Dataset Information

Greater alteration of gut microbiota occurs in childhood obesity than in adulthood obesity.

ABSTRACT: The children's gut microbiota, associated with the development of obesity, is in maturation. The impact of obesity on the gut microbiota in childhood could have a more significant effect than on adulthood and eventually be lifelong lasting, but it has been rarely studied. Aimed to discover the difference in gut microbiota between children and adults with obesity, we collected published amplicon sequencing data from National Center for Biotechnology Information (NCBI) and re-analyzed them using a uniform bioinformatic pipeline, as well as predicted the obesity using gut microbiota based on the random forest model. Summarizing common points among these cohorts, we found that the gut microbiota had a significant difference between children with and without obesity, but this difference was not observed in adult cohorts. Based on the random forest model, it was more challenging to predict childhood obesity using gut microbiota than adulthood obesity. Our results suggest that gut microbiota in childhood is more easily affected than in adulthood. Early intervention for childhood obesity is essential to improve children's health and lifelong gut microbiota-related health.

SUBMITTER: Yu Z

PROVIDER: S-EPMC9909466 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature

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Greater alteration of gut microbiota occurs in childhood obesity than in adulthood obesity.

Yu Zhongjia Z Yu Xiang-Fang XF Zhao Xiu X Su Zhe Z Ren Pei-Gen PG

Frontiers in pediatrics 20230126

The children's gut microbiota, associated with the development of obesity, is in maturation. The impact of obesity on the gut microbiota in childhood could have a more significant effect than on adulthood and eventually be lifelong lasting, but it has been rarely studied. Aimed to discover the difference in gut microbiota between children and adults with obesity, we collected published amplicon sequencing data from National Center for Biotechnology Information (NCBI) and re-analyzed them using a ...[more]

PMID: 36776907

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Project description:BackgroundObesity is a global epidemic in the industrialized and developing world, and many children suffer from obesity-related complications. Gut microbiota dysbiosis might have significant effect on the development of obesity. The microbiota continues to develop through childhood and thus childhood may be the prime time for microbiota interventions to realize health promotion or disease prevention. Therefore, it is crucial to understand the structure and function of pediatric gut microbiota.MethodsAccording to the inclusion criteria and exclusion criteria, twenty-three normal weight and twenty-eight obese children were recruited from Nanjing, China. Genomic DNA was extracted from fecal samples. The V4 region of the bacterial 16S rDNA was amplified by PCR, and sequencing was applied to analyze the gut microbiota diversity and composition using the Illumina HiSeq 2500 platform.ResultsThe number of operational taxonomic units (OTUs) showed a decrease in the diversity of gut microbiota with increasing body weight. The alpha diversity indices showed that the normal weight group had higher abundance and observed species than the obese group (Chao1: P < 0.001; observed species: P < 0.001; PD whole tree: P < 0.001; Shannon index: P = 0.008). Principal coordinate analysis (PCoA) and Nonmetric multidimensional scaling (NMDS) revealed significant differences in gut microbial community structure between the normal weight group and the obese group. The liner discriminant analysis (LDA) effect size (LEfSe) analysis showed that fifty-five species of bacteria were abundant in the fecal samples of the normal weight group and forty-five species of bacteria were abundant in the obese group. In regard to phyla, the gut microbiota in the obese group had lower proportions of Bacteroidetes (51.35%) compared to the normal weight group (55.48%) (P = 0.030). There was no statistical difference in Firmicutes between the two groups (P = 0.436), and the Firmicutes/Bacteroidetes between the two groups had no statistical difference (P = 0.983). At the genus level, Faecalibacterium, Phascolarctobacterium, Lachnospira, Megamonas, and Haemophilus were significantly more abundant in the obese group than in the normal weight group (P = 0.048, P = 0.018, P < 0.001, P = 0.040, and P = 0.003, respectively). The fecal microbiota of children in the obese group had lower proportions of Oscillospira and Dialister compared to the normal weight group (P = 0.002 and P = 0.002, respectively).ConclusionsOur results showed a decrease in gut microbiota abundance and diversity as the BMI increased. Variations in the bacterial community structure were associated with obesity. Gut microbiota dysbiosis might play a crucial part in the development of obesity in Chinese children.

Project description:ObjectiveEstrogen is a critical hormone that is mainly produced by the ovary in females. Estrogen deficiency leads to various syndromes and diseases, partly due to gut microbiota alterations. Previous studies have shown that estrogen deficiency affects the gut microbiota at 6-8 weeks after ovariectomy, but the immediate effect of estrogen deficiency on the gut microbiota remains poorly understood.MethodsTo investigate the short time and dynamic effects of decreased estrogen levels on the gut microbiota and their potential impact on estrogen deficiency-related diseases, we performed metagenomic sequencing of 260 fecal samples from 50 ovariectomy (OVX) and 15 control C57BL/6 female mice at four time points after surgery.ResultsWe found that seven gut microbiota species, including E. coli, Parabacteroides unclassified, Lachnospiraceae bacterium 8_1_57FAA, Bacteroides uniformis, Veillonella unclassified, Bacteroides xylanisolvens, and Firmicutes bacterium M10_2, were abundant in OVX mice. The abundance of these species increased with time after OVX surgery. The relative abundance of the opportunistic pathogen E. coli and the Crohn's disease-related Veillonella spp. was significantly correlated with mouse weight gain in the OVX group. Butyrate production and the Entner-Doudoroff pathway were significantly enriched in the control mouse group, while the degradation of glutamic acid and aspartic acid was enriched in the OVX mouse group. As the time after OVX surgery increased, the bacterial species and metabolic pathways significantly changed and tended to suggest an inflammatory environment, indicating a subhealthy state of the gut microbiota in the OVX mouse group.ConclusionsTaken together, our results show that the dynamic gut microbiota profile alteration caused by estrogen deficiency is related to obesity and inflammation, which may lead to immune and metabolic disorders. This study provides new clues for the treatment of estrogen deficiency-related diseases.

Project description:BackgroundAlthough the current obesity epidemic has been well documented in children and adults, less is known about long-term risks of adult obesity for a given child at his or her present age and weight. We developed a simulation model to estimate the risk of adult obesity at the age of 35 years for the current population of children in the United States.MethodsWe pooled height and weight data from five nationally representative longitudinal studies totaling 176,720 observations from 41,567 children and adults. We simulated growth trajectories across the life course and adjusted for secular trends. We created 1000 virtual populations of 1 million children through the age of 19 years that were representative of the 2016 population of the United States and projected their trajectories in height and weight up to the age of 35 years. Severe obesity was defined as a body-mass index (BMI, the weight in kilograms divided by the square of the height in meters) of 35 or higher in adults and 120% or more of the 95th percentile in children.ResultsGiven the current level of childhood obesity, the models predicted that a majority of today's children (57.3%; 95% uncertainly interval [UI], 55.2 to 60.0) will be obese at the age of 35 years, and roughly half of the projected prevalence will occur during childhood. Our simulations indicated that the relative risk of adult obesity increased with age and BMI, from 1.17 (95% UI, 1.09 to 1.29) for overweight 2-year-olds to 3.10 (95% UI, 2.43 to 3.65) for 19-year-olds with severe obesity. For children with severe obesity, the chance they will no longer be obese at the age of 35 years fell from 21.0% (95% UI, 7.3 to 47.3) at the age of 2 years to 6.1% (95% UI, 2.1 to 9.9) at the age of 19 years.ConclusionsOn the basis of our simulation models, childhood obesity and overweight will continue to be a major health problem in the United States. Early development of obesity predicted obesity in adulthood, especially for children who were severely obese. (Funded by the JPB Foundation and others.).

Dataset Information

Greater alteration of gut microbiota occurs in childhood obesity than in adulthood obesity.

Publications

Greater alteration of gut microbiota occurs in childhood obesity than in adulthood obesity.

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