创作:szx 审核:szx 2019年10月27日
  • 限时性进食(不降低卡路里的摄入量)可在多囊性肾病(PKD)大鼠模型中促进生酮作用,并导致血糖的间歇性降低;
  • 限时性进食可显著抑制PKD大鼠囊性肾脏中的mTOR信号通路、增殖及纤维化;
  • 生酮饮食与限时性进食有着类似的作用,可减少肾脏囊性负荷;
  • 急性禁食可引起囊肿衬里上皮细胞的凋亡,以迅速降低大鼠、小鼠及猫科动物的PKD模型的囊性肾脏体积;
  • 口服β-羟基丁酸(酮体)可显著抑制PKD大鼠模型的疾病进展。
少量减少食物摄入在小鼠中可延缓多囊性肾病的进展,但其作用机制尚未明确。Cell Metabolism上发表的一项最新研究,发现饮食干预可通过促进生酮作用,在多囊性肾病动物模型中抑制疾病进展。
Cell Metabolism [IF:21.567]

Ketosis Ameliorates Renal Cyst Growth in Polycystic Kidney Disease



2019-10-17, Editorial Material

Abstract & Authors:展开

Mild reduction in food intake was recently shown to slow polycystic kidney disease (PKD) progression in mouse models, but whether the effect was due to solely reduced calories or some other aspect of the diet has been unclear. We now show that the benefit is due to the induction of ketosis. Time-restricted feeding, without caloric reduction, strongly inhibits mTOR signaling, proliferation, and fibrosis in the affected kidneys in a PKD rat model. A ketogenic diet had a similar effect and led to regression of renal cystic burden. Acute fasting in rat, mouse, and feline models of PKD results in rapid reduction of cyst volume, while oral administration of the ketone β-hydroxybutyrate (BHB) in rats strongly inhibits PKD progression. These results suggest that cystic cells in PKD are metabolically inflexible, which could be exploited by dietary interventions or supplementation with BHB, representing a new therapeutic avenue to treat PKD.

First Authors:
Jacob A Torres

Correspondence Authors:
Thomas Weimbs

All Authors:
Jacob A Torres,Samantha L Kruger,Caroline Broderick,Tselmeg Amarlkhagva,Shagun Agrawal,John R Dodam,Michal Mrug,Leslie A Lyons,Thomas Weimbs