Metabolic syndrome so far is attributed to the deregulation
of the metabolic processes leading to increase triglycerides, fat, insulin
resistance etc. and thereby leading to diabetes mellitus, coronary heart
disease and hypertension. Inflammation is also one of the key factors that can
cause an onset of metabolic syndrome.
Recently, a new article in Cell Research (a Nature
publication) puts a new perspective on the role of gut micro biota as a
causative effect in the process of inflammatory response in the liver (http://www.nature.com/cr/journal/vaop/ncurrent/full/cr201255a.html)
The article highlights certain interesting points and
hypothesizes that defective inflammasome signaling in the gastro-intestinal
tract allows colitogenic microbes to prosper in the colon, and subsequently
trigger harmful inflammatory signaling pathways in systemic organs when the
gastro-intestinal barrier is breached. The fact that defective inflammasome signalling
can skew the gut micro biota towards colitogenic species of the Prevotellaceae
family and the candidate phylum TM7 is not only interesting but opens a new
dimension on the role of intestinal “niche” environment in regulating the
microbiota species and thereby controlling different aspects of well being of
humans (though the research highlighted above is in mice).
Role of gut microbes in maintaining robust immune system or
even mental health have been reported earlier. In this era of genomics, it is
therefore imperative that we use metagenomics to study gut microflora to
understand the intestinal “niche” microenvironment. This would help in
designing better targeted antibiotics for therapeutical intervention and
thereby possible prevention of many of today’s lifestyle diseases!
