New thesis on the interplay between mitochondria, primary cilium, diabetes and its complications
Noah Moruzzi from the group Growth and Metabolism will defend his thesis "Interplay between mitochondria, primary cilium, diabetes and its complications" on January 13th, 2017. Main Supervisor is professor Kerstin Brismar.
What's the main focus of your thesis?
To study the role of mitochondria and primary cilia in diabetes and its complications and to clarify the mitochondrial and cellular metabolism in response of different oxygen tension in pancreatic islets.
Which are the most important results?
Acute and chronic hyperglycemia cause a metabolic switch towards aerobic glycolysis in primary healthy human fibroblasts and endothelial cells. In pancreatic islets, both high oxygen tension and hypoxia reduced mitochondrial function and impair glucose stimulated insulin secretion. Dysfunctional cilia in pancreatic islets affect insulin signaling in beta cells through a defect in insulin receptor A recruitment at the primary cilium. ATP depletion/mitochondrial ROS production impair cilia morphology in two different cell lines in vitro. In diabetes animal models GK rats (pancreas) and db/db mice (kidney) we found evidence of impaired cilia number and morphology.
How can this new knowledge contribute to the improvement of people's health?
Unraveling the mechanism of the metabolic changes in different cells and tissues in diabetes and its complications are pivotal to find new pharmacological strategies to counteract the progression of the disease. In this work, we add knowledge to this field. Moreover, the discovery that cilia are impaired in animal models diabetes and its complications could open new venues for diabetes treatment/prevention.
What are your future ambitions?
In general, I see myself working in an established organization where I can improve my primary skills giving an impactful contribution to research/development.