Prof. Samir Bhattacharya
Prof Bhattacharya is known for his research in the area of Comparative endocrinology and molecular signalling. Currently, he is at Department of Zoology, Visva-Bharati (Central University) as an INSA Senior Scientist.

Obesity and type 2 diabetes are now recognised as global epidemic metabolic disorders. If we look at the base on which these metabolic disorders are depending upon, we could identify lipid, it is the lipid which accumulates to cause obesity, it is the lipid that affects insulin resistance and lipid begins its ravage by inducing inflammation. Centre stage of this obesity induced inflammation is occupied by adipose tissue; today we are aware that almost all crucial chronic diseases are inflammatory in nature. However, how lipid could affect adipose tissue inflammation is an interesting story. Adipocytes are the major cells in adipose tissue, there are other cells too, but these are the cells which could uptake lipid, store them and metabolize them. If there is a defect in adipocytes, it turns towards an inflammatory phenotype and secretes proinflammatory cytokines which then aggravates inflammation and cause insulin resistance. We know that TLR4 or TLR2 receptors are on the membrane of macrophage cells which serve as the prime member of innate immunity system. Interestingly, TLR4 receptors are localized on the membrane of adipocytes but for different function, it on the other hand, mediates inflammatory response. Question is how? This riddle has been fairly cleared by a current report from our laboratory. Previous findings implicated that fatty acid (FA) binds to TLR4 and triggers inflammatory signal. We showed that FA effect on adipocyte inflammation is not direct. Fet-A binds to FA and then present it to TLR4, this ternary complex activates NF-κB which then overexpresses TNFα, IL-6, IL-1β genes, these proinflammatory cytokines secreted from adipocytes cause insulin resistance.

Interestingly, lipid induced inflammation of adipose tissue attracts macrophage, they migrate towards adipose tissue and infiltrate into the tissue, lodge there and termed as adipose tissue macrophage (ATM). In the adipose tissue, macrophages are polarized from anti-inflammatory M2 subtype to proinflammatory M1 phenotype and vigorously release proinflammatory cytokines. Question is – Who drives them to adipose tissue and who converts them from M2 to M1 phenotype? All these remain unresolved. MCP1 or Monocyte chemoattractant protein 1, was thought to be acting as a chemoattractant, but recently reports showed thatMCP1 is only partially potent. One can imagine the peak inflammatory status when both adipocytes and macrophages are cohabitants and releasing inflammatory cytokines which inflicts crucial metabolic disorder. Regulatory mechanism behind the macrophage migration and polarization is yet unclear, primarily because of the lack of identification of signal(s) or factor(s), which appears to be originated from the adipose tissue ambience. We have recently discovered an endogenous signal which participates in this regulation; this will be discussed during my deliberation.