Type 2 diabetes mellitus (T2DM) is characterized by hyperglycemia, which
seriously endangers human health. The dysregulation of lncRNA LINC01018 in T2DM
has been noticed in previous studies, but whether it served as a biomarker lacks
validation. This study aimed to confirm the abnormal expression of LINC01018 in
T2DM and reveals its specific function in regulating pancreatic β cell
function. This study enrolled 77 T2DM patients and 41 healthy individuals and
compared the plasma LINC01018 levels between two groups using PCR. The
pancreatic β cell was induced with 25 mM glucose to mimic cell
injury during T2DM. The effects of LINC01018 on β cell proliferation,
dedifferentiation, and insulin production were evaluated by CCK8, western
blotting, and ELISA. Moreover, the involvement of miR-499a-5p was also evaluated
with luciferase reporter assay. Increased plasma LINC01018 was observed in T2DM
patients compared with healthy individuals, which discriminates patients with
high sensitivity and specificity. Upregulated LINC01018 was associated with
patients’ fasting blood glucose and weight loss. High glucose induced
the increasing LINC01018 in pancreatic islet β cells and suppressed cell
proliferation, insulin secretion, and promoted cell dedifferentiation. Silencing
LINC01018 could alleviate the impaired function of β cells by high
glucose, which was reversed by the knockdown by miR-499a-5p. Upregulated
LINC01018 served as a potential diagnostic biomarker for T2DM and alleviated
high glucose-induced β cell dysfunction via negatively modulating
miR-499a-5p.