Author Correction: The gut microbiota in infants of obese mothers increases inflammation and susceptibility to NAFLD

Soderborg, Taylor K.; Clark, Sarah E.; Mulligan, Christopher E.; Janssen, Rachel C.; Babcock, Lyndsey; Ir, Diana; Young, Bridget E.; Krebs, Nancy F.; Lemas, Dominick J.; Johnson, Linda K.; Weir, Tiffany L.; Lenz, Laurel; Frank, Daniel N.; Hernandez, Teri L.; Kuhn, Kristine A.; D’Alessandro, Angelo; Barbour, Linda A.; Kasmi, Karim C. El; Friedman, Jacob E.

doi:10.1038/s41467-019-10943-1

Cited by 4 publications

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“…Soderborg et al colonized germ-free mice with stool derived from 2-week-old infants born to either obese or normal weight mothers (human). 99 100 They showed that the microbiome of infants born to mothers with obesity led to liver reminiscent of steatohepatitis, with increased expression of hepatic genes involved in endoplasmic reticulum stress and innate immunity activation. Importantly, when these offspring were exposed to a Western-style diet, they had increased adiposity and accelerated development of hepatic steatosis and injury.…”

Section: Early Life Risk Factors Of Pediatric Masldmentioning

confidence: 99%

Gestational and Developmental Contributors of Pediatric MASLD

Mouzaki,

Woo,

Divanovic

2024

Semin Liver Dis

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Pediatric metabolic dysfunction-associated steatotic liver disease (MASLD) is common and can be seen as early as in utero. A growing body of literature suggests that gestational and early life exposures modify the risk of MASLD development in children. These include maternal risk factors, such as poor cardiometabolic health (e.g., obesity, gestational diabetes, rapid weight gain during pregnancy, and MASLD), as well as periconceptional dietary exposures, degree of physical activity, intestinal microbiome, and smoking. Paternal factors, such as diet and obesity, also appear to play a role. Beyond gestation, early life dietary exposures, as well as the rate of infant weight gain, may further modify the risk of future MASLD development. The mechanisms linking parental health and environmental exposures to pediatric MASLD are complex and not entirely understood. In conclusion, investigating gestational and developmental contributors to MASLD is critical and may identify future interventional targets for disease prevention.

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Section: Early Life Risk Factors Of Pediatric Masldmentioning

confidence: 99%

Gestational and Developmental Contributors of Pediatric MASLD

Mouzaki,

Woo,

Divanovic

2024

Semin Liver Dis

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“…studies, emerging translational data have provided initial insights into the pathogenesis of this condition (12)(13)(14)(15). Despite such key advances in the field, the natural history of the liver disease detected in utero and during the neonatal life is not defined.…”

Section: Translation Impactmentioning

confidence: 99%

“…Similar results were shown in a smaller study by Brumbaugh et al (11). Beyond these observational studies, emerging translational data have provided initial insights into the pathogenesis of this condition (12–15).…”

Section: Introductionmentioning

confidence: 99%

Hepatic Steatosis in Infancy: The Beginning of Pediatric Nonalcoholic Fatty Liver Disease?

et al. 2021

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Objectives: Nonalcoholic fatty liver disease is clinically silent and the age of its onset is unknown. Fatty liver can occur as early as in utero in the context of an unfavorable maternal metabolic environment. Our objective was to determine the prevalence of hepatic steatosis in a cohort of previously healthy infants less than 3 months of age. Methods: Retrospective study of all abdominal computed tomography (CT) scans performed from 2009 to 2019 for the investigation of trauma. Two independent reviewers applied published criteria to determine the presence of hepatic steatosis. Descriptive statistics were used. The groups with and without steatosis were compared using Wilcoxon-Mann Whitney or Fisher exact test. Results: Of 119 CT scans available in infants younger than 3 months of age, 65 were performed in previously healthy infants for the investigation of trauma. The included population was predominantly male, non-Hispanic, with a median age of 60 days (interquartile range, 34-73 d). Depending on the criteria used, 23% or 26% of infants had evidence of fatty liver. The prevalence of maternal obesity and/or diabetes was 11% (of the 65 pregnancies) but there was no significant difference in maternal risk factors between infants with and without evidence of steatosis. Conclusions: Findings suggest CT evidence of hepatic steatosis in up to a quarter of otherwise healthy infants ≤3 months of age. This may represent early manifestation of pediatric nonalcoholic fatty liver disease. The natural history and pathophysiology of this condition need to be studied to determine optimal detection, prevention and early intervention strategies.

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Fecal Bacterial Communities Differ by Lactation Status in Postpartum Women and Their Infants

et al. 2021

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Background: Previous research examined effects of human milk on the infant gut microbiota, but little attention has been given to the microbiota of lactating women. Research Aim: To determine associations between exclusive human milk feeding and gut microbiota characteristics in mothers and infants at 6-weeks postpartum. Methods: A sample of mother–infant dyads ( N = 24) provided fecal samples and questionnaire responses at 6-weeks postpartum as part of the Pregnancy, EAting & POstpartum Diapers study. Deoxyribonucleic acid was extracted from stool samples, followed by (V4) 16S ribosomal ribonucleic acid gene amplicon sequencing. Alpha and beta diversity, in addition to taxa differences, were compared by human milk exposure status, exclusive versus non-exclusive. A subset of dyads (those exclusively fed human milk; n = 14) was analyzed for shared bifidobacterial species using polymerase chain reaction. Results: Alpha diversity was significantly lower in exclusively human milk-fed infants. Maternal lactation status (exclusive vs. partial) and Shannon diversity were associated in univariate analysis but were no longer associated in multivariable regression including body mass index category in the model. Beta diversity (Sorensen dissimilarity) of fecal samples from women and infants was significantly associated with human milk feeding. Of six infants with Bifidobacterium longum subspecies longum in their fecal samples, all their mothers shared the same species. Conclusion: Maternal gut microbiotas differ by lactation status, a relationship potentially confounded by body mass index category. Further research is needed to identify whether lactation directly influences the maternal gut microbiota, which may be another mechanism by which lactation influences health.

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Author Correction: The gut microbiota in infants of obese mothers increases inflammation and susceptibility to NAFLD

Abstract: In addition, the following was added to the Author contributions: 'B.Y. and N.F.K. helped to design the clinical study and participated in the sample collection during the infant visits.' This has been corrected in both the PDF and HTML versions of the Article.

Cited by 4 publications

References 0 publications

Gestational and Developmental Contributors of Pediatric MASLD

Gestational and Developmental Contributors of Pediatric MASLD

Hepatic Steatosis in Infancy: The Beginning of Pediatric Nonalcoholic Fatty Liver Disease?

Fecal Bacterial Communities Differ by Lactation Status in Postpartum Women and Their Infants

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