Warning: fopen(/home/virtual/pediatrics/journal/upload/ip_log/ip_log_2024-05.txt) [function.fopen]: failed to open stream: Permission denied in /home/virtual/pediatrics/journal/ip_info/view_data.php on line 82

Warning: fwrite(): supplied argument is not a valid stream resource in /home/virtual/pediatrics/journal/ip_info/view_data.php on line 83
Gut microbiota’s impact on obesity

Volume 66(7); July

< Previous     Next >

Article Contents

Clin Exp Pediatr > Volume 66(7); 2023
Jeong: Gut microbiota’s impact on obesity


Previous studies reported that an imbalance of the gut microbiota with a relative increase in Firmicutes versus Bacteroidetes is associated with the pathogenesis of obesity [1]. A Firmicutes predominance can lead to increased production of metabolites from nondigestible polysaccharides, predisposing the host to enhanced energy extraction and augmenting weight gain [2]. This shift has also been associated with increased production of shortchain fatty acids (SCFA) and inflammation, both of which can contribute to the development of obesity and related metabolic disorders such as insulin resistance and type 2 diabetes. The role of SCFA in the onset of gut dysbiosis is described below.

Role of metabolites associated with gut dysbiosis

A growing body of evidence supports the concept that a disruption of the gut microbiota early in life can increase the likelihood of chronic diseases, including obesity. The first bacteria to colonize the intestinal tract at birth are obligate anoxic bacteria such as Bifidobacterium spp. and Bacteroides spp. Newborns born via cesarean section (CS) are initially exposed to bacteria in the external environment and skin microorganisms (e.g., Staphylococcus spp. and Corynebacterium spp.), whereas newborns born vaginally are exposed to the mother’s vaginal/fecal microflora. Therefore, newborns born vaginally have more diverse and numerous microorganisms, including Bifidobacterium spp., than newborns born by CS [3]. There is a strong association between CS and an increased body mass index (BMI) of the offspring and overweight and obesity in adulthood [4].
Cho et al. [5] reported that administering low doses of antibiotics to young mice increased adiposity and the levels of hormones involved in energy metabolism. Neonatal antibiotic exposure may be associated with these complications. Furthermore, dysbiosis is associated with microbial genes associated with SCFA production and increased colonic SCFA levels. The prominent SCFAs include acetate, propionate, and butyrate. Butyrate serves as an energy substrate for colonocytes, propionate contributes to hepatic gluconeogenesis, and acetate is utilized by the peripheral tissues [6]. SCFAs have also been shown to regulate appetite and satiety hormones, which can affect food intake and energy balance. However, the exact mechanisms by which SCFA contribute to obesity are not fully understood, and further research is required to elucidate their roles in this complex disease.
An altered gut microbiota can modulate gut permeability, resulting in lipopolysaccharide (LPS) translocation, which can initiate low-grade inflammation in the host [7]. LPS is a component of the cell walls of gram-negative bacteria, mainly including the phylum Proteobacteria and the genera Bacteroides and Prevotella. LPS plays an important role in the inflammatory process by activating the Toll-like receptor (TLR)-4, which is expressed by macrophages, neutrophils, and dendritic cells. Altered TLR-4 signaling leads to the activation of further downstream pathways, including nuclear factor-κB and proinflammatory cytokines such as interleukin (IL)-1, IL-6, IL-8, and tumor necrosis factor-α propagating the cascade of further inflammation and promoting insulin resistance. A dietary highfat intake is reportedly associated with increased plasma LPS [8]. Fig. 1 summarizes the prominent pathogenic factors related to the development of obesity and obesity-related disorders.

Impact of interventions on the gut microbiota

Pre- and probiotics also increase the microbial diversity within the gut, improve insulin sensitivity, and reduce LPS activation. Few pediatric studies have assessed the effects of probiotics on obesity and anthropometric indices. A 1-month intervention with synbiotics significantly decreased the weight and BMI of obese children and adolescents [9]. An 8-week intervention with Lactobacillus rhamnosus in obese children with the liver disease showed that L. rhamnosus GG altered the bacterial composition without any remarkable effect on the BMI z score or visceral fat. However, a 12-week intervention with Lactobacillus salivarius (Ls-33) had no significant influence on BMI z score, waist circumference, or body fat in adolescents [10]. The differences between studies could be due to variations in probiotic strains, supplement compositions, and doses, subjects’ characteristics, geographical variables, and interventional duration. In a recent meta-analysis evaluating 25 studies, 11 noted that prebiotics improved systemic inflammation in obesity. Although fecal microbiota transfer has shown promise in animal studies involving metabolic conditions, more clinical trials are required to determine its efficacy.

Future directions

The exact mechanisms of obesity are conflicting and have varied among different study models. The associations reported in human studies have not demonstrated causation. Future research on utilizing other omics technologies (metagenomics, transcriptomics, proteomics, and metabolomics) will aid the further characterization and exploration of the metabolic activity of the microbiota.


Conflicts of interest

No potential conflict of interest relevant to this article was reported.


This study received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

Fig. 1.
Dysbiosis of gut microbiota induced the inflammatory process and microbiome derived compounds implicated in the pathogenesis of obesity. LPS, lipopolysaccharide.


1. Cho KY. Association of gut microbiota with obesity in children and adolescents. Clin Exp Pediatr 2023;66:148–54.
crossref pmid pmc pdf
2. Ley RE, Turnbaugh PJ, Klein S, Gordon JI. Human gut microbes associated with obesity. Nature 2006;444:1022–3.
crossref pmid pdf
3. Biasucci G, Rubini M, Riboni S, Morelli L, Bessi E, Retetangos C. Mode of delivery affects the bacterial community in the newborn gut. Early Hum Dev 2010;86 Suppl 1:13–5.
crossref pmid
4. Cardwell CR, Stene LC, Joner G, Cinek O, Svensson J, Goldacre MJ, et al. Caesarean section is associated with an increased risk of childhood-onset type 1 diabetes mellitus: a meta-analysis of observational studies. Diabetologia 2008;51:726–35.
crossref pmid pdf
5. Cho I, Yamanishi S, Cox L, Methé BA, Zavadil J, Li K, et al. Antibiotics in early life alter the murine colonic microbiome and adiposity. Nature 2012;488:621–6.
crossref pmid pmc pdf
6. Coppola S, Avagliano C, Calignano A, Berni CR. The protective role of butyrate against obesity and obesity-related diseases. Molecules 2021;26:682.
crossref pmid pmc
7. Khan MJ, Gerasimidis K, Edwards CA, Shaikh MG. Role of gut microbiota in the aetiology of obesity: proposed mechanisms and review of the literature. J Obes 2016;2016:7353642. doi: 10.1155/2016/7353642. [Epub].
crossref pmid pmc pdf
8. Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, et al. Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes 2007;56:1761–72.
crossref pmid pdf
9. Ipar N, Aydogdu SD, Yildirim GK, Inal M, Gies I, Vandenplas Y, et al. Effects of synbiotic on anthropometry, lipid profile and oxidative stress in obese children. Benef Microbes 2015;6:775–82.
crossref pmid
10. Gøbel RJ, Larsen N, Jakobsen M, Mølgaard C, Michaelsen KF. Probiotics to adolescents with obesity: effects on inflammation and metabolic syndrome. J Pediatr Gastroenterol Nutr 2012;55:673–8.
crossref pmid
METRICS Graph View
  • 1 Web of Science
  • 1 Crossref
  •  0 Scopus
  • 1,840 View
  • 112 Download