Hans-Peter Hammes, M.D., is internationally recognized as a preeminent figure in the treatment of diabetes and its complications. As evidence of his standing in the area of diabetes, Hans-Peter was recipient of the prestigious Camillo Golgi Prize awarded by European Association for the Study of Diabetes at that organization’s 2015 annual meeting.
Hans-Peter graduated from the Medical Faculty Münster (Westfälische Wilhelms-Universität, Münster, Germany) and did his medical training at the 3rd and 1st Medical Department at the University Medical Center in Giessen, Germany.
After specializing in endocrinology, diabetology and habilitation, Hans-Peter was appointed Section Head of Endocrinology at the 5th Medical Department, University Medical Center Mannheim, University of Heidelberg, Germany, a position that he currently holds.
Areas of Expertise (5)
DR Barometer Program
Camillo Golgi Prize (professional)
European Association for the Study of Diabetes
Westfälische Wilhelms-Universität: M.D., Medicine
- German Diabetes Association : Member
- German Society of Ophthalmology : Member
- Association for the Research of Vision and Ophthalmology : Member
- German Society of Internal Medicine : Member
Media Appearances (2)
Rückenwind bei der Erforschung der diabetischen Netzhauterkrankung
Die Deutsche Diabetes-Gesellschaft unterstützt die Forschung einer Arbeitsgruppe der V. Medizinischen Klinik der Universitätsmedizin Mannheim (UMM) zur diabetischen Retinopathie, einer Erkrankung der Netzhaut als Folge des Diabetes, mit der Hans-Christian-Hagedorn-Projektförderung 2010. Der mit 25.000 Euro dotierte Förderpreis wird dem Leiter der Arbeitsgruppe, Professor Dr. Hans-Peter Hammes, Inhaber einer C3-Professur für Innere Medizin und Endokrinologie der Medizinischen Fakultät Mannheim der Universität Heidelberg, am 13. Mai 2010 im Rahmen der Jahrestagung der Deutschen Diabetes-Gesellschaft in Stuttgart verliehen.
Camillo Golgi Preis für Mannheimer Diabetes-Forscher
Für seine wissenschaftlichen Arbeiten zur diabetischen Retinopathie, einer durch die Zuckerkrankheit Diabetes mellitus hervorgerufenen Erkrankung der Netzhaut (Retina) des Auges, ist Professor Dr. Hans-Peter Hammes von der Europäischen Gesellschaft für Diabetesforschung (European Association for the Study of Diabetes, EASD) mit dem Camillo Golgi Preis ausgezeichnet worden. Den mit 20.000 Euro dotierten Preis nahm der Mannheimer Arzt und Wissenschaftler am Dienstag, den 15. September 2015 bei der 51. Jahrestagung der EASD in Stockholm entgegen.
Featured Articles (5)
Diabetic retinopathy is the most frequently occurring complication of diabetes mellitus and remains a leading cause of vision loss globally. Its aetiology and pathology have been extensively studied for half a century, yet there are disappointingly few therapeutic options. Although some new treatments have been introduced for diabetic macular oedema (DMO) (e.g. intravitreal vascular endothelial growth factor inhibitors (‘anti-VEGFs’) and new steroids), up to 50% of patients fail to respond. Furthermore, for people with proliferative diabetic retinopathy (PDR), laser photocoagulation remains a mainstay therapy, even though it is an inherently destructive procedure.
This review summarises the clinical features of diabetic retinopathy and its risk factors. It describes details of retinal pathology and how advances in our understanding of pathogenesis have led to identification of new therapeutic targets. We emphasise that although there have been significant advances, there is still a pressing need for a better understanding basic mechanisms enable development of reliable and robust means to identify patients at highest risk, and to intervene effectively before vision loss occurs.
Hyperglycemia causes micro- and macrovascular complications in diabetic patients. Elevated glucose concentrations lead to increased formation of the highly reactive dicarbonyl methylglyoxal (MG), yet the early consequences of MG for development of vascular complications in vivo are poorly understood. In this study, zebrafish were used as a model organism to analyze early vascular effects and mechanisms of MG in vivo. High tissue glucose increased MG concentrations in tg(fli:EGFP) zebrafish embryos and rapidly induced several additional malformed and uncoordinated blood vessel structures that originated out of existing intersomitic blood vessels (ISVs). However, larger blood vessels, including the dorsal aorta and common cardinal vein, were not affected. Expression silencing of MG-degrading enzyme glyoxalase (glo) 1 elevated MG concentrations and induced a similar vascular hyperbranching phenotype in zebrafish. MG enhanced phosphorylation of vascular endothelial growth factor (VEGF) receptor 2 and its downstream target Akt/protein kinase B (PKB). Pharmacological inhibitors for VEGF receptor 2 and Akt/PKB as well as MG scavenger aminoguanidine and glo1 activation prevented MG-induced hyperbranching of ISVs. Taken together, MG acts on smaller blood vessels in zebrafish via the VEGF receptor signaling cascade, thereby describing a new mechanism that can explain vascular complications under hyperglycemia and elevated MG concentrations.
The receptor for AGEs (RAGE) is linked to proinflammatory pathology in a range of tissues. The objective of this study was to assess the potential modulatory role of RAGE in diabetic retinopathy.
Cytochrome P450 (CYP) epoxygenases generate bioactive lipid epoxides which can be further metabolized to supposedly less active diols by the soluble epoxide hydrolase (sEH). As the role of epoxides and diols in angiogenesis is unclear, we compared retinal vasculature development in wild-type and sEH−/− mice. Deletion of the sEH significantly delayed angiogenesis, tip cell, and filopodia formation, a phenomenon associated with activation of the Notch signaling pathway. In the retina, sEH was localized in Müller glia cells, and Müller cell–specific sEH deletion reproduced the sEH−/− retinal phenotype. Lipid profiling revealed that sEH deletion decreased retinal and Müller cell levels of 19,20–dihydroxydocosapentaenoic acid (DHDP), a diol of docosahexenoic acid (DHA). 19,20-DHDP suppressed endothelial Notch signaling in vitro via inhibition of the γ-secretase and the redistribution of presenilin 1 from lipid rafts. Moreover, 19,20-DHDP, but not the parent epoxide, was able to rescue the defective angiogenesis in sEH−/− mice as well as in animals lacking the Fbxw7 ubiquitin ligase, which demonstrate strong basal activity of the Notch signaling cascade. These studies demonstrate that retinal angiogenesis is regulated by a novel form of neuroretina–vascular interaction involving the sEH-dependent generation of a diol of DHA in Müller cells.
This is the second iteration of the European Society of Cardiology (ESC) and European Association for the Study of Diabetes (EASD) joining forces to write guidelines on the management of diabetes mellitus (DM), pre-diabetes, and cardiovascular disease (CVD), designed to assist clinicians and other healthcare workers to make evidence-based management decisions. The growing awareness of the strong biological relationship between DM and CVD rightly prompted these two large organizations to collaborate to generate guidelines relevant to their joint interests, the first of which were published in 2007. Some assert that too many guidelines are being produced but, in this burgeoning field, five years in the development of both basic and clinical science is a long time and major trials have reported in this period, making it necessary to update the previous Guidelines.