Raktim Mukherjee

Life science professional with a strong foundation in zoology and specialized expertise in cell biology and cytogenetics. Conducted impactful research on the relationship between diet and the gut microbiome, resulting in published findings. Currently engaged in postdoctoral studies focusing on immune cell proliferation and metabolic disease at leading research institutions. Aiming to gain experience in the industrial research and development sector.

Mukherjee, Raktim, RAMUKHERJEE, Postdoctoral Researcher, City College, University of Calcutta, Kolkata, West Bengal, BS, 07/14, Zoology, Maulana Azad College, University of Calcutta, Kolkata, West Bengal, MS, 08/16, Zoology, National Institute of Science Education and Research, Bhubaneswar, Odisha, PhD, 01/22, Life Sciences, University of California, San Diego, San Diego, CA, Postdoctoral Fellow, 07/24, Atherosclerosis research, University of Michigan, Ann Arbor, MI, Postdoctoral Fellow, present, Obesity research, I am a life science enthusiast, initially trained to be a Zoologist during my bachelors and masters. During my days of studying zoology, I gradually grew interest in cell biology, particularly immune cells. I specialized at cytogenetics during master's to further my interest and ended up doing my dissertation on how food additives can impact murine cells upon short term exposure. I published our findings on the cytotoxic roles of auramine with my mentor Dr. Sushanta Roy Karmakar and my co-workers. The project made me realize that the phrase 'we are what we eat' is not merely a statement. To build upon my research interest and strengthen my knowledge, I competed for various national level examinations in India, designed to test the early aptitude of science enthusiasts. I was fortunate to score top tier ranks in three such examinations which helped me to apply for a Doctoral fellowship. I joined Professor Palok Aich's lab at National Institute of Science Education and Research, India to understand a rather unconventional component of mammalian immunology. Professor Aich's lab specialized at understanding the role of the metagenome in mammalian immunology and implemented the knowledge to identify potential probiotics. Under Professor Aich's mentorship, I asked the questions a) Will the host immune background regulate how they metabolize different macro nutrients? And b) How will the differential nutrition impact the host metagenome? I identified that an immune reactive host background sustains gram negative microbial phyla and induces adipogenesis upon consumption of saturated fat rich diet. Afterwards I moved to the University of California, San Diego to understand the role of macrophage polarization on inducing atherosclerosis. Under the mentorship of Professor Pradipta Ghosh, I identified how cellular autonomy controls its nutritional requirements and controls their survival. To further focus on the impact of over nutrition on immune metabolism, I moved to Professor Carey Lumeng's lab at University of Michigan, Ann Arbor. I am currently studying the role of glucocorticoid signaling on adipose tissue and liver immune cell proliferation and abundance. I want to further identify the major immune cell type responsible for controlling metabolic changes upon nutritional surge. Following completion of my current postdoctoral training, I would want to apply for independent research faculty position in various universities. My research interest would be related to understanding the role of adipokines in regulating metabolic disease. The AHA grant will allow me to develop key skills necessary to achieve my career goal as an independent researcher and will provide necessary financial and network development support. It would allow me to generate publications from my current research which not only serves beneficial for patient care but also for the broad scientific community., Department of Atomic Energy Ph. D. fellowship, National Institute of Science Education and Research, 2017, 2022, National Eligibility Test, Council of Scientific and Industrial Research- University Grants Commission, 2017, National Eligibility Test, Indian Council of Medical Research, 2016, Identified the anti-adipogenic role of the probiotic Lactobacillus acidophilus (LA) and the probiotic cocktail (LDB-ST) of Lactobacillus delbruckei sp. bulgaricus (LDB) and Streptococcus thermophilus (ST): In this study, we evaluated the anti-adipogenic roles of two probiotic microbes in vitro. We used differentiated 3T3-L1 cells as a murine model for obesity. We treated these cells with either LA or LDB-ST and identified that both probiotics are effective in reducing adiposity, in vitro., Guha D, Mukherjee R, Aich P, Effects of two potential probiotic Lactobacillus bacteria on adipogenesis in vitro, Life Sci, 08/01/21, 278, 119538, 33932443, Identified the impact of macronutrients on host adiposity: Here I identified the role of starch or fat-rich diets in regulating host intestinal microbiota and adipose tissue metabolism. Diet is an important component of an organism's health. The energy derived from diet impacts the intestinal microbes and through it, leads to metabolic changes. Using immune biased C57BL/6 and BALB/c mice, we demonstrated how diets rich in either starch (SRD) or fat (unsaturated and saturated, USFD and SFD) can influence the adiposity, glycemia and meta-inflammation in comparison to untreated controls. Along with this, we have also evaluated the influence of intestinal microbes in the diet mediated physiological changes. We found that with time, SRD mostly enhances lipidemia while ameliorating glycemia and meta-inflammation. Such enhancement and reduction in the said parameters were associated with the abundance of microbes from the phylum Proteobacteria and Verrucomicrobia, respectively. While, USFD had mostly ameliorative effects, SFD augmented the adipogenic, glycemia and meta-inflammation related parameters. Such effects of SFD were linked with the enhanced levels of the phyla Firmicutes, Proteobacteria and Epsilonbacteraeota., Mukherjee R, Pandey S, Ghosh A, Aich P, Effects of starch-rich or fat-rich diets on metabolism, adiposity, and glycemia in immune-biased, C57BL/6 and BALB/c mice, J Nutr Biochem, 10/01/22, 108, 109086, 35691592, Mukherjee R, Aich P, The starch-rich diet causes lipidemia while the fat-rich diet induces visceral adiposity, meta-inflammation, and insulin resistance differentially in immune biased mouse strains, Food Bioscience, 08/01/21, 42, 101136, https://www.sciencedirect.com/science/article/pii/S2212429221002613, http10.1016/j.fbio.2021.101136, Identified the role of cellular autonomy on survival: Here we identified how a circuit of two GTPAses interact with each other to transmit survival signal. In absence of the linker molecule between the two GTPAses, the circuit assembly is broken, leading to loss of the cellular survival strategy in absence of external growth factors., Mukherjee R, Sinha S, Luker GD, Ghosh P, Interlinked switch circuits of biological intelligence, Trends Biochem Sci, 04/01/24, 49, 286-289, 38341333, Identified the roles of cortisol and serotonin in regulating adipogenesis and meta-inflammation, in vitro: In this project we differentiated 3T3-L1 cells (adipocytes) and co-cultured them with RAW264.7 cells (macrophages) and treated them with the stress hormones cortisol or serotonin either alone or together. We identified that the two hormones cumulatively enhance the adiposity levels in the differentiated 3T3-L1 cells and also induce inflammatory phenotype in the macrophage., Guha D, Mukherjee R, Aich P, Macrophage plays important role in cortisol and serotonin induced adipogenesis in vitro, In Vitro Cell Dev Biol Anim, 08/01/20, 56, 511-521, 32761288, Identifying the role of T cell glucocorticoid signaling in adiposity and liver steatosis: This is an ongoing project where we are trying to identify the role of T cell glucocorticoid signaling in inducing adiposity and liver steatosis. We found that dexamethasone treatment reduces body weight and epididymal adipose tissue weight with a reduction in CD4+, CD8+ and Regulatory T cells. Also, loss of T cell glucocorticoid signaling leads to enhanced liver steatosis with a reduction in naive CD8+ T cells, during long term high fat diet feeding., 2017, Bioinformatics and Computational Biology, BB, 2017, Enzymology, BB, 2017, Quantitative Biology, AA, 2017, Advanced Cell Biology, BB, 2017, Biotechniques, BC, 2017, Advanced Molecular Biology, CC, 7.83/10

• Recipient of CSIR-NET (2017)
• ICMR-NET (2016)
• GATE (2017)