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VERSION:2.0
PRODID:-//UNL_UCBCN//NONSGML UNL Event Publisher//EN
X-WR-CALNAME:College of Agricultural Sciences and Natural Resources
CALSCALE:GREGORIAN
METHOD:PUBLISH
BEGIN:VEVENT
DTSTART:20230322T150000Z
UID:171379@events.unl.edu
DTSTAMP:20230301T222901Z
ORGANIZER;CN=Brent C Baum:MAILTO:bbaum2@unl.edu
SUMMARY:MITO (Mitochondria) Club
STATUS:CONFIRMED
DESCRIPTION:Metabolic dysfunction-associated fatty liver disease (MAFLD) is
  severe and widespread. While obesity and Western diets are known risk fac
 tors for MAFLD\, identifying the environmental and genetic modifiers causi
 ng its heterogeneous onset and progression is critical to elucidating its 
 mechanisms and developing intervention strategies. Several lines of eviden
 ce suggest reciprocal relationships between MAFLD and the dysregulation of
  copper\, a cofactor of approximately a dozen enzymes\, such as cytochrome
  oxidase and cytosolic superoxide dismutase. This project aimed to gain be
 tter insight into the roles of copper in lipid metabolism and metabolic di
 seases. We determined excess fat-induced changes in copper homeostasis and
  the impacts of copper limitation on lipid metabolism in the mouse liver a
 nd cultured hepatocytes. Our data present a fatty acid-dependent expressio
 n of copper-requiring enzymes and molecular factors involved in copper hom
 eostasis. Furthermore\, copper limitation in hepatocytes rapidly developed
  severe lipid toxicity and whole-body lipid metabolism disorders. These re
 sults indicate the critical roles of copper-dependent cellular processes i
 n lipid metabolism and provide a new conceptual framework to define previo
 usly under-appreciated contributions of copper and other micronutrients in
  preventing metabolic diseases.
LOCATION:Beadle Center Room E228
URL://events.unl.edu/casnr/2023/03/22/171379/
DTEND:20230322T150000Z
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