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.

Continue reading

Genetic Calcification Disorder May Lead To Better Treatment of Atherosclerosis

MedicalResearch.com Interview with:

Manfred Boehm M.D. Senior Investigator Laboratory of Cardiovascular Regenerative Medicine Center for Molecular Medicine NHLBI-NIH Bethesda, MD 20892

Dr. Manfred Boehm

Manfred Boehm M.D.
Senior Investigator
Laboratory of Cardiovascular Regenerative Medicine
Center for Molecular Medicine
NHLBI-NIH
Bethesda, MD 20892

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

Response: Common atherosclerosis (hardening of blood vessels) is the leading cause for vascular diseases worldwide. Vascular calcification is a critical component of atherosclerosis and an indicator of negative outcomes. This process is highly regulated and dynamic. However, the underlying mechanism is poorly understood and no direct treatment is available to stop or reverse this devastating buildup of calcium crystals in the vessel wall. Arterial calcification due to deficiency of CD73 is a rare inherited vascular disease characterized by extensive calcification of blood vessels caused by mutation in a gene encoding an enzyme that generates a compound called Adenosine outside of cells. The lack of this important enzyme, CD73, activates a compensatory mechanism to generated Adenosine by an alternative enzyme. Unfortunately, increased activity of this other enzyme is causing accelerated vascular calcification. By using the patient’s own cells, this study characterized the compensatory signaling pathway and discovered several new treatment strategies.

Continue reading