Key result
Initial methyl donor deficit during pregnancy and lactation followed by a high fat diet produced cardiomyopathy linked to inflammation and fibrosis in female rat offspring.
Why the study?
Vitamin B12 and folate deficiency is frequent during pregnancy, and experimental rat models show maternal methyl donor deficiency impairs myocardium fatty acid oxidation and mitochondrial energy metabolism at weaning.
Does a high fat diet induce cardiomyopathy in adult rats subjected to methyl donor deficiency during pregnancy and lactation?
Does a high fat diet induce cardiomyopathy in adult rats subjected to methyl donor deficiency during pregnancy and lactation?
Maternal methyl donor deficiency combined with a postnatal high-fat diet programs the development of cardiomyopathy in female rat offspring via inflammation, fibrosis, and altered energy metabolism.
Early methyl donor deficit may heighten later cardiac susceptibility to high-fat diet; leaves open relevance for human maternal supplementation trials.
SCOPE: 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. METHODS AND RESULTS: 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. CONCLUSION: 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.
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Zhen et al. (2021) studied Cardiomyopathy. Initial methyl donor deficit (iMDD) and high fat diet vs. Normal diet / no iMDD was evaluated on Cardiomyopathy (histological fibrosis, BNP, inflammation markers). Initial methyl donor deficit during pregnancy and lactation followed by a high fat diet produced cardiomyopathy linked to inflammation and fibrosis in female rat offspring.
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