02112nas a2200229 4500000000100000008004100001100001300042700001900055700001300074700001800087700001500105700001900120700001500139700001500154700001800169700001500187245010400202300001300306490000700319520154200326022001401868 2017 d1 aWong Muh1 aGlastras Sarah1 aChen Hui1 aTsang Michael1 aTeh Rachel1 aMcGrath Rachel1 aZaky Amgad1 aChen Jason1 aPollock Carol1 aSaad Sonia00aThe renal consequences of maternal obesity in offspring are overwhelmed by postnatal high fat diet. ae01726440 v123 a

AIMS/HYPOTHESIS: Developmental programming induced by maternal obesity influences the development of chronic disease in offspring. In the present study, we aimed to determine whether maternal obesity exaggerates obesity-related kidney disease.

METHODS: Female C57BL/6 mice were fed high-fat diet (HFD) for six weeks prior to mating, during gestation and lactation. Male offspring were weaned to normal chow or HFD. At postnatal Week 8, HFD-fed offspring were administered one dose streptozotocin (STZ, 100 mg/kg i.p.) or vehicle control. Metabolic parameters and renal functional and structural changes were observed at postnatal Week 32.

RESULTS: HFD-fed offspring had increased adiposity, glucose intolerance and hyperlipidaemia, associated with increased albuminuria and serum creatinine levels. Their kidneys displayed structural changes with increased levels of fibrotic, inflammatory and oxidative stress markers. STZ administration did not potentiate the renal effects of HFD. Though maternal obesity had a sustained effect on serum creatinine and oxidative stress markers in lean offspring, the renal consequences of maternal obesity were overwhelmed by the powerful effect of diet-induced obesity.

CONCLUSION: Maternal obesity portends significant risks for metabolic and renal health in adult offspring. However, diet-induced obesity is an overwhelming and potent stimulus for the development of CKD that is not potentiated by maternal obesity.

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