Programming by Methyl Donor Deficiency during Pregnancy and Lactation Produces Cardiomyopathy in Adult Rats Subjected to High Fat Diet.
Animals
Cardiomyopathies
/ chemically induced
Diet, High-Fat
/ adverse effects
Energy Metabolism
Female
Fetal Development
Folic Acid
Folic Acid Deficiency
Lactation
Lipid Metabolism
Male
Maternal Nutritional Physiological Phenomena
Myocardium
/ pathology
Pregnancy
Rats
Rats, Wistar
Receptor, Angiotensin, Type 2
Transforming Growth Factor beta1
Ventricular Function, Left
Vitamin B 12
Vitamin B 12 Deficiency
fetal programing
folate
myocardiopathy
one carbon metabolism
vitamin B12
Journal
Molecular nutrition & food research
ISSN: 1613-4133
Titre abrégé: Mol Nutr Food Res
Pays: Germany
ID NLM: 101231818
Informations de publication
Date de publication:
07 2021
07 2021
Historique:
revised:
12
04
2021
received:
21
01
2021
pubmed:
16
5
2021
medline:
29
12
2021
entrez:
15
5
2021
Statut:
ppublish
Résumé
Vitamin B12 and folate (methyl donors) deficiency is frequent during pregnancy. Experimental rat models with methyl donor deficit during pregnancy and lactation (Initial methyl donor deficit (iMDD)) produce impaired myocardium fatty acid oxidation and mitochondrial energy metabolism at weaning. The consequences of iMDD on heart of rat pups under normal diet after weaning and high fat diet (HF) between day (D) 50 and D185 are investigated. iMDD/HF induces increased histological fibrosis and increased B-type natriuretic peptide blood level. Inflammation is evidenced by increased protein expression of NFkB, Caspase1, and IL1β and fibrosis by increased expression of αSMA, col1a1, and col1a2 in females, but not in males. Fibrosis is related to increased angiotensin at D50 and D185 and increased protein expression of TGFB1 and AT1 angiotensin receptors at D185. The limited fibrosis in males is consistent with increased expression of AT2, the antagonist receptor of AT1. The increased expression of GLUT4 and decreased expression of PGC1α and PPARα reflect a shift from fatty acid oxidation to glycolysis. Developmental programming by iMDD produces cardiomyopathy in female offspring exposed to HF. The cardiomyopathy is linked to inflammation and fibrosis through angiotensin-AT2 and TGFB1 pathways and alteration of energy metabolism.
Identifiants
pubmed: 33991387
doi: 10.1002/mnfr.202100065
doi:
Substances chimiques
Receptor, Angiotensin, Type 2
0
Tgfb1 protein, rat
0
Transforming Growth Factor beta1
0
Folic Acid
935E97BOY8
Vitamin B 12
P6YC3EG204
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e2100065Informations de copyright
© 2021 Wiley-VCH GmbH.
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