Gut Bug May Prevent Obesity And Type 2 Diabetes

Date: May-15-2013A Belgian-led study published in PNAS this week suggests Akkermansia muciniphila, an intestinal microbe that is
important for maintaining the gut lining and how food is absorbed, could be used to prevent obesity and associated metabolic disorders, such as
those that lead to type 2 diabetes.

Our digestive tract is home to a vast and varied population of microbes. In fact scientists have discovered that at 3.3 million, the genes of our gut flora vastly outnumber the 23,000 or so genes in the human
genome.

This complex microbial ecosystem plays an active role in many bodily functions. But while previous studies have shown that the gut flora of people
with obesity and type 2 diabetes are different to those of healthy, lean individuals, the mechanisms of interaction between these microbe
populations and their host environment is not well understood, note the researchers.

Along the whole of the digestive tract are specialized cells that secrete mucus, a substance that lubricates the passage of food and protects the
gut lining from digestive enzymes. This mucus barrier is also an efficient system for protecting the gut lining from harmful bacteria that cause
inflammation and infection.

The most dominant bacterium that lives in the nutrient-rich mucus layer of the mammalian gut is Akkermansia muciniphila. This microbe
normally accounts for 3-5% of gut bacteria.

But when Patrice D. Cani of the Catholic University of Louvain in Belgium, and colleagues examined gut levels of A. muciniphila in
different groups of lab mice, they found them to be low in obese and type 2 diabetic mice, and high in lean and healthy mice.

They also found that giving prebiotics to obese and type 2 diabetic mice boosted gut levels of A. muciniphila, and this was accompanied by
an improved gut mucus barrier, reversal of insulin resistance (a metabolic condition that increases risk for type 2 diabetes), and reduction of other
obesity-related metabolic disorders.

When they gave mice fed a high fat diet that made them put on two to three times more fat mass than normal, lean mice, and then treated them
with the bacterium, they found the treated mice stayed bigger than the lean mice but lost about half of their extra weight. They also had lower
levels of insulin resistance.

They also noticed that giving the obese mice A. muciniphila counteracted diet-induced decreases in the mucus layer of the gut, and increased
gut levels of endocannabinoids, which studies suggest are important molecules for controlling inflammation, insulin sensitivity, and fat and
energy metabolism.

However, these effects only occured with live A. muciniphila. Treatment with heat-killed bacterium neither replenished the mucus layer
nor improved the metabolic profile of the diet-induced obese mice.

Cani and colleagues conclude that their findings provide "substantial insight into the intricate mechanisms of bacterial (ie, A. muciniphila)
regulation of the cross-talk between the host and gut microbiota."

Cani has been studying the interaction between gut bacteria and metabolism for a decade. In an article on the study in Nature News, he suggests
the bacterium communicates with the cells of the host's intestinal lining and immune system.

A. muciniphila sends a signal that appears to alter production of anti-microbial molecules, while also increasing production of
mucus.

Perhaps the bacterium is establishing a mutually beneficial relationship with the host: in exchange for more food, it will deal with any
invading harmful microbes, he suggests.

The researchers suggest their findings offer a reasonable argument for using the bacterium to develop ways to prevent or treat obesity and its
associated metabolic disorders.

In 2012, another animal study published in the Journal of Proteome Research proposed that bacteria living in the large intestine may also play a role in obesity by slowing down
the activity of energy-burning brown fat.

Written by Catharine Paddock PhD

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