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.
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.
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
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