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180 Early Life Exposure to Maternal Obesity Perturbs Renal Morphology in Mice
  1. Adele Pinnock1,
  2. Heather Blackmore1,
  3. Tom Ashmore2,
  4. Susan Ozanne1
  1. 1University of Cambridge
  2. 2University of Cambridge Metabolic


Introduction The incidence of Chronic Kidney Disease (CKD) has risen globally by 83% since 1990, concurrently with type 2 diabetes and metabolic syndrome. Studies of maternal under-nutrition during pregnancy have highlighted that the kidney can be adversely “programmed” resulting in fewer filtration units, a factor linked to the pathogenesis of CKD, hypertension and cardiovascular disease (CVD). Despite the dramatic increase in obesity in recent years, the effect of maternal over-nutrition/obesity during pregnancy on offspring kidney structure and function remains largely unexplored. The aim of the current study was to define the effects of maternal over-nutrition on offspring kidney structure using a mouse model of maternal diet-induced obesity.

Methods Female C57BL/6 mice were fed a high fat diet supplemented with sweetened condensed milk for six weeks prior to pregnancy and throughout gestation and lactation. This led to a doubling in maternal body fat. Male offspring were studied at 3 weeks of age. Kidneys were harvested, sectioned and stained with Haematoxylin and Eosin. Nephrons were counted in whole sections at even interspaces throughout the kidney to estimate the number of nephrons within a given area. Glomeruli diameters were also measured as an indicator of glomerular area.

Results There was no difference in absolute kidney weight between the 2 offspring groups (p = 0.95). Offspring exposed to a maternal obesogenic diet had significantly larger combined renal cortex and medulla areas than offspring exposed to a maternal chow diet (17.4 mm2 vs 12.5 mm2 respectively [p = 0.0136]). However, the number of nephrons/mm2 within the cortex and medulla was significantly reduced in offspring of obese pregnancies when compared to controls (2.2/mm2 vs. 3.5/mm2 respectively [p = 0.0047]). The mean glomerulus diameter was also significantly larger within offspring of obese pregnancies compared with offspring of control pregnancies (53.7 um vs. 46.3 um respectively [p < 0.0001]).

Conclusions These results suggest that there is compensatory individual glomerular hypertrophy due to a reduced glomeruli density in offspring exposed to maternal obesity during pregnancy and lactation, and that these individuals may therefore be more at risk of developing renal disease and associated CVD in later life. These findings highlight the importance of further studying the long-term consequences of these early morphological changes.

  • maternal obesity
  • programming
  • renal morphology

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