Effects of fructooligosaccharide supplementation on metabolic parameters and intestinal morphology in high-fat diet-fed mice

Background: High-fat diet (HFD) is associated with metabolic dysfunction and intestinal alterations that may contribute to chronic low-grade inflammation. Fructooligosaccharides (FOS) are prebiotic fibers that can modulate host–microbiota interactions. We evaluated the effects of FOS on metabolic parameters and intestinal morphology in HFD-fed mice.

Methods: C57BL/6 mice received a normal diet (ND) or HFD and saline (SAL) or FOS, generating ND+SAL, ND+FOS, HFD+SAL and HFD+FOS groups. Body weight, fasting glucose, insulin, resistin, ghrelin, leptin, glucose-dependent insulinotropic polypeptide (GIP), and systolic arterial pressure were evaluated. Intestinal morphology was assessed by histology, focusing on epithelial features, Paneth cell granules and lamina propria cellularity.

Results: HFD+SAL animals showed increased body weight, fasting glucose, insulin, resistin and leptin compared with ND+SAL. FOS attenuated these alterations: body weight decreased from 46.16 ± 1.5 to 39.40 ± 2.0 g, fasting glucose from 174.7 ± 7.9 to 116.7 ± 4.2 mg/dL, and insulin from 494.8 ± 117.8 to 125.8 ± 43.1 pg/mL in HFD+SAL versus HFD+FOS. Histology showed rarefaction of eosinophilic Paneth cell granules in HFD+SAL, whereas HFD+FOS showed apparent preservation of these granules. Conversely, HFD+FOS frequently presented lipid-like material in the basal region of enterocytes and/or lamina propria, together with increased mononuclear cells morphologically compatible with plasma cells.

Conclusion: FOS attenuated HFD-associated metabolic alterations and was associated with distinct intestinal morphological changes. Preservation of Paneth cell granules suggests maintenance of intestinal antimicrobial secretory morphology, whereas lipid accumulation and altered lamina propria cellularity indicate intestinal remodeling rather than complete morphological normalization.

Reference: Am. J. Physiol. Endocrinol. Metab. (2020) 319:E779.