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Insulin Resistance: Its Relationship to Certain Types of Gut Bacteria


Here’s another study on the effects of gut bacteria: done in 2008 and cited a number of times, but still not widely known.  This study treated genetically obese mice with type 2 diabetes as well as normal mice who had been overfed to induce insulin resistance with a combination of norfloxacin and ampicillin.  Afterwards, their glucose tolerance and metabolic functions improved significantly despite being fed the same diet.  Liver triglycerides dropped and liver glycogen increased.  Plasma lipids dropped, and plasma adiponectin was increased, a sign of decreased inflammation and improved insulin resistance.

This study refers to another study in humans that showed changes in the ratios of bacteria after weight loss through dietary intervention.  Specifically, the ratio to Firmicutes to Bacteroidetes was reduced.   The study also refers to another in which low-grade inflammation, induced by subcutaneous injection of low doses of bacterial wall lipopolysaccharides in mice, induced insulin resistance and excessive weight gain.

Yet a third study showed germ-free mice to maintain leanness whether fed normal chow or a high-fat diet; regular mice became obese on a high-fat diet.  The germ-free mice had the same caloric intake as the regular mice, suggesting that either the microbes contributed calories or that they induced low-grade inflammation which unbalanced the metabolism.

These studies, taken together, indicate a bidirectional relationship between low-grade inflammation and insulin resistance with weight gain, associated with specific types of bacteria resident in the gut.  The subcutaneous injections may be thought of as a simulation of the residence of large numbers of gram-negative bacteria in the gut.  Whether type 2 diabetes could be treated by antibiotics remains to be seen; it is more likely that low-calorie diets would be beneficial in changing the gut microbiome.

The 2008 study is on PDF at:

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