Ketogenic diet induces p53-dependent cellular senescence in multiple organs.
Sung-Jen WeiJoseph R SchellE Sandra ChocronMahboubeh VarmazyadGuogang XuWan Hsi ChenGloria M MartinezFelix F DongPrethish SreenivasRolando TrevinoHaiyan JiangYan DuAfaf SalibaWei QianBrandon LorenzanaAlia NazarullahJenny C ChangKumar SharmaErin MunkácsyNobuo HorikoshiDavid R GiusPublished in: Science advances (2024)
A ketogenic diet (KD) is a high-fat, low-carbohydrate diet that leads to the generation of ketones. While KDs improve certain health conditions and are popular for weight loss, detrimental effects have also been reported. Here, we show mice on two different KDs and, at different ages, induce cellular senescence in multiple organs, including the heart and kidney. This effect is mediated through adenosine monophosphate-activated protein kinase (AMPK) and inactivation of mouse double minute 2 (MDM2) by caspase-2, leading to p53 accumulation and p21 induction. This was established using p53 and caspase-2 knockout mice and inhibitors to AMPK, p21, and caspase-2. In addition, senescence-associated secretory phenotype biomarkers were elevated in serum from mice on a KD and in plasma samples from patients on a KD clinical trial. Cellular senescence was eliminated by a senolytic and prevented by an intermittent KD. These results have important clinical implications, suggesting that the effects of a KD are contextual and likely require individual optimization.
Keyphrases
- weight loss
- protein kinase
- dna damage
- endothelial cells
- cell death
- bariatric surgery
- clinical trial
- end stage renal disease
- stress induced
- physical activity
- induced apoptosis
- roux en y gastric bypass
- chronic kidney disease
- ejection fraction
- healthcare
- newly diagnosed
- high fat diet induced
- gastric bypass
- public health
- heart failure
- mental health
- peritoneal dialysis
- high intensity
- patient reported outcomes
- signaling pathway
- risk assessment
- weight gain
- health promotion
- climate change