Plasma Lipopolysaccharide Is Closely Associated With Glycemic Control and Abdominal Obesity

[ljimbo423]

Plasma Lipopolysaccharide Is Closely Associated With Glycemic Control and Abdominal Obesity
Evidence from bariatric surgery

CONCLUSIONS

Our findings support a hypothesis of translocated gut bacteria as a potential trigger of obesity and diabetes, and suggest that the antidiabetic effects of bariatric surgery might be mechanistically linked to, and even the result of, a reduction in plasma levels of LPS.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3816876/

 

[Hip]

This is actually an interesting study. I always like to see innovative investigations into the causes of obesity. The simplistic notion that obesity arises just from over-eating I've never found convincing.

In terms of how the LPS gets into the bloodstream, this study mentions the traditional idea that a leaky gut allows more LPS into the bloodstream. But it also suggests that LPS is being carried into the blood inside chylomicrons. Chylomicrons are tiny particles designed for transporting dietary fat in the intestines to other locations in the body. Here is the relevant quote from the study:

Two hypotheses have been proposed to explain the increased systemic LPS levels associated with obesity. First, LPS reaches the circulation because the gut is more permeable in obesity. A recent study showed that increased gut permeability is associated with mesenteric fat inflammation and metabolic dysfunction in obese mice. Second, LPS can be cotransported over the gut wall together with dietary fat by incorporation in triglyceride-rich chylomicrons.

The latter explanation fits well with the close correlation between fasting triglycerides and plasma LPS found in our study.

The paper also refers to another study which found that drinking orange juice with meals prevents the spike in LPS levels that normally occurs in the hours following a high-fat & high-carbohydrate meal (see figure 1).