Dietary restriction in the long-chain acyl-CoA dehydrogenase knockout mouse.
Caloric restriction
Cardiac function
Dietary restriction
Fatty acid oxidation
Inborn error of metabolism
Mouse model
Journal
Molecular genetics and metabolism reports
ISSN: 2214-4269
Titre abrégé: Mol Genet Metab Rep
Pays: United States
ID NLM: 101624422
Informations de publication
Date de publication:
Jun 2021
Jun 2021
Historique:
received:
16
03
2021
accepted:
17
03
2021
entrez:
19
4
2021
pubmed:
20
4
2021
medline:
20
4
2021
Statut:
epublish
Résumé
Patients with a disorder of mitochondrial long-chain fatty acid β-oxidation (FAO) have reduced fasting tolerance and may present with hypoketotic hypoglycemia, hepatomegaly, (cardio)myopathy and rhabdomyolysis. Patients should avoid a catabolic state because it increases reliance on FAO as energy source. It is currently unclear whether weight loss through a reduction of caloric intake is safe in patients with a FAO disorder. We used the long-chain acyl-CoA dehydrogenase knockout (LCAD KO) mouse model to study the impact of dietary restriction (DR) on the plasma metabolite profile and cardiac function. For this, LCAD KO and wild type (WT) mice were subjected to DR (70% of ad libitum chow intake) for 4 weeks and compared to ad libitum chow fed mice. We found that DR had a relatively small impact on the plasma metabolite profile of WT and LCAD KO mice. Echocardiography revealed a small decrease in left ventricular systolic function of LCAD KO mice, which was most noticeable after DR, but there was no evidence of DR-induced cardiac remodeling. Our results suggest that weight loss through DR does not have acute and detrimental consequences in a mouse model for FAO disorders.
Identifiants
pubmed: 33868931
doi: 10.1016/j.ymgmr.2021.100749
pii: S2214-4269(21)00043-4
pmc: PMC8040332
doi:
Types de publication
Journal Article
Langues
eng
Pagination
100749Subventions
Organisme : NIDDK NIH HHS
ID : P30 DK020541
Pays : United States
Organisme : NIDDK NIH HHS
ID : P60 DK020541
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK113172
Pays : United States
Informations de copyright
© 2021 The Authors.
Déclaration de conflit d'intérêts
The authors declare that they have no conflict of interest.
Références
J Inherit Metab Dis. 2017 Nov;40(6):831-843
pubmed: 28871440
Lab Invest. 2009 Dec;89(12):1348-54
pubmed: 19736549
Rapid Commun Mass Spectrom. 2003;17(12):1297-311
pubmed: 12811753
Curr Protoc Mouse Biol. 2011 Mar 1;1:71-83
pubmed: 21743841
Annu Rev Physiol. 2016;78:23-44
pubmed: 26474213
Am J Physiol Regul Integr Comp Physiol. 2002 May;282(5):R1459-67
pubmed: 11959690
J Inherit Metab Dis. 1999 May;22(3):302-6
pubmed: 10384392
Lab Anim. 2013 Oct;47(4):225-40
pubmed: 24025567
Circ Cardiovasc Imaging. 2011 Sep;4(5):558-65
pubmed: 21737602
Mol Genet Metab. 2019 May;127(1):64-73
pubmed: 31031081
J Inherit Metab Dis. 2020 Sep;43(5):969-980
pubmed: 32463482
J Pediatr. 2006 May;148(5):665-670
pubmed: 16737882
J Chromatogr A. 2009 Dec 18;1216(51):8947-52
pubmed: 19913794
J Inherit Metab Dis. 2020 May;43(3):486-495
pubmed: 31845336
JIMD Rep. 2012;6:127-9
pubmed: 23430950
Hum Mol Genet. 2013 Dec 20;22(25):5249-61
pubmed: 23933733
Proc Natl Acad Sci U S A. 1998 Dec 22;95(26):15592-7
pubmed: 9861014
FASEB J. 2014 Jul;28(7):2891-900
pubmed: 24648546
J Inherit Metab Dis. 2019 May;42(3):414-423
pubmed: 30761551
Neurobiol Aging. 1999 Mar-Apr;20(2):157-65
pubmed: 10537025
Biochim Biophys Acta. 2009 Aug;1791(8):806-15
pubmed: 19465148
J Inherit Metab Dis. 2013 Nov;36(6):973-81
pubmed: 23563854
Cardiovasc Res. 2013 Dec 1;100(3):441-9
pubmed: 24042017
Clin Chem Lab Med. 2000 May;38(5):391-401
pubmed: 10952221
PLoS One. 2014 May 02;9(5):e96290
pubmed: 24789369
J Inherit Metab Dis. 2020 Jul;43(4):787-799
pubmed: 31955429