Dr. J.W.M. Höppener

Höppener ZW

Molecular Biologist
Associate Professor
Laboratory of Translational Immunology
University Medical Center Utrecht
Heidelberglaan 100, 3584 CX Utrecht, The Netherlands

Dr. Höppener graduated (cum laude) in 1981 in Biology at Utrecht University. He did his Ph.D. (cum laude) in 1988 with Prof. Lips and Prof. Jansz, studying “The human calcitonin/CGRP genes: structure, chromosomal localization and expression in tumors” Part of the Ph.D. study was performed at the Johns Hopkins Hospital (Baltimore, USA). He was research fellow at Utrecht University until 1989 (financed by STW [Foundation for Technical Sciences]), when he was awarded a 5-year fellowship from the Royal Netherlands Academy of Arts and Sciences (KNAW). He was appointed senior research scientist in the Faculty of Medicine (presently UMC Utrecht) at the Division of Internal Medicine in 1994.

He was appointed Associate Professor at the Division of Biomedical Genetics at UMC Utrecht in 2005 and joined the Laboratory of Translational Immunology at UMC Utrecht in 2013. His research has been supported by UMC Utrecht, Dutch Cancer Society (NKB/KWF), Dutch Diabetes Research Fund, European Union and industry.

The group of Dr. Höppener has been working in the field of molecular endocrinology, focussing on peptides belonging to the calcitonin/calcitonin gene–related peptide (CGRP) gene family. The major research theme of his group is the role of IAPP (Islet amyloid polypeptide/amylin), and particularly its (pre-) fibrillary depositions, in pancreatic islet ß-cell dysfunction in Type 2 diabetes mellitus (DM2). To this end they have generated and characterized a transgenic mouse model, in which the amyloidogenic human IAPP is expressed in the pancreatic islet ß-cells. Particularly when obesity and insulin resistance are induced, islet amyloid develops in these mice and contributes to the pathogenesis of DM2 by reducing the insulin producing capacity, involving islet remodeling by inflammation and fibrosis. This unique animal model is used for pioneering research with respect to the pathogenesis, diagnosis and therapy of DM2. In addition to this in vivo model, isolated and cultured mouse pancreatic islets are used as an ex vivo modelsystem.

Keynote papers

Engel MF, Khemtémourian L, Kleijer CC, Meeldijk HJ, Jacobs J, Verkleij AJ, de Kruijff B, Killian JA, Höppener JWM. Membrane damage by human islet amyloid polypeptide through fibril growth at the membrane. Proc Natl Acad Sci U S A. 2008; 105:6033-8.


Höppener JWM, B Ahrén, CJM Lips. Islet amyloid and type 2 diabetes mellitus. The New England Journal of Medicine 2000; 343:411-9.

Höppener JWM, C Oosterwijk, MG Nieuwenhuis, et al., B Ahrén, CJM Lips. Extensive islet amyloid formation is induced by development of type 2 diabetes mellitus and contributes to its progression. Pathogenesis of diabetes in a transgenic mouse model. Diabetologia 1999; 42:427-34.