Skip to main content

Gut Bacteria Blamed For Heart Disease

It's hard to have our steak and eat it too. Red meat was once implicated in a wave of studies and linked to heart disease and other maladies, before being absolved.


But the microbiome and the surge in advertising for probiotics to promote 'healthy' gut bacteria has implicated red meat again - this time by correlating a nutrient that the authors say is changed by gut bacteria into an atherosclerosis-causing metabolite, which means hardening of the arteries.

Writing in Cell Metabolism, Dr. Stanley Hazen, of the Cleveland Clinic and colleagues implicated a bacteria in the gut that converts L-carnitine, a nutrient abundant in red meat, into a compound called trimethylamine, which in turn changes to a metabolite named trimethylamine-N-oxide (TMAO), which promotes atherosclerosis. Now they believe another metabolite, called gamma-butyrobetaine, is generated to an even greater extent by gut bacteria after L-carnitine is ingested, and it too contributes to atherosclerosis. 

The researchers found that gamma-butyrobetaine is produced as an intermediary metabolite by microbes at a rate that is 1,000-fold higher than the formation of trimethylamine in the gut, making it the most abundant metabolite generated from dietary L-carnitine by microbes in the mouse models examined. Moreover, gamma-butyrobetaine can itself be converted into trimethylamine and TMAO. Interestingly, however, the bacteria that produce gamma-butyrobetaine from L-carnitine are different from the bacterial species that produce trimethylamine from L-carnitine.

That's not causation but they believe it is important that metabolism of L-carnitine involves two different gut microbial pathways, as well as different types of bacteria, and to them this suggests new targets for preventing atherosclerosis—for example, by inhibiting various bacterial enzymes or shifting gut bacterial composition with probiotics and other treatments. 


Comments

Post a Comment

Popular posts from this blog

Fussy eaters: the favoured food of Salmonella

Image
As antibiotic resistance increases the search for new anti-bacterial treatments becomes more and more important. One way to design anti-bacterials is to find specific biochemical pathways that the bacteria require to survive, and develop drugs that block off these pathways. Some pathways are better targets than others and for  Salmonella bacteria it was thought that pathways dealing with nutrient metabolises would be a lost cause. Salmonella lives in the intestine, which hosts a whole variety of different nutrients, so surely preventing the bacteria from using a specific one wouldn’t cause them much undue distress. It’s been found, however, that as they grow and spread in the inflamed intestine the bacteria are heavily reliant on one particular nutrient: fructose-asparagine. The chemical structure of fructose-asparagine, image from the reference. The importance of fructose-asparagine metabolism was originally discovered durin...
Read more

Timing is key for bacteria surviving antibiotics

For bacteria facing a dose of antibiotics, timing might be the key to evading destruction. In a series of experiments, Princeton researchers found that cells that repaired DNA damaged by antibiotics before resuming growth had a much better chance of surviving treatment. When antibiotics hit a population of bacteria, often a small fraction of "persister" cells survive to pose a threat of recurrent infection. Unlike bacteria with genetic resistance to antibiotics, evidence suggests that persisters stay alive in part by stalling cellular processes targeted by the drugs. In a new study, Princeton researchers examined a class of antibiotics that target bacterial DNA. In bacterial populations, some cells repair damaged DNA before resuming growth, and others resume growth before making repairs. The researchers found that those that make repairs before resuming growth generally are the ones that survive as persisters. The research advances a long-term goal to make ...
Read more