Altering the makeup of bugs in the gut could be a way of tackling insulin resistance and related problems such as non alcoholic fatty liver disease, according to new research published this week.
The study also has implications for the treatment of associated conditions such as type 2 diabetes, obesity and heart disease.
The research shows that the type of microbes found in the guts of mice with a certain genetic makeup causes them to be pre-disposed to insulin resistance and non-alcoholic fatty liver disease (NAFLD). On a high fat diet, these microbes transform the nutrient choline, found in food and essential for metabolising fat, into methylamines.
Scientists believe that these methylamines, which can only be produced by the microbes in the gut, lead to insulin resistance. In addition, because choline is needed to transport fat out of the liver, altering choline metabolism leads to fat accumulating in the liver and NAFLD.
This is good news. Why? Bacteria can be defeated. Any time I read about how some disease is caused by chronic infection it makes me more optimistic. We can develop drugs and vaccines that'll stop pathogens. Better that chronic diseases of old age be caused by pathogens than by the body simply wearing out. The pathogens are easier to stop than the wearing out of cells.
Here is part of the abstract from the PNAS paper for this report. Bacteria reduce choline availability while also increasing exposure to harmful methylamines.
Multivariate statistical modeling of the spectra shows that the genetic predisposition of the 129S6 mouse to impaired glucose homeostasis and NAFLD is associated with disruptions of choline metabolism, i.e., low circulating levels of plasma phosphatidylcholine and high urinary excretion of methylamines (dimethylamine, trimethylamine, and trimethylamine-N-oxide), coprocessed by symbiotic gut microbiota and mammalian enzyme systems. Conversion of choline into methylamines by microbiota in strain 129S6 on a high-fat diet reduces the bioavailability of choline and mimics the effect of choline-deficient diets, causing NAFLD. These data also indicate that gut microbiota may play an active role in the development of insulin resistance.
The practical question: Can we use this information now? We need answers to some basic questions: Which human stomach bacteria convert choline to methylamines? Do they all do this? Are antibiotics or the consumption of competing bacteria the best way to shift the balance of bacteria in the stomach away from bacteria that convert choline to methylamine?
Anyone know the answers to these questions?
|Share |||Randall Parker, 2006 August 21 09:49 PM Biotech Pathogen Control|