Partha Chakrabarti

Dr. Partha Chakrabarti

Senior Scientist

* PhD, Boston University School of Medicine, USA, 2009
* MD Biochemistry, Banaras Hindu University, India, 2005
* MBBS, Calcutta Medical College, University of Calcutta, India, 2000

    • MOLECULAR METABOLISM, the concept of it has had a makeover from what we used to perceive some time ago. As biological sciences continue to expand the horizons of its knowledge domains, it is becoming manifest that metabolism is at the centre of all the cellular processes both in physiology and in pathophysiology. At the Metabolic Diseases Laboratory we put effort in understanding the molecular basis of human disorders through the scope of metabolism. To this end we work with genes, proteins, cells, mice and human patients.
      Currently we are working on several broad aspects in the plethora of Metabolic Disorders –

      We have identified ubiquitin-proteasome system as novel regulator of hepatic fat turnover. We showed that ubiquitin ligase COP1 promotes NAFLD by targeting adipose triglyceride lipase (ATGL) for proteasomal degradation. In liver, ATGL serves as a major triacylglycerol lipase and controls bulk of intracellular lipid turnover. COP1 thus controls hepatocyte fat content, fatty acid mobilization and oxidation, the metabolic outcomes that require ATGL. Depleting COP1 gene in mice with NAFLD significantly reduced disease burden.

    • Mitochondrial metabolism: Crosstalk between nutrients and muscle aging

    Burn more fat to make your muscles younger: Our study show implications that in age associated muscle frailty, the PPARa-ATGL axis could partially maintain the muscle mitochondrial metabolism (which otherwise declines with age).

    • Metabolic reprogramming in cancer

    Latest research from MDL has shown that cancer cells in order to sustain high proliferative rates inhibit glucose production particularly of tissues were the gluconeogenic program is active like liver and kidney tissues.

    • Pathophysiology of Indian type 2 diabetes (T2DM)

      We took multi pronged approaches in investigating T2DM in Indian patients with an emphasis on incretin pathway. Intestinal mucosa produces certain factors named incretin peptides such as glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) which have the capacity to reduce blood glucose level by directly acting on the pancreatic beta cells. We have found that the negative regulator of incretin peptides, dipeptidyl peptidase-4 (DPP4) plays a critical role in the pathogenesis of T2DM in Indian patients.

    1. Adak A, Das D, Niyogi S, Challa N, Ray D, Chakrabarti P. Inflammasome activation in Kupffer cells confers a protective response in nonalcoholic steatohepatitis through pigment epithelium–derived factor expression. (2018) FASEB J. (Accepted)
    2. Palit S, Mukherjee S, Niyogi S, Banerjee A, Patra D, Chakraborty A, Chakrabarti S, Chakrabarti P*, Dutta S*. Quinoline-glycomimetic conjugates reducing lipogenesis and lipid accumulation in hepatocytes. (2018) ChemBiochem (Accepted)
    3. Khan MW, Layden BT, Chakrabarti P. Inhibition of mTOR complexes protects cancer cells from glutamine starvation induced cell death by restoring Akt stability. Biochim Biophys Acta. 2018 Mar 17;1864(6 Pt A):2040-2052. doi: 10.1016/j.bbadis.2018.03.013.
    4. Nargis T, Chakrabarti P. Significance of circulatory DPP4 activity in metabolic diseases. IUBMB Life. 2018 Feb;70(2):112-119. doi: 10.1002/iub.1709. Epub 2018 Jan 13. Review.
    5. Nargis T, Kumar K, Ghosh AR, Sharma A, Rudra D, Sen D, Chakrabarti S, Mukhopadhyay S, Ganguly D, Chakrabarti P. KLK5 induces shedding of DPP4 from circulatory Th17 cells in type 2 diabetes. Mol Metab. 2017 Nov;6(11):1529-1539. doi: 10.1016/j.molmet.2017.09.004. Epub 2017 Sep 27.
    6. Basu M, Sengupta I, Khan MW, Srivastava DK, Chakrabarti P, Roy S, Das C. Dual histone reader ZMYND8 inhibits cancer cell invasion by positively regulating epithelial genes. Biochem J. 2017 May 19;474(11):1919-1934. doi: 10.1042/BCJ20170223.
    7. Basu M, Khan MW, Chakrabarti P, Das C. Chromatin reader ZMYND8 is a key target of all trans retinoic acid-mediated inhibition of cancer cell proliferation. Biochim Biophys Acta. 2017 Apr;1860(4):450-459. doi: 10.1016/j.bbagrm.2017.02.004. Epub 2017 Feb 14.
    8. Ghosh M, Niyogi S, Bhattacharyya M, Adak M, Nayak DK, Chakrabarti S, Chakrabarti P. Ubiquitin Ligase COP1 Controls Hepatic Fat Metabolism by Targeting ATGL for Degradation. (2016) Diabetes. Sep 22. pii: db160506. [Epub ahead of print]

    9. Ghosh AR, Bhattacharya R, Bhattacharya S, Nargis T, Rahaman O, Duttagupta P, Raychaudhuri D, Chen Liu CS, Roy S, Ghosh P, Khanna S, Chaudhuri T, Tantia O, Haak S, Bandyopadhyay S, Mukhopadhyay S, Chakrabarti P, Ganguly D. Adipose Recruitment and Activation of Plasmacytoid Dendritic Cells Fuel Metaflammation. (2016) Diabetes. Aug 25. doi: db160331. [Epub ahead of print].

    10. D Biswas, M Ghosh, S Kumar, P Chakrabarti PPARα-ATGL pathway improves muscle mitochondrial metabolism: implication in aging. (2016) FASEB J. 30(11):3822-3834.

    11. Khan MD, Biswas D, Ghosh M, Mandloi S, Chakrabarti S, Chakrabarti P. mTORC2 controls cancer cell survival by modulating gluconeogenesis. (2015) Nature: Cell Death Discovery; 1:15016. doi:10.1038/cddiscovery.2015.16

    12. Khan MD, Chakrabarti P. Gluconeogenesis combats cancer: opening new doors in cancer biology. Nature: Cell Death and Disease. 2015; 6, e1872; doi:10.1038/cddis.2015.245

    1. Partha Chakrabarti, Taylor English, Shakun Karki, Li Qiang, Rong Tao, Juyoun Kim, Zhijun Luo, Stephen R. Farmer and Konstantin V. Kandror. SIRT1 controls lipolysis in adipocytes via FoxO1-mwdiated expression of ATGL. (2011) J Lipid Res, Jul (Epub ahead of print).

    2. Partha Chakrabarti, Taylor English, Jun Shi, Synthia M. Smas and Konstantin V. Kandror. Mammalian target of rapamycin complex 1 suppresses lipolysis, stimulates lipogenesis and promotes fat storage. (2010)Diabetes,59: 775-781.

    3. Partha Chakrabarti and Konstantin V. Kandror. FoxO1 controls insulin-dependent ATGL expression and lipolysis in adipocytes. (2009) J. Biol. Chem. 284, 13296-13300. (Featured in Nature Lipodomics gateway

    4. Partha Chakrabarti, Takatoshi Anno, Brendan Manning, Zhijun Luo and Konstantin V. Kandror. The mammalian target of rapamycin complex 1 regulates leptin biosynthesis in adipocytes at the level of translation: the role of the 5′-untranslated region in the expression of leptin messenger ribonucleic acid. (2008) Mol. Endocrinol. 22: 2260-2267.

    5. Ramkrishna Gupta, Partha Chakrabarti, Madhu Dikshit and Debabrata Dash. Late signaling in the activated platelets upregulates tyrosine phosphatase SHP1 and impairs platelet adhesive functions: Regulation by calcium and Src kinase. (2007) Biochim. Biophys. Acta,1773: 131-140.

    6. Partha Chakrabarti, Bimal K. Panda and Debabrata Dash. Detection of Gγ(Aγδβ)0 thalassemia in North India. (2006) Clin Chim Acta, 364: 363-364.

    7. Partha Chakrabarti, Ramkrishna Gupta, Asutosh Misra, Madhukar Rai, Vijay Pratap Singh and Debabrata Dash. Spectrum of b-thalassemia mutations in North-Indian states: a b-thalassemia trait with two mutations in cis. (2005) Clin Biochem, 38: 576-578.

    8. Partha Chakrabarti, Zubair Ahmed Karim, Ramkrishna Gupta, Vinita Vadhawan, Saikat Mukhopadhyay and Debabrata Dash. Biochemical characterization of Glanzmann’s Thrombasthenia, a rare genetic disorder affecting platelet function. (2004) Ind J Med Biochem, 8:56-60.

    1. Partha Chakrabarti and K.V. Kandror. The role of mTOR in lipid homeostasis and diabetes progression. Curr Opin Endocrinol Diabetes Obes 2015, 22:000–000 DOI:10.1097/MED.0000000000000187

    2. Partha Chakrabarti* and Konstantin V. Kandror. Adipose Triglyceride Lipase: A New Target in the Regulation of Lipolysis by Insulin. (2011) Current Diabetes Review, 7: 270-277

    3. Partha Chakrabarti*. Promoting adipose specificity: the adiponectin promoter. (2010) Endocrinology, 151: 2408-2410 (Invited News and Views review)