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Supriya Srinivasan, PhD

Professor - NE

Department of Neuroscience

Supriya Srinivasan, PhD

Research Focus

Dr. Srinivasan’s research program investigates the gut-brain axis as a fundamental organizer of metabolic physiology, with a particular emphasis on the neuroendocrine and enteroendocrine signaling systems through which the intestine and nervous system communicate to regulate energy homeostasis, feeding behavior, fat metabolism, and longevity. Her laboratory employs C. elegans as a genetically tractable model system to identify conserved molecular mechanisms underlying these processes, leveraging the organism’s well-defined neural circuitry and amenability to large-scale genetic and small-molecule screens. Central to this work is the question of how animals sense and integrate information about internal physiological state and translate these inputs into coordinated systemic responses via GPCRs, neuropeptides, and insulin-like signaling cascades. Her program has increasingly extended into mammalian intestinal biology, examining how enteroendocrine cell-derived signals govern lipid mobilization, mucosal immunity, and inflammation. Spanning invertebrate genetics and mammalian physiology, her research addresses fundamental questions with direct relevance to obesity, type 2 diabetes, inflammatory bowel disease, and the biology of healthy aging.

Looking ahead, the laboratory is pursuing several interconnected lines of inquiry at the interface of neuroscience, endocrinology, and aging biology. A primary focus is deepening the mechanistic understanding of how gut-derived signals act on the nervous system to modulate metabolic state across the lifespan, with the goal of identifying conserved molecular targets relevant to cardiometabolic disease and healthspan. In parallel, the program is expanding its investigation of mammalian intestinal signaling, exploring how enteroendocrine and immune crosstalk shapes systemic metabolic and inflammatory outcomes. A longer-term ambition is to integrate findings across model systems to build a unified framework for understanding how the gut-brain axis changes with age and how those changes contribute to the decline in metabolic resilience that characterizes aging.

Select Publications


  • Lee, B. H.; Liu, J.; Wong, D.; Srinivasan, Supriya; Ashrafi, K. Hyperactive neuroendocrine secretion causes size, feeding, and metabolic defects of c. Elegans bardet-biedl syndrome mutants. PLoS Biology 2011, 9, e1001219.

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  • Srinivasan, Supriya; Sadegh, L.; Elle, I. C.; Christensen, A. G.; Faergeman, N. J.; Ashrafi, K. Serotonin regulates c-elegans fat and feeding through independent molecular mechanisms. Cell Metabolism 2008, 7, 533-544.

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  • Conklin, B. R.; Hsiao, E. C.; Claeysen, S.; Dumuis, A.; Srinivasan, Supriya; Forsayeth, J. R.; Guettier, J. M.; Chang, W. C.; Pei, Y.; McCarthy, K. D.; Nissenson, R. A.; Wess, J.; Bockaert, J.; Roth, B. L. Engineering GPCR signaling pathways with RASSLs. Nature Methods 2008, 5, 673-678.

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  • Kok, B. P.; Galmozzi, A.; Littlejohn, N. K.; Albert, V.; Godio, C.; Kim, W.; Kim, S. M.; Bland, J. S.; Grayson, N.; Fang, M. L.; Meyerhof, W.; Siuzdak, Gary; Srinivasan, Supriya; Behrens, M.; Saez, Enrique Intestinal bitter taste receptor activation alters hormone secretion and imparts metabolic benefits. Molecular Metabolism 2018, 16, 76-87.

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  • Srinivasan, Supriya; Santiago, P.; Lubrano, C.; Vaisse, C.; Conklin, B. R. Engineering the melanocortin-4 receptor to control constitutive and ligand-mediated g(s) signaling in vivo. PLoS One 2007, 2, e668.

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  • Govaerts, C.; Srinivasan, Supriya; Shapiro, A.; Zhang, S. M.; Picard, F.; Clement, K.; Lubrano-Berthelier, C.; Vaisse, C. Obesity-associated mutations in the melanocortin 4 receptor provide novel insights into its function. Peptides 2005, 26, 1909-1919.

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  • Srinivasan, Supriya; Lubrano-Berthelier, C.; Govaerts, C.; Picard, F.; Santiago, P.; Conklin, B. R.; Vaisse, C. Constitutive activity of the melanocortin-4 receptor is maintained by its n-terminal domain and plays a role in energy homeostasis in humans. Journal of Clinical Investigation 2004, 114, 1158-1164.

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