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Edematous Severe Acute Malnutrition is Characterized by Hypomethylation of DNA

ABSTRACT: Edematous Severe Acute Malnutrition is Characterized by Hypomethylation of DNA

PROVIDER: PRJNA449392 | ENA |

REPOSITORIES: ENA

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Edematous Severe Acute Malnutrition is Characterized by Hypomethylation of DNA

Project description:A slower transmethylation of one-carbon substrates in the edematous form of severe acute malnutrition (ESAM) suggests that downstream aberrations in DNA methylation could drive differences in acute pathogenesis between ESAM and non-edematous malnutrition (NESAM). Here, we integrate genome-wide assessments of DNA methylation with corresponding gene expression profiles and sequence variation to show that relative to NESAM, acute ESAM is characterized by significant hypomethylation at 99% of differentially methylated loci in two SAM cohorts, whereas recovered adults show no significant differences in methylation. Hypomethylated loci correlate with both up- and down-regulation of proximal genes, which are associated with the clinical sub-phenotypes of kwashiorkor and enriched for GWAS hits linked to over-nutrition, including fatty liver and diabetes. Methylation at these loci also appears to be influenced by nearby genetic variation in a manner that varies with nutritional status. Our findings implicate epigenetic and genetic variation in ESAM pathophysiology and support methyl-group supplementation in ESAM management.

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Edematous severe acute malnutrition is characterized by hypomethylation of DNA.

Project description:Edematous severe acute childhood malnutrition (edematous SAM or ESAM), which includes kwashiorkor, presents with more overt multi-organ dysfunction than non-edematous SAM (NESAM). Reduced concentrations and methyl-flux of methionine in 1-carbon metabolism have been reported in acute, but not recovered, ESAM, suggesting downstream DNA methylation changes could be relevant to differences in SAM pathogenesis. Here, we assess genome-wide DNA methylation in buccal cells of 309 SAM children using the 450 K microarray. Relative to NESAM, ESAM is characterized by multiple significantly hypomethylated loci, which is not observed among SAM-recovered adults. Gene expression and methylation show both positive and negative correlation, suggesting a complex transcriptional response to SAM. Hypomethylated loci link to disorders of nutrition and metabolism, including fatty liver and diabetes, and appear to be influenced by genetic variation. Our epigenetic findings provide a potential molecular link to reported aberrant 1-carbon metabolism in ESAM and support consideration of methyl-group supplementation in ESAM.

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