The American journal of clinical nutrition · 2026
Differential effects of stearic, palmitic and oleic acid enriched diets on gut microbiome, bile acid and cholesterol metabolism in mildly hypercholesterolemic post-menopausal females: A secondary analysis of a randomized controlled trial.
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Zhang Wen, Matuszek Gregory, Dolnikowski Gregory G, Lamon-Fava Stefania, Ausman Lynne M, Lichtenstein Alice H, Matthan Nirupa R
Аннотация
BACKGROUND: Stearic acid (18:0), a saturated fatty acid (SFA), does not raise plasma LDL cholesterol concentrations compared with palmitic acid (16:0), and has similar effects to oleic acid (18:1), but underlying mechanisms remain unclear.
OBJECTIVES: To determine if the hypocholesterolemic effects of dietary 18:0 and 18:1 relative to 16:0 are mediated by alterations in gut microbiome, bile acid (BA), and cholesterol metabolism.
METHODS: Secondary analysis of a randomized controlled crossover trial in mildly hypercholesterolemic postmenopausal females (n=17) who consumed isocaloric diets enriched in 18:0, 16:0 or 18:1 for 5-weeks each with 2-week washouts. Gut microbiome composition, plasma and fecal BA profiles, cholesterol absorption and synthesis markers, and related gene expression were assessed at the end of each dietary phase. Diet effects and multi-omics associations were evaluated using mixed-effects and multivariate models, accounting for repeated measures.
RESULTS: Fecal microbiome diversity was stable across diets, with modest species-level differences. Both 18:0 and 18:1 diets resulted in lower fasting total primary BAs (-159.1 (-313.0,-5.7), and -200.2 (-353.0,-47.7), mean difference (95% CI), respectively) and higher non-fasting unconjugated PBA concentrations (2.7 (1.1,6.4) and 2.4 (1.1,5.6), geometric mean ratio (95% CI), respectively) compared to the 16:0 diet. The 18:0 diet resulted in lower fecal secondary BAs compared to the 18:1 diet (-15.2 (-27.8, -2.6), mean difference (95% CI)) and higher non-fasting conjugated BAs compared to the 16:0 diet (1.4 (0.8,2.3) geometric mean ratio (95% CI)). FXR and SHP expression were 3-4 fold higher (p<0.01), and cholesterol synthesis:absorption ratio 22-24% lower, after both 18:0 and 18:1 compared to the 16:0 diet (p <0.05). Multi-omics analyses identified moderate-to-strong correlations (r = 0.43 to 0.72) among microbes, BAs, gene expression, cholesterol metabolism markers, and lipid profiles.
CONCLUSIONS: The cholesterol-lowering effects of 18:0 and 18:1 relative to 16:0 involved shared hepatic regulation of BA and cholesterol metabolism, while 18:0 uniquely modulated specific microbial taxa and BAs, suggestive of altered enterohepatic BA recycling.
CLINICAL TRIAL REGISTRY: https://clinicaltrials.gov/study/ NCT02145936.
OBJECTIVES: To determine if the hypocholesterolemic effects of dietary 18:0 and 18:1 relative to 16:0 are mediated by alterations in gut microbiome, bile acid (BA), and cholesterol metabolism.
METHODS: Secondary analysis of a randomized controlled crossover trial in mildly hypercholesterolemic postmenopausal females (n=17) who consumed isocaloric diets enriched in 18:0, 16:0 or 18:1 for 5-weeks each with 2-week washouts. Gut microbiome composition, plasma and fecal BA profiles, cholesterol absorption and synthesis markers, and related gene expression were assessed at the end of each dietary phase. Diet effects and multi-omics associations were evaluated using mixed-effects and multivariate models, accounting for repeated measures.
RESULTS: Fecal microbiome diversity was stable across diets, with modest species-level differences. Both 18:0 and 18:1 diets resulted in lower fasting total primary BAs (-159.1 (-313.0,-5.7), and -200.2 (-353.0,-47.7), mean difference (95% CI), respectively) and higher non-fasting unconjugated PBA concentrations (2.7 (1.1,6.4) and 2.4 (1.1,5.6), geometric mean ratio (95% CI), respectively) compared to the 16:0 diet. The 18:0 diet resulted in lower fecal secondary BAs compared to the 18:1 diet (-15.2 (-27.8, -2.6), mean difference (95% CI)) and higher non-fasting conjugated BAs compared to the 16:0 diet (1.4 (0.8,2.3) geometric mean ratio (95% CI)). FXR and SHP expression were 3-4 fold higher (p<0.01), and cholesterol synthesis:absorption ratio 22-24% lower, after both 18:0 and 18:1 compared to the 16:0 diet (p <0.05). Multi-omics analyses identified moderate-to-strong correlations (r = 0.43 to 0.72) among microbes, BAs, gene expression, cholesterol metabolism markers, and lipid profiles.
CONCLUSIONS: The cholesterol-lowering effects of 18:0 and 18:1 relative to 16:0 involved shared hepatic regulation of BA and cholesterol metabolism, while 18:0 uniquely modulated specific microbial taxa and BAs, suggestive of altered enterohepatic BA recycling.
CLINICAL TRIAL REGISTRY: https://clinicaltrials.gov/study/ NCT02145936.