Chris is a renowned leader in the field of diabetes, obesity and metabolism research, with a career spanning over three decades. He has more than 180 published manuscripts, and has held industry and academic leadership roles at top institutions that include Harvard Medical School and the University of Washington. Chris is also Professor Emeritus at the University of Chicago, Department of Medicine.
Chris’ research journey began in 1984 when he received his PhD in Biochemistry from the University of London. Soon after, he was quickly established as a pioneering force in the field of diabetes research—beginning with postdoctoral fellowships at the Joslin Diabetes Center/ Harvard Medical School and the University of Cambridge, then following with academic appointments and industry roles among some of the most venerated institutions in the US and the UK.
Chris’ diabetes research has centered on the molecular mechanisms of insulin production and secretion, as well as signal transduction pathways that control pancreatic beta-cells growth and death in relation to the pathogenesis of diabetes. His work has earned him numerous awards and honors, as well as research funding from esteemed organisations such as the Juvenile Diabetes Research Foundation, American Diabetes Association and the National Institutes of Health. He also was a member of the National Institutes of Health Endocrinology and CADO Study Sections, an associate editor for Diabetes, the journal of the American Diabetes Association, a reviewer for multiple other peer-reviewed journals and is a frequent visiting professor and lecturer.
In 2015, Christopher joined AstraZeneca and in his role as Chief Scientist, is responsible for developing and growing the CVRM research base in the US and the UK, as well as contributing to the product development goals and vision across the CVRM therapeutic area. His research continues to focus on the molecular pathogenesis of both type 1 and type 2 diabetes, as well as the regulation of biosynthesis and production of polypeptide hormones; signal transduction mechanisms for insulin sensitivity; and novel pharmacological biologic targets for the treatment of metabolic diseases.
In May 2019, Chris’s was announced as the new Chair of AstraZeneca’s postdoctoral programme. His wealth of experience, strong links to academia and passion for biomedical education means he has the ideal background to continue to build this industry-leading programme.
AstraZeneca’s postdoc programme offers outstanding training, intellectual freedom, high-impact publishing opportunities, and, ultimately, a springboard for a great scientific career. With a dedicated supervisor from one of AstraZeneca’s two R&D organisations (BioPharmaceuticals or Oncology), complemented by an academic mentor, postdocs work at the interface of academia and industry, and gain a unique combination of experience from both worlds.
I grew up in an artistic musical family, which instilled in me very early on the essence of creativity. Science requires original thinking and cultivating ideas, and using that creativity is fundamental to innovation and momentous discovery.
Announced as Chair of AstraZeneca’s Postdoc programme
UNIVERSITY OF CAMBRIDGE
While at the University of Cambridge, Chris was an instrumental member of the team that discovered enzyme activities for proinsulin to insulin processing
PACIFIC NORTHWEST DIABETES RESEARCH INSTITUTE
Helped to build a diabetes research institute in Seattle, WA
UNIVERSITY OF CHICAGO
Built the research department and helped found the Kovler Diabetes Center, at the University of Chicago
Named Professor Emeritus at the University of Chicago
Awards and honors
Juvenile Diabetes Foundation International Fellowship and Career Development Awards
Mary Jane Kugel Award, Juvenile Diabetes Foundation International Kroc Lecture in Diabetes
David Rumbough Award, JDRF
The Kovler Family Professor, Endowed Chair of Medicine
Golden Key Award, University of Chicago
Chair, American Diabetes Association 65th and 66th Scientific Sessions Meetings
Chair, Medical & Scientific Research Committees, JDRF
Chair, American Diabetes Association Council for Molecular, Cellular & Biochemical Aspects of Diabetes (2005-2007)
Newly synthesised proinsulin/insulin and stored insulin are released from pancreatic B-cells predominantly via a regulated, rather than a constitutive pathway.
Rhodes CJ, Halban PA. J Cell Biol. 1987; 105:145-153.
Intraorganellar Ca and pH control proinsulin cleavage in the pancreatic ß-cell via two site-specific endopeptidases.
Davidson HW, Rhodes CJ, Hutton JC. Nature 1988; 333:93-96.
Preferential Cleavage of des 31, 32 Proinsulin, over Intact Proinsulin by the Insulin Secretory Granule Type-II Endopeptidase: Implication of a Favored Route for Prohormone Processing.
Rhodes CJ, Lincoln B & Shoelson S. J. Biol. Chem. 1992; 267: 22719-22727.
Chronic exposure to free fatty acid reduces pancreatic ß-cell insulin content bi increasing basal insulin secretion that is not compensated for by a corresponding increase in proinsulin biosynthesis translation.
Bollheimer LC, Skelly RH, Chester MC, McGarry JD & Rhodes CJ. J. Clin. Invest. 1998; 101: 1094-1101.
Ca2+-dependent dephosphorylation of kinesin heavy chain on beta-granules in pancreatic beta-cells. Implications for regulated beta-granule transport and insulin exocytosis.
Donelan MJ, Morfini G, Julyan R et al. J Biol Chem 2002; 277:24232-24242.
Protein kinase B/Akt prevents fatty Acid-induced apoptosis in pancreatic beta -cells (INS-1).
Wrede CE, Dickson LM, Lingohr MK, Briaud I, Rhodes CJ. J. Biol. Chem. 2002; 277:49676-49684.
Type-2 diabetes – A matter of ß-cell life and death?
Type-2 diabetes – A matter of ß-cell life and death? Rhodes CJ. Science 2005 307:380-4.
A cis-element in the 5' untranslated region of the preproinsulin mRNA (ppIGE) is required for glucose regulation of proinsulin translation.
Wicksteed BL Uchizono Y, Alarcón C, McCuaig JF, Shalev A, Rhodes CJ. Cell Metab. 2007 5: 221-227.
Specific Regulation of IRS-2 Expression by Glucose in Rat Primary Pancreatic Islet ß-cells.
Lingohr MK, Briaud I, Dickson LM et al. 2006 J. Biol. Chem. 281:15884-92
Regulated autophagy controls hormone content in secretory-deficient pancreatic endocrine ß-cells.
Marsh BJ, Alarcón C, Soden C et al. Mol. Endo. 2007 21: 2255-2269.
FoxO Feedback Control of Basal IRS-2 Expression in Pancreatic ß-Cells is Distinct From that in Hepatocytes.
Tsunekawa S, Demozay D, Briaud I et al. Diabetes 2011 60: 2883-2891.
Specific Glucose-Induced Control of Insulin Receptor Substrate-2 Expression is Mediated via Ca2+-Dependent Calcineurin/NFAT Signaling in Primary Pancreatic Islet ß-cells.
Demozay D, Tsunekawa S, Shah R, Rhodes CJ. Diabetes. 2011 60: 2892-2902.
A Direct Autocrine Action of Insulin on ß-Cells: Does it make Physiological Sense?
Rhodes CJ, White, MF, Leahy, J, Kahn SE. 2013 Diabetes 62: 2157-2163.
Pancreatic ß-Cell Adaptive Plasticity in Obesity Increases Insulin Production but Adversely Affects Secretory Function.
Alarcón C, Boland B, Uchizono Y et al. 2016 Diabetes 65: 438-50.
A brain to pancreatic islet map reveals differential glucose regulation from distinct hypothalamic regions.
Rosario W, Singh I, Wautlet A et al. 2016 Diabetes. 65(9):2711-23
Inhibition of upper small intestinal mTOR lowers plasma glucose levels by inhibiting glucose production.
Waise T, Rasti M, Duca F et al. 2019 Nat. Comm. 10: 714
Pancreatic β-Cell Rest Replenishes Insulin Secretory Capacity and Attenuates Diabetes in an Extreme Model of Obese Type 2 Diabetes.
Boland B, Brown C Jr, Boland M et al. 2019 Diabetes. 68:131-140.
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