International journal for vitamin and nutrition research. Internationale Zeitschrift fur Vitamin- und Ernahrungsforschung. Journal international de vitaminologie et de nutrition · 2026
Fructooligosaccharide Upregulates Colonic Vitamin D Receptors and Modulates Inflammatory Status in High-Fat Diet-Induced Obese Male C57BL/6 Mice.
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Brunelle Kelly, Butler Emily, Nobles Zack, Lewis Lauren, Hernandez Sophia, Koh Gar Yee
Аннотация
BACKGROUND: Vitamin D (VD) deficiency is commonly observed in obesity, which may increase morbidity risk. This study explores the effect of fructooligosaccharide (FOS) on VD signaling and inflammatory status in diet-induced obese mice.
METHODS: Therefore, 5-week-old male C57BL/6J mice were randomly assigned (n = 10/group) to groups that received either a (1) standard purified maintenance AIN-93G control diet (CON), (2) CON + 5% FOS (CON-FOS), (3) high-fat diet (HFD) of which 60% kcal was from fat, or (4) HFD + 5% FOS (HFD-FOS) for 10 weeks.
RESULTS: Mice fed an HFD exhibited reduced serum 25-hydroxycholecalciferol (25D) levels (p < 0.01) and a 70% decrease in the expression of colonic vitamin D receptor (Vdr) mRNA (p = 0.018) compared to the mice fed the CON. A 2-fold increase in colonic Vdr mRNA expression was observed in the mice fed the HFD-FOS compared to the HFD (p < 0.01), although the increased FOS did not alter the serum 25D levels in the HFD group. The mRNA and protein expression of colonic Toll-like receptor 4 (Tlr4) was downregulated in the HFD-FOS group compared to the HFD group, which was negatively correlated to colonic Vdr expression (r = -0.747; p < 0.001). Additionally, the addition of FOS resulted in a 44% reduction in circulating proinflammatory cytokine Interleukin-6 (IL-6) in the HFD group (p < 0.01). The observed upregulation of β-defensin 1 (p = 0.017) and zona-occluden 1 (Zo-1) mRNA expression in mice fed FOS and an HFD compared with the HFD group further suggests that FOS supplementation can improve epithelial barrier integrity in HFD-induced obese mice.
CONCLUSIONS: Our data suggest that FOS may be a potential dietary strategy for preventing obesity-induced complications.
METHODS: Therefore, 5-week-old male C57BL/6J mice were randomly assigned (n = 10/group) to groups that received either a (1) standard purified maintenance AIN-93G control diet (CON), (2) CON + 5% FOS (CON-FOS), (3) high-fat diet (HFD) of which 60% kcal was from fat, or (4) HFD + 5% FOS (HFD-FOS) for 10 weeks.
RESULTS: Mice fed an HFD exhibited reduced serum 25-hydroxycholecalciferol (25D) levels (p < 0.01) and a 70% decrease in the expression of colonic vitamin D receptor (Vdr) mRNA (p = 0.018) compared to the mice fed the CON. A 2-fold increase in colonic Vdr mRNA expression was observed in the mice fed the HFD-FOS compared to the HFD (p < 0.01), although the increased FOS did not alter the serum 25D levels in the HFD group. The mRNA and protein expression of colonic Toll-like receptor 4 (Tlr4) was downregulated in the HFD-FOS group compared to the HFD group, which was negatively correlated to colonic Vdr expression (r = -0.747; p < 0.001). Additionally, the addition of FOS resulted in a 44% reduction in circulating proinflammatory cytokine Interleukin-6 (IL-6) in the HFD group (p < 0.01). The observed upregulation of β-defensin 1 (p = 0.017) and zona-occluden 1 (Zo-1) mRNA expression in mice fed FOS and an HFD compared with the HFD group further suggests that FOS supplementation can improve epithelial barrier integrity in HFD-induced obese mice.
CONCLUSIONS: Our data suggest that FOS may be a potential dietary strategy for preventing obesity-induced complications.