Abstract
Objective Type 2 diabetes mellitus (T2DM) is a common metabolic disorder
with rising incidence worldwide. This study explored the anti-T2DM role of
vitamin D, thereby providing novel therapeutic strategies.
Methods C57BL/6 J mice and MIN6 cells were used to induce
in vivo T2DM and damaged β-cell models, respectively. Body
weights, fasting blood glucose, and fasting insulin were measured in mice. Oral
glucose tolerance test (OGTT) and insulin tolerance test (ITT) were conducted on
mice. Lipid indices (TG, TC, LDL-C, and HDL-C) were detected in mouse serum.
Hematoxylin-eosin staining was used to evaluate pancreatic tissue injury. ELISA
was used to assess insulin and oxidative stress (OS) markers (MDA, GSH, and SOD)
in mice and MIN6 cells. Production of ROS was detected in islet β-cells
and MIN6 cells. Cell viability and apoptosis were evaluated using CCK-8 and flow
cytometry, respectively. QRT-PCR and western blotting were used to detect
pro-inflammatory factors (TNF-α and IL-6) and endoplasmic reticulum
stress (ERS) markers (CHOP and GRP78), respectively.
Results Vitamin D reduced body weights, fasting blood glucose, and insulin
and ameliorated glucose tolerance and insulin sensitivity in T2DM mice. Besides,
vitamin D decreased serum TG, TC, LDL-C, and increased HDL-C in T2DM mice.
Vitamin D inhibited pancreatic histopathological injury, cell apoptosis, OS, and
β-cell decline in T2DM mice. Moreover, vitamin D alleviated cell death,
insufficient insulin secretion, inflammation, OS, and ERS in damaged MIN6 cells.
Notably, N-acetyl-L-cysteine (an OS inhibitor) enhanced these effects of vitamin
D.
Conclusions Vitamin D relieved T2DM symptoms by alleviating OS-induced
β-cell impairment.
Key words
type 2 diabetes mellitus - vitamin D - β-cell - oxidative stress - insulin
