Eugene Chang, PhD: No relevant financial relationship(s) with ineligible companies to disclose.
Objectives: Recent evidence demonstrates intestinal inflammation and permeability in obese humans. Numerous epidemiological and clinical studies demonstrate a negative association between vitamin D status and obesity. The specific aim of this study was to investigate the molecular mechanism by which dietary vitamin D supplementation influences obesity-related intestinal inflammation and permeability in high fat diet-fed obese mice.
Methods: Male C57BL/6J mice were fed either a low-fat diet (1000 IU vitamin D/kg diet) or high-fat diet (HFD, 1000 or 10,000 IU vitamin D). Body weight and food intake were measured weekly. Serum NO and TNF-α, levels and colon AMPK activity were measured using commercial ELISA kits. mRNA levels involved in inflammation and permeability were measured by RT-qPCR.
Results: Vitamin D supplementation improved HFD-induced adipose tissue mass without changing body weight and food intake. However, circulating levels of proinflammatory cytokines such as NO and TNF-α were significantly decreased by vitamin D supplementation in HFD-fed obese mice. Additionally, vitamin D supplementation significantly decreased mRNA levels IL-6, MCP-1, and TNF-α related to inflammation in colon from obese mice. Occluding and zo-1 gene expression involved in permeability was suppressed by vitamin D supplementation in accompanied with the increment of AMPK activity in the colon.
Conclusions: This study indicates that intestinal inflammation in obese mice was reversed by vitamin D supplementation in HFD-fed obese mice in accompanied with increased gene expression related to permeability and AMPK activity. It suggests the favorable effects of vitamin D on obesity-induced intestinal inflammation along with the improvement of intestinal permeability.
Funding Sources: This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIT) (2020R1I1A1A01068463 & RS-2023-00242630).
