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CC BY-NC-ND 4.0 · Exp Clin Endocrinol Diabetes 2023; 131(12): 656-666
DOI: 10.1055/a-2191-9969
Article

Vitamin D Alleviates Type 2 Diabetes Mellitus by Mitigating Oxidative Stress-Induced Pancreatic β-Cell Impairment

Jia Liu   ‡
1   Department of Endocrinology, Gansu Provincial Hospital, Lanzhou, Gansu, China
,
Yuanjun Zhang   ‡
1   Department of Endocrinology, Gansu Provincial Hospital, Lanzhou, Gansu, China
,
Derong Shi
2   Gansu University of Chinese Medicine, Gansu, China
,
Cuihuan He
2   Gansu University of Chinese Medicine, Gansu, China
,
Guanghao Xia
1   Department of Endocrinology, Gansu Provincial Hospital, Lanzhou, Gansu, China
› Author Affiliations
Funding This work was supported by (Effect of Vitamin D on pancreatic β cell injury induced by lipotoxicity and underlying mechanisms) under grant (number 20JR10RA397) and (Effect and mechanism of Vitamin D on pancreatic β cell injury induced by lipotoxicity) under grant (number ZX-62000001-2021-191).
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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

‡ Co-first Author: These authors contributed equally to this work: Jia Liu, Yuanjun Zhang




Publication History

Received: 14 June 2023
Received: 28 August 2023

Accepted: 11 September 2023

Article published online:
07 November 2023

© 2023. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial-License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/).

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