Liver Key To Development of Diabetic Vascular Complications

MedicalResearch.com Interview with:

Dr. Mauricio Berriel Diaz Deputy Director & Head of Division Metabolic Dysfunction and Cancer Institute for Diabetes and Cancer IDC Helmholtz Center Munich and Joint Heidelberg-IDC Translational Diabetes Program Heidelberg University Hospital, Molecular Metabolic Control Medical Faculty, Technical University Munich Neuherberg, Germany

Dr. Berriel Diaz

Dr. Mauricio Berriel Diaz
Deputy Director & Head of Division Metabolic Dysfunction and Cancer
Institute for Diabetes and Cancer IDC
Helmholtz Center Munich and
Joint Heidelberg-IDC Translational Diabetes Program
Heidelberg University Hospital, Molecular Metabolic Control
Medical Faculty, Technical University Munich
Neuherberg, Germany 

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: Our institute takes part in a german collaborative research consortium (https://www.klinikum.uni-heidelberg.de/index.php?id=132204&L=1), in which the key objective is to understand why in diabetes mellitus late complications occur even when blood sugar is well controlled.

Our study focused the role of the liver and of inflammatory signaling, as the latter is known to be increased in metabolic diseases such as obesity and diabetes mellitus. We found that TNF-α-induced reactive oxygen species (ROS) formation in the liver abolished the function of the transcription factor GAbp. Impaired hepatic GAbp function resulted in transcriptional inactivation of the cellular energy sensor AMPK, which in turn induced hepatic cholesterol secretion, hypercholesterolemia and eventually atherosclerotic lesion formation.

MedicalResearch.com: What should readers take away from your report?

Response: Our study identifies the GAbp transcriptional complex as a molecular gatekeeper at the interface between inflammation, dyslipidemia, and atherosclerosis. Also, it emphasizes the role of the liver for the development of vascular diseases in diabetes. Targeting the anti-atherogenic properties of hepatic GAbp might provide a potential innovative treatment options in diabetic long-term complications.

MedicalResearch.com: What recommendations do you have for future research as a result of this study?

Response: The study supports the hypothesis that changes of important endogenous proteins by reactive metabolites strongly contribute to the development of diabetic complications. Reactive metabolites, which are the focus of the research, are dicarbonyls such as methylglyoxal and reactive oxygen species (ROS). Further understanding on how increased levels in reactive metabolites occur in diabetes and how they cause cellular damage will pave the way for therapeutic procedures aiming at prevention and reversal of diabetic complications. 

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Citation:

Katharina Niopek, Bilgen Ekim Üstünel, Susanne Seitz, Minako Sakurai, Annika Zota, Frits Mattijssen, Xiaoyue Wang, Tjeerd Sijmonsma, Yvonne Feuchter, Anna M. Gail, Barbara Leuchs, Dominik Niopek, Oskar Staufer, Maik Brune, Carsten Sticht, Norbert Gretz, Karin Müller-Decker, Hans-Peter Hammes, Peter Nawroth, Thomas Fleming, Michael D. Conkright, Matthias Blüher, Anja Zeigerer, Stephan Herzig, Mauricio Berriel Diaz. A Hepatic GAbp-AMPK Axis Links Inflammatory Signaling to Systemic Vascular Damage. Cell Reports, 2017; 20 (6): 1422 DOI: 10.1016/j.celrep.2017.07.023

Note: Content is Not intended as medical advice. Please consult your health care provider regarding your specific medical condition and questions. 

 

 

 

 

 

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