Iqbal · Journal of bacteriology 2025 · narrative review · n=?

Unraveling the gut microbiota's role in obesity: key metabolites, microbial species, and therapeutic insights.

Cited 45 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Narrative review summarizing mechanisms without systematic methodology or primary human trial data.

PubMed 40183584 · doi:10.1128/jb.00479-24 · record verified 2026-08-27

What was done

This narrative review synthesized literature examining the mechanisms by which gut microbiota, specific bacterial taxa, and microbial metabolites (such as lipopolysaccharides and short-chain fatty acids) influence metabolic pathways, inflammation, gut barrier integrity, and adipose tissue regulation in obesity.

What was found

The abstract reports no quantitative numbers or effect sizes. It describes qualitative associations where species such as *Clostridium* XIVb, *Dorea* spp., *Enterobacter cloacae*, and *Collinsella aerofaciens* promote obesity phenotypes via increased energy harvest, elevated gut permeability, and systemic lipopolysaccharide translocation. Conversely, *Akkermansia muciniphila*, *Lactobacillus* spp., and *Bifidobacterium* spp. correlate with improved metabolic health by strengthening barrier integrity, producing short-chain fatty acids (SCFAs), and modulating fasting-induced adipose factor. Additionally, SCFAs (acetate, propionate, butyrate) signal through G-protein coupled receptors to stimulate white adipose tissue browning and thermogenesis, whereas lipopolysaccharides exacerbate insulin resistance and fat storage.

Why it matters

The paper summarizes actionable microbial targets and metabolic pathways—specifically short-chain fatty acid signaling and adipose tissue browning—relevant to developing microbiota-targeted obesity therapies.

Limits

As a narrative review, the paper provides no original empirical data, quantitative meta-analyses, or study count metrics. Most described mechanistic pathways derive from non-human or preclinical models, and high inter-individual microbiome heterogeneity limits generalizability to clinical populations.

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