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SUMMARY:Interrogating Amino Acid Metabolism in Metabolic Disorders
DTSTART:20230501T123000
DTEND:20230501T133000
DTSTAMP:20260513T030844Z
UID:1781476c13759a4c81e480db6f71d7ebd5d61db77c138eb8a5c63951
CATEGORIES:Conferences - Seminars
DESCRIPTION:Michal Handzlik\, Ph.D.\, The Salk Institute for Biological St
 udies\, La Jolla\, CA (USA)\nBIOENGINEERING SEMINAR\n \nAbstract:\nType 2
  Diabetes (T2D) represents a disease spectrum with metabolic dysfunction d
 amaging multiple organ systems including liver\, kidneys\, and peripheral 
 nerves. Although insulin resistance and dyslipidemia link onset and progre
 ssion of these co-morbidities\, aberrant amino acid metabolism also contri
 butes to pathogenesis of diabetes and potentially its complications. Serin
 e and glycine are closely related non-essential amino acids that are consi
 stently reduced in metabolic syndrome patients\, but the mechanistic drive
 rs of serine deficiency and the downstream metabolic and phenotypic conseq
 uences remain unclear. Low systemic serine\, a serine-opathy\, is emerging
  as a hallmark of retinopathy and peripheral neuropathy\, correlating with
  impaired visual acuity and peripheral neuropathy (PN). Our data demonstr
 ate that aberrant serine homeostasis in the liver drives serine and glycin
 e deficiencies in genetically obese mice. This serine-opathy can be diagno
 sed with a serine tolerance test that quantifies systemic serine disposal.
  Mimicking serine deficiency via dietary serine/glycine restriction togeth
 er with high fat intake dramatically accelerates thermal hypoalgesia in mi
 ce and reduces epidermal sensory nerve density\, which are accompanied by 
 extensive sciatic nerve lipid remodeling. These phenotypes were subsequent
 ly normalized by myriocin\, linking serine-associated PN with sphingolipid
  metabolism. These findings identify systemic serine deficiency and dyslip
 idemia as novel risk factors for PN that may be exploited therapeutically.
 \n\nBio:\nDr. Michal Handzlik trained as a physiotherapist before obtainin
 g a Master's degree in Exercise Physiology (Loughborough University\, UK) 
 with Prof. Mike Gleeson and a Ph.D. in Biomedical Sciences (University of 
 Nottingham\, UK) with Prof. Paul Greenhaff. Inspired by his diabetic patie
 nts\, he continued his NIH-supported postdoctoral training with Prof. Chri
 stian Metallo (UC San Diego/Salk Institute\, US)\, developing a strong int
 erest in in vivo stable isotope tracing\, mass spectrometry\, and inter-o
 rgan crosstalk to dissect the contribution of aberrant amino acid homeost
 asis toward the diabetic phenotype and complications.\n\n\nZoom link for 
 attending remotely: https://epfl.zoom.us/j/65946248975\n 
LOCATION:SV 1717 https://plan.epfl.ch/?room==SV%201717 https://epfl.zoom.u
 s/j/65946248975
STATUS:CONFIRMED
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