Food Restriction Ameliorates the Development of Polycystic Kidney Disease

Autosomal dominant polycystic kidney disease (ADPKD) is a genetic disorder characterized by the accumulation of kidney cysts that ultimately leads to loss of renal function and kidney failure. At present, the treatment for ADPKD is largely supportive. Multiple studies have focused on pharmacologic a...

Full description

Saved in:
Bibliographic Details
Published in:Journal of the American Society of Nephrology Vol. 27; no. 5; pp. 1437 - 1447
Main Authors: Warner, Gina, Hein, Kyaw Zaw, Nin, Veronica, Edwards, Marika, Chini, Claudia C S, Hopp, Katharina, Harris, Peter C, Torres, Vicente E, Chini, Eduardo N
Format: Journal Article
Language:English
Published: United States American Society of Nephrology 01-05-2016
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Autosomal dominant polycystic kidney disease (ADPKD) is a genetic disorder characterized by the accumulation of kidney cysts that ultimately leads to loss of renal function and kidney failure. At present, the treatment for ADPKD is largely supportive. Multiple studies have focused on pharmacologic approaches to slow the development of the cystic disease; however, little is known about the role of nutrition and dietary manipulation in PKD. Here, we show that food restriction (FR) effectively slows the course of the disease in mouse models of ADPKD. Mild to moderate (10%-40%) FR reduced cyst area, renal fibrosis, inflammation, and injury in a dose-dependent manner. Molecular and biochemical studies in these mice indicate that FR ameliorates ADPKD through a mechanism involving suppression of the mammalian target of the rapamycin pathway and activation of the liver kinase B1/AMP-activated protein kinase pathway. Our data suggest that dietary interventions such as FR, or treatment that mimics the effects of such interventions, may be potential and novel preventive and therapeutic options for patients with ADPKD.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
G.W. and K.Z.H. contributed equally to this work.
ISSN:1046-6673
1533-3450
DOI:10.1681/asn.2015020132