Diabetes Research and Clinical Practice - Volume 120 - Supplement 1 - October 2016

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Kaohsiung Veterans General Hospital, 6Division of Endocrinology and
Metabolism, Kaohsiung Veterans General Hospital, Kaohsiung City,
Taiwan
The anti-diabetic drug Metformin has been shown to have the
potential as a preventive and therapeutic drug for several
cancers, including gastric cancer (GC). The long non-coding
RNAs (lncRNAs) are non-protein coding transcripts that are
more than 200 nucleotides in length. LncRNA has been
reported to be dysfunction in diverse human cancers.
However, its impact on metformin-induced gastric cancer
cells death remains unclear. In this study, we found that
metformin could suppress GC cells growth and invasion in a
dose- and time-dependent manner. We also found that
metformin inhibited gastric cancer cell proliferation by
inducing significant cell cycle arrest at the G2/M phases. In
order to identify metformin-induced lncRNAs, we performed
the transcriptome profiles of HR control cell line and HR cell
line treating with metformin by microarray approach (includ-
ing 27958 protein-coding genes and 7419 lncRNAs). We
identified 2704 genes and 2458 genes that were significantly
upregulated and downregulated in the HR cells following
treatment with metformin, respectively. Bioinformatics ana-
lysis showed that metformin-associated genes simultan-
eously participated in cell growth, cell cycles and apoptosis.
Among these metformin-associated genes, we found that
the expression level of Loc10050669 was significantly sup-
pressed in dose- and time course-dependent manner after
gastric cancer cells treatment with metformin. Knockdown of
Loc10050669 expression could significantly suppress gastric
cancer cell growth, invasion ability and induce cell cycle arrest
at G2/M phases. These results implied that Loc10050669 may
play a critical role on metformin-induced suppression of
gastric cancer cell growth and motility. Our findings reveal a
new insight for lncRNAs regulation by metformin and provide
an application for gastric cancer therapy.
PD-16
Clinical effectiveness study of dapagliflozin as add-on for 33
inadequate glycemic control patients using liraglutide and
OADs
Yuan-Ching LIU1,2, Ching-Yi LIN1, I-Ying CHIU1,
Neng-Chun YU1*. 1Neng-Chun Diabetes Clinic, 2Department of
Nursing, School of Medicine, National Taiwan University, Taipei,
Taiwan
Background: Liraglutide and dapagliflozin have two different
anti-diabetical action mechanisms. They have shown ability
to improve the glycemic and body weight control. In this study,
for those patients who used OADs and liraglutide but fail to
meet the glycemic control criteria, dapagliflozin was added to
evaluate the effectiveness of liraglutide on glycemic and
body weight.
Methods: The design was a real-world, observational study. A
retrospective case note audit of type 2 diabetes patients who
were added dapagliflozin to their liraglutide regimens was
performed in a diabetes clinic located at Yilan County, Taiwan.
Datum of A1C, body weight (BW), and adverse events were
collected to analyze the effectiveness of initiating dapagli-
flozin for 6 months.
Results: 33 patients were included in the final analysis. The
average age at baseline was 54.1 ± 11.3 and the mean DM
duration was 12.7 ± 6.6 years. 60.6% of patients were male and
the average A1C and BMI at baseline were 8.0 ± 1.0% and
29.7 ± 5.7 kg/m 2, respectively. The mean duration of using
liraglutide before initiating dapagliflozin was 100.2 ± 30.0
weeks. 54.5% of patients used 1.2 mg daily liraglutide and
45.5% of patients used 1.8 mg daily liraglutide at baseline. After
adding dapagliflozin for 6 months, A1C has been reduced in 24
patients (72.7%), and the overall A1C has been significantly
reduced by 0.71 ± 0.95% (t = −4.33, p < 0.001). A1C has been
reduced by equal and more than 1% in 55.6% of 18 patients
with 1.2 mg liraglutide and 26.7% of 15 patients with 1.8 mg
liraglutide. BWhas been reduced in 29 patients (87.9%), and the
overall BW has been significantly reduced by 2.13 ± 2.24 kg
(t = −5.46, p < 0.001). Body weight has been reduced by equal
and more than 3 kg in 38.9% of 18 patients with 1.2 mg
liraglutide and 26.7% of 15 patients with 1.8 mg liraglutide.
Before dapagliflozin being initiated, the incidence of hypogly-
cemia was 21.2%. After using dapagliflozin for 3 months, the
incidence of hypoglycemia was 15.2% (5 out of 33 patients).
However, one urogenital infection case has been self-reported.
Conclusions: Dapagliflozin improved glycemic and weight
control in patients who used OADs and liraglutide but fail to
meet the glycemic control criteria. Reductions in A1C and body
weight were not affected by the dose of liraglutide used at
baseline. After using dapagliflozin for 3 months, the incidence
of hypoglycemia was not increased but one urogenital
infection case was self-reported.
PD-17
Clinical effectiveness of liraglutide as add-on therapy after
OADs failure for two years in 77 type 2 diabetes cases
Yuan-Ching LIU1,2, Ching-Yi LIN1, I-Ying CHIU1,
Neng-Chun YU1*. 1Neng-Chun Diabetes Clinic, 2Department of
Nursing, School of Medicine, National Taiwan University, Taipei,
Taiwan
Background: Liraglutide, a glucagon-like peptide-1 (GLP-1)
analogue, has been shown to possess beneficial effects on
body weight and glycemic control. The long-term effective-
ness of liraglutide for type 2 diabetes patients has been
evaluated in this study.
Methods: A systematic clinical case note audit of patients
with type 2 diabetes who used liraglutide for two years was
performed in a diabetes clinic located at Yilan County, Taiwan.
After liraglutide was initiated, clinical parameters were
collected at baseline, then collected every 3 months for two
years. Adverse events were also investigated at the first 3
months.
Results: A total of 77 patients who were 56.2 ± 9.4 years old
were selected in this study. The mean duration of diabetes was
12.5 ± 6.2 years. 54.5% of these selected patients were male.
The average A1C and BMI of these people were 8.7 ± 0.7% and
29.3 ± 4.2 kg/m2, respectively. 77.9% of patients were treated
with a mixed formula that included metformin, and sulfony-
lurea. 77 patients have used 1.2 mg liraglutide for 2 years. A1C
has been reduced in 61 patients (79.2%), and the overall A1C
has been significantly reduced by 0.92 ± 0.98% (t = −8.27,
p < 0.001). The body weight (BW) has been reduced in 65
patients (84.4%), and the overall BW has been significantly
reduced by 2.78 ± 3.56 kg (t = −6.84, p < 0.001). In these selected
patients, 30 patients used 1.2 mg liraglutide for 109.4 ± 16.9
weeks, then switched to 1.8 mg liraglutide. At the beginning of
1.8 mg liraglutide being used, their average A1C and BMI were
8.4 ± 0.8% and 29.7 ± 5.3 kg/m2, respectively. After 3 month,
A1C has been reduced in 21 patients (70.0%), and the overall
A1C has been significantly reduced by 0.56 ± 0.91% (t = −3.38,
p = 0.002). BW has been reduced in 22 patients (73.3%), and the
overall BW has been significantly reduced by 1.47 ± 2.03 kg
(t = −3.97, p < 0.001). During the first week of treatment,
adverse events including nausea (29.3%) and loss of appetite
(62.7%) were self-reported. However, they reduced to 5.3% and
37.3% after 3 months, respectively.
Conclusions: Long-term liraglutide treatment effectively
improves glycemic and body weight control for 2 years.
During the first week of treatment, adverse events including
nausea and loss of appetite were self-reported more fre-
quently, then they gradually decreased.
Poster Presentations / Diabetes Research and Clinical Practice 120S1 (2016) S65–S211 S96