Human gastrointestinal tract habitats trillions of microbes play a central role in physiology. These microbes evolved to establish a host-microbe interaction for beneficial outputs; however, a few also reported to cause harmful events [1]. It has been well established that gut Microbiota has a central role in infectious diseases, inflammation, neurological disorders, obesity, and associated metabolic syndromes. Extensive research over a period brought an understanding of how these microbes modulate the energy balance (energy harvest and storage) and the onset of obesity. Further, a few microbes profiled were associated with the initiation of low-level inflammation (induce Lipopolysaccharide (LPS) based inflammation) and various metabolic syndromes (T2D, CVD and obesity) [2]. These microbes were also indulged in the remodeling of Endocannabinoid (e-CB) system; however, the exact mechanism for Endocannabinoid (e-CB) signaling under the influence of gut microbes is not explored yet. Additionally, a few studies have suggested LPS-eCB is involved in altered energy balance and leads to obesity. The key problem in this context remains intact as how these microbes reprogram the gut barrier and result in metabolic endotoxemia [3]. Further, aberrant gut Microbiota and their metabolites mimic several other receptors such lipopolysaccharides (LPS), Toll-Like Receptor (TLR), nucleotide-binding oligomerization domain-like receptors (NOD) and NOD-like receptors (NLRs) over natural ligand and alter the fate of native signaling cascade [4].

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Citation

Citation: Mahendra Kumar Verma and Samba Naik A. “Gut Dysbiosis; An Altered Gut Microbial Ecology Major Risk Factor for Human Diseases". Acta Scientific Biotechnology 1.10 (2020): 01-02.

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Copyright: © 2020 Mahendra Kumar Verma and Samba Naik A. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.