Lunch Pitch with Cemal Erdem and Elin Chorell
February 28 @ 12:00 - 13:00
Lunch Pitches with Cemal Erdem and Elin Chorell
Pitch 1: Cemal Erdem: Make computational models great again
Assistant professor, Department of Medical BiosciencesPitch 2: Elin Chorell: The sphinx of our metabolism
Assistant Professor, Department of Public Health and Clinical MedicineThe global rise in obesity and type 2 diabetes poses a significant health risk, accompanied by comorbidities like cardiovascular diseases and certain cancers. Recent findings challenge the notion of type 2 diabetes as a lifelong condition, revealing that a reduction of organ fat can induce disease remission meaning that lipid mechanisms are of key importance to both disease progression and remission. While diabetes can be managed with lifestyle changes and medication, the underlying mechanism remains unclear, hindering efficient risk prediction and treatment.
Our expertise lies in mass spectrometry-based lipidomics screening, focusing on insulin signaling tissues, disease progression, and remission. We explore obesity-related states, studying the impact of exercise and diet through human studies, mouse models, and cell experiments. Our research indicates that sphingolipid metabolism, specifically in pancreatic islets and skeletal muscle, are detrimental for the insulin signaling machinery. The sphingolipid metabolism, like its namesake ‘the Sphinx’, remain an enigma due to their diverse chemical composition and therefore a challenge to measure.
In the quest to understand obesity-associated disease, we are focused on unraveling bioactive lipids chemical composition for better understanding of biological activity. Our current focus involves connecting altered tissue metabolism with circulating markers, providing insights into tissue-crosstalk and potential therapeutic markers for risk assessment and monitoring of this global health threat.
Interested in: We are seeking collaborators experienced in sorting cell populations and/or tissue/single cell bioimaging to further unravel the spatial orientation of the bioactive sphingolipid derivatives we have identified in our model systems.
Our overall aim is to deepen our understanding of the clearance and production of sphingolipid derivatives, which may interfere with insulin signaling mechanisms and contribute to disease progression.