Adverse Effects of Autoclaved Diets on the Progression of Chronic Kidney Disease and Chronic Kidney Disease-Mineral Bone Disorder in Rats.


Journal

American journal of nephrology
ISSN: 1421-9670
Titre abrégé: Am J Nephrol
Pays: Switzerland
ID NLM: 8109361

Informations de publication

Date de publication:
2020
Historique:
received: 06 12 2019
accepted: 20 02 2020
pubmed: 9 3 2020
medline: 27 5 2021
entrez: 9 3 2020
Statut: ppublish

Résumé

Autoclaving rodent diets is common in laboratory animals, but autoclaving increases the formation of dietary advanced glycation end-products (AGE). We studied the effect of autoclaved (AC) diet alone or in combination with a diet high in bioavailable phosphorus on biochemistries of chronic kidney disease-mineral and bone disorder (CKD-MBD), intestinal gene expression, and oxidative stress. Male CKD rats (Cy/+) and normal littermates were fed 1 of 3 diets: AC 0.7% phosphorus grain-based diet for 28 weeks (AC); AC diet for 17 weeks followed by non-autoclaved (Non-AC) 0.7% phosphorus casein diet until 28 weeks (AC + Casein); or Non-AC diet for 16 weeks followed by a Non-AC purified diet until 30 weeks (Non-AC + Casein). AC diets contained ~3× higher AGEs and levels varied depending on the location within the autoclave. Rats fed the AC and AC + Casein diets had higher total AGEs and oxidative stress, irrespective of kidney function. Kidney function was more severely compromised in CKD rats fed AC or AC + Casein compared to Non-AC + Casein. There was a disease-by-diet interaction for plasma phosphorus, parathyroid hormone, and c-terminal fibroblast growth factor-23, driven by high values in the CKD rats fed the AC + Casein diet. Compared to Non-AC + Casein, AC and AC + Casein-fed groups had increased expression of receptor of AGEs and intestinal NADPH oxidase dual oxidase-2, independent of kidney function. Autoclaving rodent diets impacts the progression of CKD and CKD-MBD, highlighting the critical importance of standardizing diets in experiments.

Sections du résumé

BACKGROUND
Autoclaving rodent diets is common in laboratory animals, but autoclaving increases the formation of dietary advanced glycation end-products (AGE). We studied the effect of autoclaved (AC) diet alone or in combination with a diet high in bioavailable phosphorus on biochemistries of chronic kidney disease-mineral and bone disorder (CKD-MBD), intestinal gene expression, and oxidative stress.
METHODS
Male CKD rats (Cy/+) and normal littermates were fed 1 of 3 diets: AC 0.7% phosphorus grain-based diet for 28 weeks (AC); AC diet for 17 weeks followed by non-autoclaved (Non-AC) 0.7% phosphorus casein diet until 28 weeks (AC + Casein); or Non-AC diet for 16 weeks followed by a Non-AC purified diet until 30 weeks (Non-AC + Casein).
RESULTS
AC diets contained ~3× higher AGEs and levels varied depending on the location within the autoclave. Rats fed the AC and AC + Casein diets had higher total AGEs and oxidative stress, irrespective of kidney function. Kidney function was more severely compromised in CKD rats fed AC or AC + Casein compared to Non-AC + Casein. There was a disease-by-diet interaction for plasma phosphorus, parathyroid hormone, and c-terminal fibroblast growth factor-23, driven by high values in the CKD rats fed the AC + Casein diet. Compared to Non-AC + Casein, AC and AC + Casein-fed groups had increased expression of receptor of AGEs and intestinal NADPH oxidase dual oxidase-2, independent of kidney function.
CONCLUSIONS
Autoclaving rodent diets impacts the progression of CKD and CKD-MBD, highlighting the critical importance of standardizing diets in experiments.

Identifiants

pubmed: 32146472
pii: 000506729
doi: 10.1159/000506729
pmc: PMC7228841
mid: NIHMS1573681
doi:

Substances chimiques

Glycation End Products, Advanced 0

Types de publication

Comparative Study Journal Article Research Support, N.I.H., Extramural Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

381-389

Subventions

Organisme : NIAMS NIH HHS
ID : P30 AR072581
Pays : United States
Organisme : NIDDK NIH HHS
ID : K01 DK102864
Pays : United States
Organisme : NIAMS NIH HHS
ID : T32 AR065971
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR002529
Pays : United States
Organisme : NIDDK NIH HHS
ID : T32 DK120524
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK110871
Pays : United States
Organisme : BLRD VA
ID : I01 BX001471
Pays : United States

Informations de copyright

© 2020 S. Karger AG, Basel.

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Auteurs

Annabel Biruete (A)

Division of Nephrology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Indiana, USA.

Shruthi Srinivasan (S)

Division of Nephrology, Indiana University School of Medicine, Indianapolis, Indiana, USA.

Kalisha D O'Neill (KD)

Division of Nephrology, Indiana University School of Medicine, Indianapolis, Indiana, USA.

Colby J Vorland (CJ)

Department of Applied Health Science, School of Public Health-Bloomington, Indiana University, Bloomington, Indiana, USA.
Department of Nutrition Science, Purdue University, West Lafayette, Indiana, USA.

Kathleen M Hill Gallant (KM)

Division of Nephrology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Department of Nutrition Science, Purdue University, West Lafayette, Indiana, USA.

Weijing Cai (W)

Division of Nephrology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.

Jaime Uribarri (J)

Division of Nephrology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.

Nancy Johnston (N)

Laboratory Animal Resource Center, Indiana University School of Medicine, Indianapolis, Indiana, USA.

Matthew R Allen (MR)

Division of Nephrology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Roudebush Veterans Affairs Medical Center, Indianapolis, Indiana, USA.

Neal X Chen (NX)

Division of Nephrology, Indiana University School of Medicine, Indianapolis, Indiana, USA.

Sharon M Moe (SM)

Division of Nephrology, Indiana University School of Medicine, Indianapolis, Indiana, USA, smoe@iu.edu.
Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Indiana, USA, smoe@iu.edu.
Roudebush Veterans Affairs Medical Center, Indianapolis, Indiana, USA, smoe@iu.edu.

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Classifications MeSH