Table 1.

Gut microbiota in relation to dyslipidemia.

Reference	Study Description	Subjects	Methods	Main Findings
Fu et al., 2015 [70]	Large cohort study	893 participants of the LifeLines-DEEP cohort	Lipid panels of total cholesterol, HDL-C, TGs, LDL-C. Sample genotyping. Fecal sample gut microbiota profiling with 16s rRNA gene sequencing. Operational taxonomic unit (OTU) picking and OTU richness. Microbial Shannon diversity index calculation. Cross validation analysis.	In total, 34 bacterial taxa correlated with plasma lipid levels and BMI. Specifically, family Clostridiaceae/Lachnospiracease was correlated with LDL. Coprococcus (Firmicutes) and Collinsella had strong correlation with TGs. Cross validation analysis revealed that GM explained ≤25.9% of HDL-C variance and that microbiota explained 6% of the variance in TGs.
Rebolledo et al., 2017 [71]	Case control study	30 hypercholesterolemic subjects, 27 controls with normal cholesterol levels	Anthropometric data. Serum fasting glucose and lipid profile. Stool sample analysis of GM by gel electrophoresis with denaturing gradient (DGGE) technique and nonmetric multidimensional scaling (NMDS). Shannon–Weaver, Simpson, and Richness microbial community diversity indices.	DGGE banding profiles differed between case and control, confirmed by 2 separate groups forming on NMDS scaling analysis. Significant (p < 0.05) decrease of all three bacterial DNA indices of microbial diversity.
Vojinovic et al., 2019 [72]	Prospective cohort study of two large cohorts.	2309 individuals from the Rotterdam and the LifeLines-DEEP cohort.	Fasting plasma metabolite profiling with 1H-nuclear magnetic resonance (NMR). Fecal sample gut microbiota profiling with 16s rRNA gene sequencing.	Significant (p < 0.05) associations between 18 families and genera of bacteria with VLDL of different sizes, 22 with HDL, 13 with HDL and VLDL, and 15 with serum triglycerides
Le Roy et al., 2019 [73]	Mouse study	Hypercholesterolemic female Apoe−/− and LDLr−/− mice	Depletion of all microbes in hypercholesterolemic mice with a combination of 4 antibiotics. Human feces intestinal microbiota transplantation. Further on mice: Plasma lipid and lipoprotein profile analysis. Bile acid synthesis measurement with labeled (14C) cholesterol dissolved in olive oil. Liver, ileum, and jejunum gene expression with qPCR. Sterol quantification in liver and bile. 16S rRNA gene sequencing of fecal gut microbiota.	Depletion of microbiota in mice raises cholesterol, mainly VLDL and LDL. Depletion also enhances liver uptake of cholesterol. Depletion increases cholesterol de novo synthesis by liver. Cholesterol level is transmissible in mice by microbiota transplantation from humans with altered cholesterol levels to microbiota depleted Apoe−/− mice.
Yun et al., 2020 [74]	Cross sectional study	1141 subjects from the Kangbuk Samsung Health Study in South Korea, divided into dyslipidemic (G0) and normal lipid (G1) groups based on total cholesterol, LDL-C, TG, HDL-C, ApoB and ApoA1 levels.	Anthropometric data. Blood sample after 10 h fasting of total cholesterol, triglycerides, LDL-C, HDL-C, and apoA1 (HDL particle component) and ApoB (LDL-C and other particle component) determination. Gut microbiota 16s rRNA gene sequencing of fecal sample.	The group with high TGs had lower alpha diversity indices (Shannon’s index and Faith’s phylogenetic diversity, both p < 0.001, Pielou’s evenness p < 0.030). Abnormally low ApoA1 group had higher alpha diversity. No association with alpha diversity for other lipid parameters. 12 taxa associated with TGs: The high TGs group had high amount of the genus Fusobacterium and low levels of Oscillospira, which produces butyrate (a SCFA) 10 and 6 taxa were associated with ApoA1 and ApoB levels, respectively.