IBCS Seminar
Understanding saturated fatty acid-mediated β-cell dysfunction and its implications on diabetes
IBCS Seminar – Professor Yusuf Ali (Lee Kong Chian School of Medicine) Wednesday 19th February 2020 15:00 – 16:30 St Luke’s G18
| A seminar | |
|---|---|
| Date | 19 February 2020 |
| Time | 15:00 to 16:30 |
| Place | G18 |
Event details
Abstract
Brief Bio
Yusuf Ali is an Assistant Professor of Metabolic Disease in the Lee Kong Chian School of Medicine, Nanyang Technological University Singapore. He received his PhD in Integrative Sciences and Engineering (NUS) in 2008. He subsequently completed his postdoctoral fellowships in A*STAR and at the Karolinska Institute in Stockholm, Sweden. Asst Prof Ali has published several landmark scientific papers describing mechanisms of aberrant pancreatic hormone release in diabetes. Currently, his laboratory is focused on tackling insulin insufficiency in type-2 diabetes (T2D) with emphasis on localised low-grade inflammation, lipid stress and islet plasticity. Loss of β-cell function is a characteristic of the Asian diabetic phenotype and finding ways to mitigate this loss will undoubtedly improve diabetes incidence and help patients better manage diabetic complications
Abstract
Oils from palm and coconut are high in saturated fatty acid (SFA) content and high SFA intake is associated with cardiovascular disease and diabetes. Palmitate, an abundant SFA in these oils have been long been associated with raising circulating LDL and cholesterol. On top of this, excess palmitate (and other SFAs) induces cellular toxicity (lipotoxicity) more so than unsaturated fatty acids (UFAs) and the mechanism underpinning this difference in response is slowly unravelling. Our interest in mechanisms of pancreatic insulin-producing cell (β-cells of the Islets of Langerhans) dysfunction and death, especially in type-2 diabetes, led us to study intracellular lipid droplet biogenesis, with the latter showing profound differences when exposed to different FAs. I will present largely unpublished data and provide a new mechanism by which SFAs, but not UFAs, induce β-cell stress and dysfunction. I will also discuss the subsequent impact of this mechanism on glucose homeostasis.
