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Kidney Week

Abstract: FR-OR008

Ketosis Inhibits and Reverses Renal Cyst Growth in Polycystic Kidney Disease

Session Information

Category: Genetic Diseases of the Kidneys

  • 1001 Genetic Diseases of the Kidneys: Cystic


  • Torres, Jacob A., University California Santa Barbara, Santa Barbara, California, United States
  • Kruger, Samantha L., University of California Santa Barbara, Santa Barbara, California, United States
  • Broderick, Caroline M., University of California, Santa Barbara, Goleta, California, United States
  • Amarlkhagva, Tselmeg, UCSB, Goleta, California, United States
  • Agrawal, Shagun, UCSB, Goleta, California, United States
  • Mrug, Michal, University of Alabama at Birmingham, Birmingham, Alabama, United States
  • Lyons, Leslie A., College of Veterinary Medicine, University of Missouri, Columbia, Missouri, United States
  • Weimbs, Thomas, University of California Santa Barbara, Santa Barbara, California, United States

PKD cells have been shown to exhibit an altered metabolism, favoring aerobic glycoysis. Our lab recently found that a mild reduction in food intake slowed progression of PKD in a mouse model of the disease. We hypothesized that the effects we observed in the PKD mouse model were not due to calorie restriction per se, but were instead due to the effects brought on by the state of ketosis.


To test if ketosis was capable of ameliorating PKD, we use the Han rat model of PKD or the Nestin-Cre Pkd1 mouse model. Animals were treated beginning at age week 3 to week 8 or from week 8 to week 12 with induction of ketosis utilizing several methods including, 1-time-restricted feeding, 2-ketogenic diet, 3-acute starvation and 4-beta-hydroxybutyrate supplementation. Both male and female animals were tested using these approaches of inducing ketosis.


Treatment using approaches that induce a state of ketosis produced profound effects in the animals tested, reducing or reversing the progression of PKD in treated animals. Interestingly, we found that supplementation with the ketone body, beta-hydroxybutyrate, was capable of eliciting the beneficial effects in a dominant way in the context of a normal rodent diet.


Our research shows that dietary interventions that induce a state of ketosis are capable of preventing PKD progression in a rodent model of PKD and that the small molecule beta-hydroxybutyrate underlies the effects observed by the diet. These findings have significant implications for the treatment of human ADPKD and may be readily transferrable to clinical practice.


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