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Dietary Intervention with Brown Top Millet Starch Ameliorates Dyslipidaemia and Gut Leakiness in High Fat Diet Fed Models

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Editor's note
Dietary resistant starches may repair the intestinal barrier damage caused by high-fat diets—a practical intervention point given how common such diets are and how difficult pharmacological approaches remain. This work extends existing evidence that specific carbohydrate sources modulate barrier function beyond caloric restriction alone, though the mechanism remains incompletely characterized. Gastroenterologists, metabolic specialists, and researchers studying obesity-related dysbiosis should assess whether these findings translate to human dietary guidance.

Source: openalex · Origin: IN · Ashish R. Chaudhari, Nandkishor R. Kotagale, Sandip Rahangdale · International Journal of Drug Delivery Technology · 2026-05-25

URL: https://doi.org/10.25258/ijddt.16.32s.54

AI rationale (4/5, tier: unclassified): Directly addresses gut barrier integrity and intestinal permeability in HFD models; mechanistic focus on leakiness aligns with corpus scope.

High-fat diet (HFD) consumption promotes obesity-associated hyperglycaemia, dyslipidaemia, metabolic inflexibility and impaired intestinal barrier integrity, highlighting the need for effective non-pharmacological dietary strategies. This study investigated whether brown top millet starch (BTMS) and Modified BTMS can mitigate HFD-induced metabolic derangements and gut leakiness in adult male Sprague–Dawley rats. BTMS was isolated by water steeping from authenticated millet seeds, purified to remove protein/lipid, and evaluated for amylase hydrolytic resistance using pancreatic α-amylase/amyloglucosidase digestion followed by GOPOD colorimetry. Rats (n=30) were fed normal pellet diet (NPD) or HFD for 8 weeks (n=15 each), then subdivided (n=5/group) for an additional 4 weeks to continue NPD or HFD alone, or to receive diets in which carbohydrate was replaced with purified unprocessed starch (HFDP/NPDP; 24 g/100 g diet) or modified starch (MHFD/MNPD). Body weight, food and water intake were monitored; fasting glycaemia and intraperitoneal glucose tolerance tests (2 g/kg) were performed on days 1, 57 and 85. Plasma/serum lipids (triglycerides, total cholesterol, LDL, HDL), short-chain fatty acids (SCFA), free fatty acids (FFA), glycerol and βhydroxybutyrate (BHB) were quantified using commercial assays; serum lipopolysaccharide-binding protein (LBP) and ileal tight-junction proteins (ZO-1, occludin) were measured by ELISA, and plasma corticosterone was assayed by HPLC. HFD produced significant weight gain with reduced water intake, hyperglycaemia and impaired glucose tolerance (e.g., Diet×Days effect for fasting glucose F(10,72)=28.1, P<0.001), dyslipidaemia (triglycerides, cholesterol and LDL increased; HDL decreased; all P<0.001), reduced SCFA with elevated glycerol, FFA and BHB (all P<0.001), and increased LBP with decreased ZO-1/occludin (all P<0.001). Modified BTMS (MHFD) significantly improved fasting and post-load glycaemia across time points, normalized lipid and metabolite profiles (increased SCFA; decreased glycerol/FFA/BHB), reduced LBP, and restored ZO-1 and occludin, whereas unprocessed starch showed limited glycaemic benefit (mainly at later GTT time points) and partial lipid improvement. These findings indicate that modified resistant (11.6 ± 0.8%) starch from brown top millet counteracts HFD-induced metabolic syndrome features and intestinal barrier dysfunction, supporting its potential as a dietary intervention to reduce HFD-related complications.

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Published 2026-05-28 · Last kit-update 2026-05-28