Photo of Rupangi Vasavada

Rupangi Vasavada

  • ASSOCIATE PROFESSOR Medicine, Endocrinology, Diabetes and Bone Disease
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    Diabetes, a major metabolic disease, affects ~10% of the US population, with an expected growth rate of 20-33% by 2050, according to the CDC, causing one of the highest life expectancy and economic tolls to the health system. All forms of diabetes ultimately result from the loss of functional pancreatic beta cells that produce insulin. It is now known that even patients with long-term diabetes retain residual beta cells with the potential to proliferate and regenerate. Therefore, enhancing a patient’s own functional beta cell mass, through improved function, survival and/or proliferation of existing beta cells, or through the formation of new beta cells from precursor cells, represent potential future therapeutic approaches for the treatment of diabetes.

    My lab has been interested in understanding the pathways and mechanisms that regulate beta cell growth, survival and function, with the ultimate objective being to enhance regeneration of functional beta cells in vivo. We have focused on the role of specific growth factors, parathyroid hormone-related protein (PTHrP), lactogens, and more recently, osteporotegerin (OPG), in normal beta cell physiology. We use transgenic overexpression as well as conditional knockout mouse models to determine the in vivo effects of these growth factors and their downstream signaling and molecular pathways on beta cell proliferation, survival and function.

    The ultimate objective of our research is to find ways to enhance preservation and regeneration of functional beta cells in vivo, for the treatment of diabetes. There are several approaches we have taken towards this therapeutic goal. 1) To test the effects of acute and systemic administration of molecules in rodent models of depleted beta cell mass and in the pathophysiological settings of type 1 and type 2 diabetes. 2) To assess the effects of these molecules on human beta cells in vitro, and in vivo, in rodent models of islet transplantation. 3) More recently, we have focused attention on discovering ways to quantify human beta cell proliferation in collaboration with Dr. Garcia-Ocana. The currently used methods can label dividing cells but have not convincingly demonstrated an increase in beta cell numbers. As the ultimate goal in the treatment of diabetes is to increase human beta cell mass, we are developing a novel labeling tool to address this problem.

    This work is currently funded by the NIH/NIDDK, and the Juvenile Diabetes Research Foundation.


Cebrian A, García-Ocaña A, Takane KK, Sipula D, Stewart AF, Vasavada RC. Overexpression of parathyroid hormone-related protein inhibits pancreatic beta-cell death in vivo and in vitro. Diabetes 2002 Oct; 51(10).

Fujinaka Y, Sipula D, Garcia-Ocaña A, Vasavada RC. Characterization of mice doubly transgenic for parathyroid hormone-related protein and murine placental lactogen: a novel role for placental lactogen in pancreatic beta-cell survival. Diabetes 2004 Dec; 53(12).

Vasavada RC, Garcia-Ocaña A, Zawalich WS, Sorenson RL, Dann P, Syed M, Ogren L, Talamantes F, Stewart AF. Targeted expression of placental lactogen in the beta cells of transgenic mice results in beta cell proliferation, islet mass augmentation, and hypoglycemia. The Journal of biological chemistry 2000 May; 275(20).

Vasavada RC, Cozar-Castellano I, Sipula D, Stewart AF. Tissue-specific deletion of the retinoblastoma protein in the pancreatic beta-cell has limited effects on beta-cell replication, mass, and function. Diabetes 2007 Jan; 56(1).

Fujinaka Y, Takane K, Yamashita H, Vasavada RC. Lactogens promote beta cell survival through JAK2/STAT5 activation and Bcl-XL upregulation. The Journal of biological chemistry 2007 Oct; 282(42).

Vasavada RC, Gonzalez-Pertusa JA, Fujinaka Y, Fiaschi-Taesch N, Cozar-Castellano I, Garcia-Ocaña A. Growth factors and beta cell replication. The international journal of biochemistry & cell biology 2006; 38(5-6).

Vasavada RC, Wang L, Fujinaka Y, Takane KK, Rosa TC, Mellado-Gil JM, Friedman PA, Garcia-Ocaña A. Protein kinase C-zeta activation markedly enhances beta-cell proliferation: an essential role in growth factor mediated beta-cell mitogenesis. Diabetes 2007 Nov; 56(11).

Harb G, Vasavada RC, Cobrinik D, Stewart AF. The retinoblastoma protein and its homolog p130 regulate the G1/S transition in pancreatic beta-cells. Diabetes 2009 Aug; 58(8).

Cozar-Castellano I, Harb G, Selk K, Takane K, Vasavada R, Sicari B, Law B, Zhang P, Scott DK, Fiaschi-Taesch N, Stewart AF. Lessons from the first comprehensive molecular characterization of cell cycle control in rodent insulinoma cell lines. Diabetes 2008 Nov; 57(11).

Zhang H, Zhang J, Pope CF, Crawford LA, Vasavada RC, Jagasia SM, Gannon M. Gestational diabetes mellitus resulting from impaired beta-cell compensation in the absence of FoxM1, a novel downstream effector of placental lactogen. Diabetes 2010 Jan; 59(1).

Vasavada RC, Wang L, Fujinaka Y, Takane KK, Rosa TC, Mellado-Gil JM, Friedman PA, Garcia-Ocaña A. Protein kinase C-zeta activation markedly enhances beta-cell proliferation: an essential role in growth factor mediated beta-cell mitogenesis. Diabetes 2007 Nov; 56(11).

Mellado-Gil J, Rosa TC, Demirci C, Gonzalez-Pertusa JA, Velazquez-Garcia S, Ernst S, Valle S, Vasavada RC, Stewart AF, Alonso LC, Garcia-Ocaña A. Disruption of hepatocyte growth factor/c-Met signaling enhances pancreatic beta-cell death and accelerates the onset of diabetes. Diabetes 2011 Feb; 60(2).

Guthalu Kondegowda N, Joshi-Gokhale S, Harb G, Williams K, Zhang XY, Takane KK, Zhang P, Scott DK, Stewart AF, Garcia-Ocaña A, Vasavada RC. Parathyroid hormone-related protein enhances human ß-cell proliferation and function with associated induction of cyclin-dependent kinase 2 and cyclin E expression. Diabetes 2010 Dec; 59(12).

Velazquez-Garcia S, Valle S, Rosa TC, Takane KK, Demirci C, Alvarez-Perez JC, Mellado-Gil JM, Ernst S, Scott DK, Vasavada RC, Alonso LC, Garcia-Ocaña A. Activation of protein kinase C-ζ in pancreatic β-cells in vivo improves glucose tolerance and induces β-cell expansion via mTOR activation. Diabetes 2011 Oct; 60(10).

González-Pertusa JA, Dubé J, Valle SR, Rosa TC, Takane KK, Mellado-Gil JM, Perdomo G, Vasavada RC, García-Ocaña A. Novel proapoptotic effect of hepatocyte growth factor: synergy with palmitate to cause pancreatic {beta}-cell apoptosis. Endocrinology 2010 Apr; 151(4).

Kondegowda NG, Mozar A, Chin C, Otero A, Garcia-Ocaña A, Vasavada RC. Lactogens protect rodent and human beta cells against glucolipotoxicity-induced cell death through Janus kinase-2 (JAK2)/signal transducer and activator of transcription-5 (STAT5) signalling. Diabetologia 2012 Jun; 55(6).

Demirci C, Ernst S, Alvarez-Perez JC, Rosa T, Valle S, Shridhar V, Casinelli GP, Alonso LC, Vasavada RC, García-Ocana A. Loss of HGF/c-Met signaling in pancreatic β-cells leads to incomplete maternal β-cell adaptation and gestational diabetes mellitus. Diabetes 2012 May; 61(5).

Metukuri MR, Zhang P, Basantani MK, Chin C, Stamateris RE, Alonso LC, Takane KK, Gramignoli R, Strom SC, O'Doherty RM, Stewart AF, Vasavada RC, Garcia-Ocaña A, Scott DK. ChREBP mediates glucose-stimulated pancreatic β-cell proliferation. Diabetes 2012 Aug; 61(8).

Williams K, Abanquah D, Joshi-Gokhale S, Otero A, Lin H, Guthalu NK, Zhang X, Mozar A, Bisello A, Stewart AF, Garcia-Ocaña A, Vasavada RC. Systemic and acute administration of parathyroid hormone-related peptide(1-36) stimulates endogenous beta cell proliferation while preserving function in adult mice. Diabetologia 2011 Nov; 54(11).

Alvarez-Perez JC, Rosa TC, Casinelli GP, Valle SR, Lakshmipathi J, Rosselot C, Rausell-Palamos F, Vasavada RC, García-Ocaña A. Hepatocyte growth factor ameliorates hyperglycemia and corrects ß-cell mass in IRS2 deficient mice. Molecular endocrinology (Baltimore, Md.) 2014 Oct;.

Wang P, Fiaschi-Taesch NM, Vasavada RC, Scott DK, García-Ocaña A, Stewart AF. Diabetes mellitus-advances and challenges in human β-cell proliferation. Nature reviews. Endocrinology 2015 Feb;.

Industry Relationships

Physicians and scientists on the faculty of the Icahn School of Medicine at Mount Sinai often interact with pharmaceutical, device and biotechnology companies to improve patient care, develop new therapies and achieve scientific breakthroughs. In order to promote an ethical and transparent environment for conducting research, providing clinical care and teaching, Mount Sinai requires that salaried faculty inform the School of their relationships with such companies.

Dr. Vasavada has not yet completed reporting of Industry relationships.

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