomerular injury in @entity28 Zucker XXXX .

@entity28 @entity34021 @entity628 @entity633 @entity5753 @entity412 @entity35 @entity165
@entity28 Zucker @entity35 develop @entity633 and spontaneous @entity628 ( @entity628 ) at an early age, despite normal glomerular capillary pressures and nephron plasma flows. To investigate the role of abnormal lipid metabolism in the pathogenesis of @entity628 , pharmacologic agents were used to reduce serum lipids in male, @entity28 Zucker @entity35 . Eight @entity35 were treated from 8 to 40 weeks of age with the @entity165 synthesis inhibitor, @entity5753 (group I). A separate group of seven @entity28 @entity35 was treated with the structurally-unrelated lipid lowering agent, @entity34021 (group II). Results from these two groups were compared to controls injected with vehicle only (group III). Body weight and food intake were similar in all three groups. @entity5753 reduced both serum @entity165 and fasting @entity412 levels while @entity34021 lowered only serum @entity165 . Urine albumin excretion was reduced in groups I and II compared to group III. Mesangial matrix expansion and cellularity were both reduced by @entity5753 and @entity34021 . In addition, the percent of glomeruli with @entity628 was much less in groups I (0.4 +/- 0.1%) and II (1.3 +/- 0.7%) compared to group III (4.6 +/- 0.7%, P less than 0.05). Micropuncture studies, carried out in separate groups of @entity28 @entity35 , demonstrated that @entity5753 and @entity34021 did not affect glomerular hemodynamic function. Although the precise mechanism remains to be defined, these results suggest that abnormal lipid metabolism may be important in the pathogenesis of @entity628 .
