The non pungent analogue of capsaicin i.e. evodiamine also boosted energy consumption and prevented weight gain in HFD fed mice and obese humans via multiple mechanisms. Recently, it has been shown that capsaicin and its non-pungent analog, capsiate can activate BAT via either TRPV1 activation or sympathetic/adrenergic stimulation. TRPV1 neurons co-express with SP, CGRP and are modulated by NGF, NPY and BDNF. Given that these peptides have significant roles to play in weight gain and energy expenditure, one cannot rule out the potential effects of their interactions with TRPV1. Approaches to augment “brite” cell population in WAT are gaining significant importance. It has been reported that various KO strains that resist body weight gain on HFD have higher number of “brite” cells. Advances have been made to understand and study pharmacological and nutritional/ dietary agents as well as the signalling pathways that can contribute to browning of WAT. Some pharmacological agents that can promote browning are sympathetic activators like BDNF and leptin, prostaglandins like PGE2 and PGI2, cardiac natriuretic peptides and neuropeptides, PPAR modulators, some hormones like irisin and FGF-2. These agents act through different mechanisms. Numerous nutritional and dietary factors have been linked with browning including dietary methionine/leucine restriction, maternal under-nutrition and high fat/Dinaciclib CDK inhibitor calorie diet-induced sympathetic inputs to adipose tissue, dietary chemicals such as fucoxanthin, olive oil constituents, conjugated linoleic acid, PUFA from marine sources, resveratrol, capsaicin and its analogue as well as others. The exact mechanism of action of capsaicin is controversial i.e. whether TRPV1 agonism, TRPV1 or capsaicin sensitive neuron desensitization/blockade or browning of WAT or any other mechanism independent of TRPV1/direct action is responsible for its effect. A better understanding of the role of capsaicin, TRPV1 and their interplay is warranted. Herein, we investigated in detail the anti-adipogenic effect of capsaicin and the modulatory role of TRPV1 receptors in adipogenesis using in vitro and in vivo model systems. Looking at the rather in-conclusive pattern of expression of proadipogenic genes, we looked at anti-adipogenic genes as well, which have shown quite consistent results. Thirteen anti-adipogenic genes were identified and most showed decreased expression during adipogenesis while only two genes, ADRB2 and LRP5, showed higher expression. These genes function via multiple pathways whose enhanced expression upon capsaicin treatment resulted in inhibition of adipogenesis. Due to changes in the gene expression of PPARc, we hypothesized that capsaicin may play a role in developing “brite” cells or brown phenotype within white adipocytes. Therefore, we investigated the effect of capsaicin on “browning” specific genes by targeting brown-specific genes responsible for formation of proteins that show their activity right from the cell membrane to the nucleus.