Event Title

Effect of Fasting and Deoxycholic Acid Feeding in Xbp1-Knockout and Xbp1-Flox Control Mice

Session Number

C14

Advisor(s)

Richard Green, Northwestern University

Location

B-131 Grainger

Start Date

28-4-2016 10:15 AM

End Date

28-4-2016 10:40 AM

Disciplines

Biology

Abstract

The unfolded protein response (UPR) is a protective response which helps the cell adapt to intracellular stressors. Recent data indicates that the UPR affects hepatic lipid and glucose metabolism. This study analyzes how the individual and combined effects of bile acid feeding followed by fasting or non-fasting periods affect phosphorylated inositol requiring enzyme 1 alpha (IRE1α), a UPR protein. Cre+ X-box binding protein 1 (Xbp1) knock-out mice (lacking hepatic Xbp1) and Cre- mice (containing hepatic Xbp1) were either fed chow or 0.3% deoxycholic acid (a bile salt) for three days. After feeding, the mice were either left non-fasted or were fasted for 4 hours before sacrifice. Western blots indicate that phosphorylated- IRE1α is prominent in 4 hours fasted DCA-fed Cre+ mice and 4 hours fasted chow-fed Cre+ mice, which may be due to loss of suppression by XBP1 in knockout mice. Further testing will examine how IRE1α alters with different fasting periods in chow and DCA-fed mice. Additionally, XBP1 will be studied to analyze its interaction with its upstream target, IRE1α. By studying mechanisms of the UPR through fasting and feeding contexts, critical information can be formulated about UPR proteins role in bile acid and lipid regulation.


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Apr 28th, 10:15 AM Apr 28th, 10:40 AM

Effect of Fasting and Deoxycholic Acid Feeding in Xbp1-Knockout and Xbp1-Flox Control Mice

B-131 Grainger

The unfolded protein response (UPR) is a protective response which helps the cell adapt to intracellular stressors. Recent data indicates that the UPR affects hepatic lipid and glucose metabolism. This study analyzes how the individual and combined effects of bile acid feeding followed by fasting or non-fasting periods affect phosphorylated inositol requiring enzyme 1 alpha (IRE1α), a UPR protein. Cre+ X-box binding protein 1 (Xbp1) knock-out mice (lacking hepatic Xbp1) and Cre- mice (containing hepatic Xbp1) were either fed chow or 0.3% deoxycholic acid (a bile salt) for three days. After feeding, the mice were either left non-fasted or were fasted for 4 hours before sacrifice. Western blots indicate that phosphorylated- IRE1α is prominent in 4 hours fasted DCA-fed Cre+ mice and 4 hours fasted chow-fed Cre+ mice, which may be due to loss of suppression by XBP1 in knockout mice. Further testing will examine how IRE1α alters with different fasting periods in chow and DCA-fed mice. Additionally, XBP1 will be studied to analyze its interaction with its upstream target, IRE1α. By studying mechanisms of the UPR through fasting and feeding contexts, critical information can be formulated about UPR proteins role in bile acid and lipid regulation.