Role of macrophages in regulating stress hormone induced adipogenesis Raktim Mukherjee*, Dipanjan Guha*,# & Palok Aich* *School of Biological Sciences, National Institute of Science Education and Research (NISER), HBNI, P.O. Bhimpur-Padanpur, Dist. Khurda, Jatni, Odisha 752050, India #Present address: S.N. Bose Innovation Centre, University of Kalyani, Kalyani, West Bengal, India Unrestrained body fat accumulation can result in various metabolic disorders such as Obesity, Type-II diabetes and cardiovascular diseases. Various factors can contribute to the development of metabolic disorders such as unhealthy feeding habit, sedentary life style and psychological stress. Among these, chronic psychological stress has become a salient feature of present-day lifestyle which often acts as a pioneer for metabolic diseases. The effects of stress induced metabolic abnormalities are mainly regulated by primordial stress hormones, which not only augments lipid storage but also attracts several innate immune cells at the site of lipid deposition. This results in chronic mild inflammation, also known as metainflammation. In the present work, we investigated how stress hormones can regulate lipid build-up in murine adipocytes and whether macrophage induced inflammation can augment the process. For this, we treated terminally differentiated murine adipocyte cell line 3T3-L1 with two potent stress hormones, cortisol and serotonin. We found that the said hormones alone and together, gradually augmented lipid storage in differentiated 3T3-L1 cells. The quantity of lipid storage was further enhanced when the cortisol and serotonin treated, differentiated 3T3-L1 cells were co-cultured with murine macrophage RAW264.7 cells. Further, the macrophage cells became gradually pro-inflammatory following this co-culturing from an initial anti-inflammatory phenotype. Our results confirm that stress hormones can potentiate adipogenesis which can be further enhanced by the proximity of immunologically polarized macrophages in murine model. This finding can direct towards using immune modulation as an intervention of metabolic disorders potentiated by chronic stress, following further pre-clinical and clinical studies.
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