Gut microbial communication with immune cells and cells of target organs, pathways leading to obesity. Microbiota adipose tissue axis: metabolites of gut microbiota promote adipogenesis by triggering LPS based inflammation and SCF induced adipocyte differentiation. Gut-liver axis: microbiota dysbiosis alters the gut permeability enhancing the release of bacteria derived bioactive molecules in the liver. LPS interacts with TLR4 of the Kupffer cells enhancing the recruitment of MyD88 protein, IRAK, TRAF6, and NIK which promotes activation of MAPK, JNK, p38, and NF-κB signaling pathways leading to inflammation and insulin resistance ultimately causing nonalcohol fatty liver (NAFLD). Metabolites like bile acid, SCF, and choline play a vital role in causing NAFLD. Gut-brain axis: neuroactive peptides, lactate, SCF, and LPS of gut microbiota activate vagal afferent neurons and gut hormones leading to alteration in appetite and neuroinflammation.