Dietary Fructooligosaccharide Is Associated with Improved Insulin Resistance, Reduced Romboutsia ilealis Abundance, and Modulation of GLP-1 Production in High-Fat Diet-Induced Obese Mice
- 1Nutrition and Foods Program, School of Family and Consumer Sciences, College of Applied Arts, Texas State University, San Marcos, TX 78666, USA
Abstract
Background/Objectives: Obesity disrupts glucose homeostasis and insulin signaling, partly through altered gut hormone secretion and intestinal inflammation. Our previous work demonstrated that fructooligosaccharides (FOS), a prebiotic fiber, suppressed colonic inflammation, and modulated gut microbiota when administered with vitamin D supplementation. However, the effects of FOS on metabolic alterations, glucagon-like peptide-1 (GLP-1) production under obesogenic stimulation remains unclear. Here, we examined the effects of FOS on insulin resistance and GLP-1 production in high-fat diet (HFD)—induced obese mice. Methods: Six-week-old male and female C57BL/6J mice were assigned to control or HFDs ± 5% FOS for 10 weeks. Body weight, visceral fat, fasting glucose, insulin, triglycerides, and insulin resistance index (HOMA-IR) were assessed. Serum GLP-1 was quantified by ELISA. Colonic expressions of Glp1r, Pi3k, and Akt were evaluated by qRT-PCR and western blotting, respectively. Cecal abundance of Akkermansia muciniphila (AM), Dubosiella newyorkensis (DN), and Romboutsia ilealis (RI) was quantified by qPCR. Results: FOS attenuated HFD-induced metabolic dysfunction, lowering serum insulin and HOMA-IR in both sexes. Notably, FOS elicited sex-dependent physical improvements of which it suppressed body weight gain by 10% in male mice and reduced visceral fat accumulation by 36% in female mice. The phenotypic changes in male mice were associated with an increase in GLP-1. Further, FOS modulated colonic PI3K/Akt signaling in a sex-dependent manner and downregulated HFD-associated increases in Glp1r mRNA expression. Consistent with our previous work, FOS suppressed RI abundance, and this reduction was associated with lower colonic Tlr4 mRNA expression and improved insulin-resistance index. Conclusions: FOS improves insulin sensitivity in HFD-induced obesity and specifically enhanced GLP-1 production in male mice. Though the mechanism remained elucidated, the observed phenotype changes may be attributed to a combination of altered colonic PI3K/Akt pathways and targeted bacterial shifts. These effects appear to be sex-dependent and support FOS as a promising dietary strategy for maintenance of metabolic health.
Related
- Selinexor enhances temozolomide efficacy in glioblastoma through modulation of multiple resistance-associated mechanisms
- IL-16 production is a mechanism of resistance to BTK inhibitors and R-CHOP in lymphomas
- Nutritional Modulation of the Immuno–Biomineral Interface: From Vascular Calcification to a Hypothesis-Generating Framework for Tumor-Associated Biomineralization
- Differential Modulation of WNT/β‐Catenin Pathway‐Associated Molecular Responses by Palmitate and Oleate in Lipid‐Loaded HepG2 Cells
- Pre‐Exercise Conditioned Pain Modulation Is Associated With Exercise‐Induced Hypoalgesia in Patients With Painful Rotator Cuff Tears
BibTeX
@article{kamia2026dietary,
title = {{Dietary Fructooligosaccharide Is Associated with Improved Insulin Resistance, Reduced Romboutsia ilealis Abundance, and Modulation of GLP-1 Production in High-Fat Diet-Induced Obese Mice}},
author = {Lais Yuki Tuzino Kamia and Lauren Lewis and Zack Nobles and Gar Yee Koh},
journal = {Nutrients},
year = {2026},
month = oct,
doi = {10.3390/nu18193258},
url = {https://www.mdpi.com/2072-6643/18/19/3258},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Dietary Fructooligosaccharide Is Associated with Improved Insulin Resistance, Reduced Romboutsia ilealis Abundance, and Modulation of GLP-1 Production in High-Fat Diet-Induced Obese Mice
AU - Lais Yuki Tuzino Kamia
AU - Lauren Lewis
AU - Zack Nobles
AU - Gar Yee Koh
PY - 2026
DA - 2026/10/02
JO - Nutrients
DO - 10.3390/nu18193258
UR - https://www.mdpi.com/2072-6643/18/19/3258
AB - Background/Objectives: Obesity disrupts glucose homeostasis and insulin signaling, partly through altered gut hormone secretion and intestinal inflammation. Our previous work demonstrated that fructooligosaccharides (FOS), a prebiotic fiber, suppressed colonic inflammation, and modulated gut microbiota when administered with vitamin D supplementation. However, the effects of FOS on metabolic alterations, glucagon-like peptide-1 (GLP-1) production under obesogenic stimulation remains unclear. Here, we examined the effects of FOS on insulin resistance and GLP-1 production in high-fat diet (HFD)—induced obese mice. Methods: Six-week-old male and female C57BL/6J mice were assigned to control or HFDs ± 5% FOS for 10 weeks. Body weight, visceral fat, fasting glucose, insulin, triglycerides, and insulin resistance index (HOMA-IR) were assessed. Serum GLP-1 was quantified by ELISA. Colonic expressions of Glp1r, Pi3k, and Akt were evaluated by qRT-PCR and western blotting, respectively. Cecal abundance of Akkermansia muciniphila (AM), Dubosiella newyorkensis (DN), and Romboutsia ilealis (RI) was quantified by qPCR. Results: FOS attenuated HFD-induced metabolic dysfunction, lowering serum insulin and HOMA-IR in both sexes. Notably, FOS elicited sex-dependent physical improvements of which it suppressed body weight gain by 10% in male mice and reduced visceral fat accumulation by 36% in female mice. The phenotypic changes in male mice were associated with an increase in GLP-1. Further, FOS modulated colonic PI3K/Akt signaling in a sex-dependent manner and downregulated HFD-associated increases in Glp1r mRNA expression. Consistent with our previous work, FOS suppressed RI abundance, and this reduction was associated with lower colonic Tlr4 mRNA expression and improved insulin-resistance index. Conclusions: FOS improves insulin sensitivity in HFD-induced obesity and specifically enhanced GLP-1 production in male mice. Though the mechanism remained elucidated, the observed phenotype changes may be attributed to a combination of altered colonic PI3K/Akt pathways and targeted bacterial shifts. These effects appear to be sex-dependent and support FOS as a promising dietary strategy for maintenance of metabolic health.
SN - 2072-6643
ER -