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Volume 4
Endocrinology & Diabetes Research
October 01-02, 2018 Osaka, Japan
12
th
International Conference on
Endocrinology, Diabetes and Metabolism
Endocrinology Summit 2018
October 01-02, 2018
Gong Deuk Bae et al., Endocrinol Diabetes Res 2018, Volume 4
DOI: 10.4172/2470-7570-C3-015
Effect of liquiritigenin on apoptotic beta-cell death by palmitate-induced lipotoxicity in
INS-1
cells
Gong Deuk Bae
1
, Hee-Sook Jun
1
, Yoon Sin Oh
2
1
Lee Gil Ya Cancer and Diabetes Institute, Department of Molecular Medicine, Incheon, Republic of Korea
2
Department of Food and Nutrition, Eulji University, Seongnam, Republic of Korea
Objective:
Activation of estrogen receptor signaling plays an important role to preserve functional beta‑cell mass in treatment
of diabetes. Liquiritigenin (LQ), a flavonoid isolated from Glycyrrhiza uralensis, is an estrogenic compound which acts as an
agonist for the estrogen receptor β. In this study, we investigated protective effect of LQ on palmitate (PA)-induced apoptosis
in
INS-1 cells
.
Methods:
To examine effect of LQ on beta cells, glucose stimulated insulin secretion (GSIS) by enzyme immunoassay (EIA)
method and cell viability by MTT were measured in rat beta-cell line INS-1 cells. To induce lipotoxicity, PA (400 μM) was
treated for 24 h and amount of apoptotic cells were analyzed using a flow cytometer with annexin-V staining. Expression
level of apoptotic proteins and endoplasmic reticulum (ER) stress markers were analyzed by western blot analysis after LQ
treatment. Tunicamycin and thapsigargin were used to ER stress inducer and AKT inhibitor (
AKTi-1/2
) was used to inhibit
LQ-induced AKT phosphorylation at ser 473.
Results:
Exposure of
INS-1 cells
to 5 μM of LQ significantly increased GSIS as well as cell viability. PA treatment increased
annexin-V stained cells and apoptotic proteins such as cleaved caspase-3, cleaved poly (ADP-ribose) polymerase and bax,
but these increases were significantly inhibited by LQ treatment. LQ treatment inhibited cell death by ER stress inducers and
PA induced ER stress marker proteins such as CHOP and phosphorylated forms of PERK and eIF2α was also significantly
downregulated inLQtreated cells. LQphosphorylatedAKTat ser 473 via estrogen receptor element dependent pathway andblocking
AKT signaling inhibited LQ induced decrease in level of phosphorylated PERK, consequently cell viability was not recovered.
Conclusion:
Our data demonstrated that LQ has anti-apoptotic effect against PA induced lipotoxicity and AKT mediated ER
stress inhibition was involved in the anti-apoptotic effect of LQ.
Biography
Gong Deuk Bae is a PhD course student in Gachon university. His research topic is The effect of natural products on the prevention and treatment of type 2 diabetes
focusing on pancreatic beta-cells.
chocoba819@naver.com