Abstract

BackgroundThe term “metabolically healthy obese (MHO)” denotes a hale and salutary status, yet this connotation has not been validated in children, and may, in fact, be a misnomer. As pertains to obesity, the gut microbiota has garnered attention as conceivably a nosogenic or, on the other hand, protective participator.ObjectiveThis study explored the characteristics of the fecal microbiota of obese Chinese children and adolescents of disparate metabolic statuses, and the associations between their gut microbiota and circulating proinflammatory factors, such as IL-6, TNF-α, lipopolysaccharide-binding protein (LBP), and a cytokine up-regulator and mediator, leptin.ResultsBased on weight and metabolic status, the 86 Chinese children (ages 5–15 years) were divided into three groups: metabolically healthy obese (MHO, n = 42), metabolic unhealthy obese (MUO, n = 23), and healthy normal weight controls (Con, n = 21). In the MUO subjects, the phylum Tenericutes, as well as the alpha and beta diversity, were significantly reduced compared with the controls. Furthermore, Phylum Synergistetes and genus Bacteroides were more prevalent in the MHO population compared with controls. For the MHO group, Spearman’s correlation analysis revealed that serum IL-6 positively correlated with genus Paraprevotella, LBP was positively correlated with genus Roseburia and Faecalibacterium, and negatively correlated with genus Lactobacillus, and leptin correlated positively with genus Phascolarctobacterium and negatively with genus Dialister (all p < 0.05).ConclusionAlthough there are distinct differences in the characteristic gut microbiota of the MUO population versus MHO, dysbiosis of gut microsystem is already extant in the MHO cohort. The abundance of some metabolism-related bacteria associates with the degree of circulating inflammatory compounds, suggesting that dysbiosis of gut microbiota, present in the MHO children, conceivably serves as a compensatory or remedial response to a surfeit of nutrients.

Highlights

  • The global epidemic of childhood obesity, and the accompanying rise in the prevalence of endocrine, metabolic, and cardiovascular comorbidities, is perhaps the most impactful and ubiquitous public health disorder of the modern world [1]

  • An altered gut microbiota has been implicated in obesity and type 2 diabetes mellitus (T2DM) insofar as a decrement in certain species and gene richness have been linked to adiposity, dyslipidemia, and insulin resistance [7]

  • Weight, BMI, BMI-Z, waist-to-height ratio (WHtR), SBP, TG and low density lipoprotein cholesterol (LDL-c) in the MUO group were significantly higher than the Con and metabolically healthy obese” (MHO) children, and high-density lipoprotein cholesterol (HDL-c) in the in the MUO group were significantly lower than the Con and MHO children

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Summary

Introduction

The global epidemic of childhood obesity, and the accompanying rise in the prevalence of endocrine, metabolic, and cardiovascular comorbidities, is perhaps the most impactful and ubiquitous public health disorder of the modern world [1]. The distinctive gut microbiota prevalent in obese subjects is recognized as promoting an unhealthy metabolic obese (MUO) phenotype with attendant comorbidities, such as increased endotoxemia, intestinal and systemic inflammation, as well as insulin resistance. The clinical repercussions aside, it is plausible that differences in the gut microbiota could dictate whether an obese child is metabolically fit (MHO) or not (MUO) [8, 9]. The gut microbiota has garnered attention as conceivably a nosogenic or, on the other hand, protective participator

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