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Perinatal Obesity Sensitizes for Premature Kidney Aging Signaling

Jaco Selle1, Katrin Bohl2,3, Katja Höpker2,4

  • 1Translational Experimental Pediatrics-Experimental Pulmonology, Department of Pediatric and Adolescent Medicine, University Hospital Cologne, 50931 Cologne, Germany.

International Journal of Molecular Sciences
|February 11, 2023
PubMed

Insights

Perinatal obesity, caused by maternal high-fat diet, triggers premature aging and DNA damage in newborn mouse kidneys. This early-life kidney aging may increase susceptibility to chronic kidney disease (CKD) later in life.

Area of Science:

  • Nephrology
  • Developmental Biology
  • Aging Research

Background:

  • Chronic Kidney Disease (CKD) is a global health issue linked to aging, hypertension, and diabetes, often exacerbated by obesity.
  • Perinatal metabolic disturbances, including maternal obesity, can negatively impact kidney development and lifelong function.
  • Understanding CKD susceptibility mechanisms, especially early-life influences, is crucial for public health.

Purpose of the Study:

  • To investigate if perinatal obesity sensitizes newborn mouse kidneys to aging-associated mechanisms.
  • To identify molecular pathways involved in kidney aging due to early-life high-fat diet exposure.
  • To explore the link between perinatal obesity, premature aging, and CKD susceptibility.

Main Methods:

  • Mice dams were fed a high-fat diet (HFD) during gestation to induce perinatal obesity.
  • Kidney tissues from newborn offspring were analyzed for DNA damage (γH2AX, 8-Oxo-dG) and oxidative stress markers.
  • Comprehensive transcriptomics identified differentially regulated pathways in perinatal obesity-exposed kidneys.
  • Comparative transcriptomic analysis was performed against naturally aged and prematurely aged mouse kidney data (Ercc1 hypomorph).
  • Biochemical assays validated inflammaging pathways.

Main Results:

  • Perinatal obesity led to increased DNA damage and oxidative stress in newborn mouse kidneys.
  • Transcriptomic analysis revealed compartment-specific signaling pathway alterations.
  • Kidney aging signatures in perinatal obesity models showed similarities to naturally and prematurely aged kidneys, including inflammatory signaling.
  • Biochemical validation confirmed the presence of inflammaging pathways.

Conclusions:

  • Perinatal obesity induces premature aging-associated processes in the developing kidney.
  • These early-life changes may represent a critical window for developing susceptibility to chronic kidney disease.
  • Findings highlight the long-term impact of maternal diet and obesity on offspring kidney health.

Keywords:
DNA damage responsechronic kidney diseasekidney agingperinatal obesity

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