Tandrika Chattopadhyay

Assoc Principal Res Scientist, CIMPS

Research Area:

  • Impact of Nutrition on Liver Physiology
  • Inflammation Biology of Liver
  • Disease Biology of Non-Alcoholic Fatty Liver Disease
  • Liver and Vitamin-D biology

Education & Training:

  • 2007: M.Sc., Department of Biochemistry, University of Delhi, Delhi, India.
  • 2013: PhD, National Institute of Immunology, Delhi, India.

Professional Experience:

  • 2013-15: Research Associate, National Institute of Immunology (NII), Delhi
  • 2015-19: Visiting Fellow, Tata Institute of Fundamental Research (TIFR), Mumbai
  • 2019-2022: Post-Doctoral Fellow, IISER, Pune
  • 2022 Onwards: Associate Principal Research Scientist, CIMPS, DRILS

Research Interests:

Maintenance of systemic homeostasis and response to nutritional and environmental challenges require the coordination of multiple organs and tissues. Multiple organ systems work together to absorb, store, sense and use chemical energy, and must communicate with one another to maximize the efficiency of these processes. Dysfunction of these systems results in metabolic syndrome/diseases, which is rapidly becoming one of the most pressing current public-health concerns. Metabolic syndrome is a group of conditions, including hyperglycemia, hypertension, abdominal obesity and dyslipidemia that increase the risk of cardiovascular disease, diabetes, cancer and associated morbidities.

Work over several decades suggest that liver acts as the main hub for the orchestration of cellular and physiological responses to various dietary and metabolic conditions. Liver dysfunction is often associated with metabolic pathologies such as obesity, non-alcoholic fatty liver disease (NAFLD), insulin resistance and diabetes mellitus, atherosclerosis and cardiovascular disease. Both acute and chronic liver dysfunction represents a major global health burden and an important cause of morbidity and lethality in India and worldwide, with widespread socio-economic consequences. Studies show that liver dysfunction is preceded by inflammation, and elements of both the innate and adaptive immune systems are pivotal in both initiating and regulating the disease progression. Our interest lies in investigating the mechanism of cross-talk between nutrition and chronic activation of tissue-associated immune cells and the cellular mechanisms that mediate the resolution of fibrosis and restoration of tissue homeostasis. Specifically, how liver metabolism rewires tissue resident macrophages, thereby contributing towards liver pathology is also of interest to us.

Many lines of evidence indicate that chronic over-nutrition causes metabolic abnormalities and predispose patients to non-alcoholic fatty liver disease (NAFLD), which put them at risk of developing cardiovascular diseases (CVD) and diabetes. However underlying reasons for the ensuing caloric imbalance remain poorly understood.

Thus the main focus of my research program is:

  1. Investigating nutrient/diet dependent regulation of cellular mechanisms (epigenetic, transcriptional and signaling) maintaining metabolic homeostasis with emphasis on liver physio/patho-physiology
  2. Bidirectional relationship between the heterogeneous cellular milieu regulating energy intake and utilization – Role of Immune Cell homeostasis
  3. Inter-organ communication via endocrine/secreted mediators.



  • Chattopadhyay T, Maniyadath B, Bagul HP, Chakraborty A, Shukla N, Budnar S, Rajendran A, Shukla A, S. Kamat S, Kolthur-Seetharam U. Spatiotemporal gating of SIRT1 functions by O-GlcNAcylation is essential for liver metabolic switching and prevents hyperglycemia. Proc Natl Acad Sci U S A. 2020 Mar 24;117(12):6890-6900. (Impact Factor – 11.2)
  • Maniyadath B*, Chattopadhyay T*, Verma S, Kumari S, Kulkarni P, Banerjee K, Lazarus A, Kokane SS, Shetty T, Anamika K, Kolthur-Seetharam U. Loss of Hepatic Oscillatory Fed microRNAs Abrogates Refed Transition and Causes Liver Dysfunctions. Cell Rep. 2019 Feb 19;26(8):2212-2226.e7. (*Equal contribution) (Impact Factor – 9.42)
  • Deota S*, Chattopadhyay T*, Ramachandran D, Armstrong E, Camacho B, Maniyadath B, Fulzele A, Gonzalez-de-Peredo A, Denu JM, Kolthur-Seetharam U. Identification of a tissue-restricted isoform of SIRT1 defines a regulatory domain that encodes specificity. Cell Rep. 2017 Mar 28;18(13):3069-3077. (*Equal contribution) (Impact Factor – 9.42)
  • Chattopadhyay T, Singh RR, Gupta S, Surolia A. Bone Morphogenetic Protein-7 (BMP-7) augments insulin sensitivity in mice with Type-II diabetes mellitus by potentiating PI3K/AKT pathway. Biofactors. 2017 Mar;43(2):195-209. (Impact Factor – 6.113)
  • Gupta S, Chattopadhyay T, Pal Singh M, Surolia A. Supramolecular insulin assembly II for a sustained treatment of type 1 diabetes mellitus. Proc Natl Acad Sci U S A. 2010 Jul 27;107(30):13246-51. (Impact Factor – 11.2)


Compositions useful for the treatment of diabetes and other chronic disorder” (WO/2009/125423)

  • Indian Patent Application no: 914/DEL/2008
  • Granted in US, Patent No: 8,426,362
  • Granted in Republic of South Africa, Patent No: 2009/02374
  • Granted by the European Patent Office.

Open Positions:
PhD, M.Sc. dissertation, Project Fellows

Interested candidates may send across their CV at: tandrikac@dril.org