Parental obesity predisposes offspring to kidney dysfunction and increased susceptibility to ischemia/reperfusion injury in a sex-dependent manner

We examined the impact of parental obesity on offspring kidney function, morphology, and markers of kidney damage after acute kidney injury (AKI). Offspring from normal (N) diet-fed C57BL/6J parents were fed either N (NN) or a high fat (H) diet (NH) from weaning until adulthood. Offspring from obese H diet-fed parents were fed N (HN) or H diet (HH) after weaning. All offspring groups were submitted to bilateral AKI by clamping the left and right renal pedicles for 30 min. Compared to male NH and NN offspring from lean parents, male HH and HN offspring from obese parents exhibited higher kidney injury markers such as urinary, renal osteopontin, plasma creatinine, urinary albumin excretion, and NGAL levels, and worse histological injury score at 22 weeks of age. Only albumin excretion and NGAL were elevated in female HH offspring from obese parents compared to lean and obese offspring from lean parents. We also found an increased mortality rate and worse kidney injury scores after AKI in male offspring from obese parents, regardless of the diet consumed after weaning. Female offspring were protected from major kidney injury after AKI. These results indicate that parental obesity leads to increased kidney injury in their offspring after ischemia/reperfusion in a sex-dependent manner, even when their offspring remain lean.PMID:38511219 | DOI:10.1152/ajprenal.00294.2023
Source: American Journal of Physiology. Renal Physiology - Category: Physiology Authors: Source Type: research