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Chronic Activation of Liver X Receptor Induces β-Cell Apoptosis Through Hyperactivation of Lipogenesis

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Author(s)
Sung Sik ChoeA Hyun ChoiJoo-Won LeeKang Ho KimJun-Jae ChungJiyoung ParkKyeong-Min LeeKeun-Gyu ParkIn-Kyu LeeJae Bum Kim
Keimyung Author(s)
Park, Keun Gyu
Department
Dept. of Internal Medicine (내과학)
Journal Title
Diabetes
Issued Date
2007
Volume
56
Issue
6
Abstract
Liver X receptor (LXR) and LXR play important roles in
fatty acid metabolism and cholesterol homeostasis. Although
the functional roles of LXR in the liver, intestine,
fat, and macrophages are well established, its role in
pancreatic -cells has not been clearly defined. In this
study, we revealed that chronic activation of LXR contributes
to lipotoxicity-induced -cell dysfunction. We observed
significantly elevated expression of LXR in the
islets of diabetic rodent models, including fa/fa ZDF rats,
OLETF rats, and db/db mice. In primary pancreatic islets
and INS-1 insulinoma cells, activation of LXR with a synthetic
ligand, T0901317, stimulated expression of the lipogenic
genes ADD1/SREBP1c, FAS, and ACC and resulted in
increased intracellular lipid accumulation. Moreover,
chronic LXR activation induced apoptosis in pancreatic
islets and INS-1 cells, which was synergistically promoted
by high glucose conditions. Taken together, we suggest
lipid accumulation caused by chronic activation of LXR in
-cells as a possible cause of -cell lipotoxicity, a key step
in the development of type 2 diabetes. Diabetes 56:1534
–1543, 2007
Keimyung Author(s)(Kor)
박근규
Publisher
School of Medicine
Citation
Sung Sik Choe et al. (2007). Chronic Activation of Liver X Receptor Induces β-Cell
Apoptosis Through Hyperactivation of Lipogenesis. Diabetes, 56(6), 1534–1543. doi: 10.2337/db06-1059
Type
Article
ISSN
0012-1797
DOI
10.2337/db06-1059
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/35561
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Internal Medicine (내과학)
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