Research

Macro partitioning

Gut dysbiosis in obesity increases intestinal permeability, allowing lipopolysaccharide (LPS) to enter circulation, which triggers adipose tissue macrophages to switch from an anti-inflammatory (M2) to a pro-inflammatory (M1) phenotype via TLR4, thereby driving low-grade chronic inflammation.

If you have obesity, your gut health may be driving inflammation. A high-fat or high-sugar diet can damage your gut barrier, letting bacterial toxins (LPS) into your blood. This triggers immune cells in your fat tissue to become pro-inflammatory, worsening insulin resistance and fat storage. Improving gut health through fiber and reducing processed foods may help reduce this inflammation.

ModerateSupportsMEDIUM confidence
The obesity-associated decrease in the Bifidobacterium levels leads to the reduced production of GLP-2... eventually destroying the tight junction integrity of the epithelial barrier and enhancing the intestinal permeability... LPS enters circulation... Adipose tissue macrophages are response to LPS activation and transform to M1 phenotype.
Ji Wang et al. · Frontiers in Microbiology · 2020

Why this rating

This is a mini-review summarizing multiple studies; the evidence is indirect and mechanistic rather than a single clinical trial.

Source

The Relationship Between Gut Microbiota and Inflammatory Diseases: The Role of Macrophages

Ji Wang et al. · Frontiers in Microbiology · 2020

DOI 10.3389/fmicb.2020.01065

narrative_reviewCited 258×
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DOI resolved against Crossref · corpus check 2026-06-10

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