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This research examines how a fructo-oligosaccharide and sea buckthorn complex influences glucose and lipid metabolism in type 2 diabetic rats.

April 26, 2026Food & Function0 citationsOpen Access

A fructo-oligosaccharide and sea buckthorn complex ameliorates glucose and lipid metabolism in type 2 diabetic (T2DM) rats via metabolic and anti-inflammatory pathways

LCL ChenGuangzhou University HLHualin LiuZhongshan Hospital YCYanwu ChenZhongshan Hospital

Key Points

This research examines how a fructo-oligosaccharide and sea buckthorn complex influences glucose and lipid metabolism in type 2 diabetic rats.
Induced T2DM in rats via a high-fat diet and alloxan administration.
Utilized zebrafish experiments to verify hypoglycemic and hypolipidemic effects.
Conducted 16S rDNA sequencing and transcriptomic analysis to assess gut microbiota and gene expression.
FS significantly reduced fasting blood glucose, triglycerides, total cholesterol, and LDL-C.
16S rDNA sequencing indicated gut microbiota reshaping with enrichment of beneficial genera.
Transcriptomic analysis showed reversal of inflammation and metabolism-related gene expression.

Abstract

This study investigated the effects and underlying mechanisms of a fructo-oligosaccharide (FOS) and sea buckthorn complex (FS) on blood glucose and lipid metabolism in type 2 diabetic mellitus (T2DM) rats. The T2DM model was induced by a high-fat diet (HFD) combined with alloxan administration. Prior to rat experiments, the synergistic hypoglycemic and hypolipidemic effects of FOS and sea buckthorn have been verified by zebrafish experiments. FS intervention significantly reduced fasting blood glucose, triglycerides (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) in rats, although high-density lipoprotein cholesterol (HDL-C) showed a non-significant increasing trend. 16S rDNA sequencing revealed that FS significantly reshaped gut microbiota; it enriched beneficial genera (e.g., Akkermansia, Bifidobacterium) and suppressed inflammation-associated taxa (e.g., Escherichia-Shigella). Transcriptomic analysis indicated that FS reversed aberrant expression of inflammation-related genes (e.g., Retnlg, Retnlb, Bmp2 in the colon) and metabolism-related genes (e.g., Gpam, Cpt1a in the liver), activating pathways including fat digestion and absorption and fatty acid metabolism, while inhibiting immune-inflammatory pathways (e.g., the "TNF signaling pathway", "Th17 cell differentiation"). Serum bile acid (BA) profiling showed FS modulated levels of primary and secondary BAs (e.g. CA, α-MCA, HDCA, GHDCA), restoring metabolic homeostasis. Pearson correlation analyses demonstrated robust associations among key microbiota, BAs, blood glucose/lipid indices, and farnesoid X receptor (FXR/Nr1h4) expression, supporting a regulatory network involving the gut-liver axis. This study elucidates the multi-target mechanisms by which FS ameliorates glucolipid metabolic disorders in T2DM, via gut microbiota remodeling, attenuation of intestinal/hepatic inflammation, and BA metabolism crosstalk, providing a theoretical basis for prebiotic-based precision nutrition.

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