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Cited by 1,163Gut microbiota and healthFatty Acid Research and HealthOral microbiology and periodontitis research

Dietary lipids, gut microbiota and lipid metabolism

Open access
Schoeler, Marc, Caesar, Robert·2019·Reviews in Endocrine and Metabolic Disorders
DOI 10.1007/s11154-019-09512-0PMC PMC6938793
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Abstract

The gut microbiota is a central regulator of host metabolism. The composition and function of the gut microbiota is dynamic and affected by diet properties such as the amount and composition of lipids. Hence, dietary lipids may influence host physiology through interaction with the gut microbiota. Lipids affect the gut microbiota both as substrates for bacterial metabolic processes, and by inhibiting bacterial growth by toxic influence. The gut microbiota has been shown to affect lipid metabolism and lipid levels in blood and tissues, both in mice and humans. Furthermore, diseases linked to dyslipidemia, such as non-alcoholic liver disease and atherosclerosis, are associated with changes in gut microbiota profile. The influence of the gut microbiota on host lipid metabolism may be mediated through metabolites produced by the gut microbiota such as short-chain fatty acids, secondary bile acids and trimethylamine and by pro-inflammatory bacterially derived factors such as lipopolysaccharide. Here we will review the association between gut microbiota, dietary lipids and lipid metabolism

AI snapshot

Written from the paper’s full text.

TL;DR

This review synthesizes evidence that dietary lipids shape gut microbiota composition and function, while microbiota-derived metabolites influence host lipid metabolism and dyslipidemia-related disease. It highlights mechanistic mouse studies and human associations, but notes that specific fatty acid roles and long-term therapeutic benefits remain uncertain.

Key findings

  • Dietary fat amount and source alter gut microbiota in mice: lard-rich saturated fat versus fish oil n-3 PUFA was associated with lower phylogenetic diversity and lower *Akkermansia muciniphila*, *Lactobacillus*, and *Bifidobacterium*, plus reduced insulin sensitivity and increased white adipose tissue inflammation via TLR4; milk fat increased *Bilophila wadsworthia* and colitis in susceptible mice.
  • The microbiota affects host lipid handling: germ-free mice are protected against diet-induced obesity, and the microbiota increases circulating triglycerides, HDL, and total cholesterol in mice on a high-fat diet. In humans, low microbial gene richness is associated with higher total serum cholesterol and triglycerides and lower HDL; Fu et al. attributed 6% of serum triglyceride variance and 4% of HDL variance to gut microbiota composition.
  • Mechanisms include short-chain fatty acids signaling through GPR43/GPR41, bile acids acting via FXR/TGR5, LPS/TLR4 linking metabolic endotoxemia to dyslipidemia, NAFLD, and atherosclerosis, and TMA/TMAO associated with cardiovascular risk and atherosclerosis, though the TMAO role remains debated.
  • Clinical interventions show mixed evidence: a meta-analysis of 11 minor trials using fermented milk/probiotics reported beneficial serum lipid effects; a *Lactobacillus* meta-analysis improved total cholesterol and LDL but not triglycerides or HDL; a meta-analysis of 25 trials using pre-, pro-, or symbiotics reduced AST and ALT in NAFLD; obeticholic acid improved NASH after 72 weeks but raised serum LDL.

Methods

  • Narrative review; no primary experimental data are reported.
  • Synthesizes mechanistic mouse and gnotobiotic studies plus human observational, metagenomic, and clinical intervention studies on dietary lipids, gut microbiota, and lipid metabolism.
  • Main analysis is qualitative synthesis of cited literature; no systematic search strategy or formal meta-analysis is described.

Limitations

  • Stated: the role of specific fatty acids is not known; how lipids combine with other nutrients such as dietary fibers to affect the microbiota remains to be investigated; the diet–microbiota–dyslipidemia association needs study in large human cohorts; individual microbiota differences likely require patient stratification and individual-based therapies.
  • Stated: clinical studies targeting the microbiota for dyslipidemia and NAFLD are heterogeneous, with small cohorts and short intervention periods, so long-term benefits remain uncertain; prevention of atherosclerosis by microbiota modulation has not been studied in humans, and mouse data are conflicting.
  • Evident: as a narrative review, it lacks a systematic search and risk-of-bias assessment, and conclusions rely on studies with varying designs and inconsistent human findings.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1007/s11154-019-09512-0

Cites

143 of 143 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 49 cited sources checked · 0 supported · 0 flagged

  • Premisecitation

    The gut microbiota is a central regulator of host metabolism.

    “The gut microbiota is a central regulator of host metabolism.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [1] Sonnenburg JL, Backhed F. Diet-microbiota interactions as moderators of human metabolism. Nature. 2016;535(7610):56–64. https://doi.org/10.1038/nature18846 . source

      Not checked in the free run.

  • Premisenone given

    Microbial imbalance, sometimes termed dysbiosis, is associated with metabolic perturbations.

    “Microbial imbalance, sometimes termed dysbiosis, is associated with metabolic perturbations, and several studies have demonstrated a causal relationship between microbial function and metabolic perturbations.”
    Quote in the paperSubstantial claim
  • Premisecitation

    Diseases linked to dyslipidemia, such as non-alcoholic liver disease and atherosclerosis, are associated with changes in gut microbiota profile.

    “Furthermore, diseases linked to dyslipidemia, such as non-alcoholic liver disease and atherosclerosis, are associated with changes in gut microbiota profile.”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [40] Koren O, Spor A, Felin J, Fak F, Stombaugh J, Tremaroli V, et al. Human oral, gut, and plaque microbiota in patients with atherosclerosis. Proc Natl Acad Sci U S A. 2011;108(Suppl 1):4592–8. https://doi.org/10.1073/pnas.1011383107 . source

      Not checked in the free run.

    • cites [41] Karlsson FH, Fak F, Nookaew I, Tremaroli V, Fagerberg B, Petranovic D, et al. Symptomatic atherosclerosis is associated with an altered gut metagenome. Nat Commun. 2012;3:1245. https://doi.org/10.1038/ncomms2266 . source

      Not checked in the free run.

    • cites [43] Da Silva HE, Teterina A, Comelli EM, Taibi A, Arendt BM, Fischer SE, et al. Nonalcoholic fatty liver disease is associated with dysbiosis independent of body mass index and insulin resistance. Sci Rep. 2018;8(1):1466. https://doi.org/10.1038/s41598-018-19753-9 . source

      Not checked in the free run.

  • Premisenone given

    The composition and function of the gut microbiota is dynamic and affected by diet properties such as the amount and composition of lipids.

    “The composition and function of the gut microbiota is dynamic and affected by diet properties such as the amount and composition of lipids.”
    Quote in the paperSubstantial claim
  • Premisecitation

    The gut microbiota affects lipid metabolism and lipid levels in blood and tissues in mice and humans.

    “The gut microbiota has been shown to affect lipid metabolism and lipid levels in blood and tissues, both in mice and humans.”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [29] Backhed F, Manchester JK, Semenkovich CF, Gordon JI. Mechanisms underlying the resistance to diet-induced obesity in germ-free mice. Proc Natl Acad Sci U S A. 2007;104(3):979–84. https://doi.org/10.1073/pnas.0605374104 . source

      Not checked in the free run.

    • cites [31] Rabot S, Membrez M, Bruneau A, Gerard P, Harach T, Moser M, et al. Germ-free C57BL/6J mice are resistant to high-fat-diet-induced insulin resistance and have altered cholesterol metabolism. FASEB J. 2010:4948–59. https://doi.org/10.1096/fj.10-164921 . source

      Not checked in the free run.

    • cites [37] Cotillard A, Kennedy SP, Kong LC, Prifti E, Pons N, Le Chatelier E, et al. Dietary intervention impact on gut microbial gene richness. Nature. 2013;500(7464):585–8. https://doi.org/10.1038/nature12480 . source

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  • May combine two claims. 16
  • Classified as probably not a substantial claim. 2

  • May combine two claims.

    Premisecitation

    Lipids affect the gut microbiota both as substrates for bacterial metabolic processes and by inhibiting bacterial growth by toxic influence.

    “Lipids affect the gut microbiota both as substrates for bacterial metabolic processes, and by inhibiting bacterial growth by toxic influence.”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [14] Jackman JA, Yoon BK, Li D, Cho NJ. Nanotechnology Formulations for Antibacterial Free Fatty Acids and Monoglycerides. Molecules (Basel, Switzerland). 2016;21(3):305. https://doi.org/10.3390/molecules21030305 . source

      Not checked in the free run.

    • cites [15] Shilling M, Matt L, Rubin E, Visitacion MP, Haller NA, Grey SF, et al. Antimicrobial effects of virgin coconut oil and its medium-chain fatty acids on Clostridium difficile. Journal of medicinal food. 2013;16(12):1079–85. https://doi.org/10.1089/jmf.2012.0303 . source

      Not checked in the free run.

    • cites [16] Sheu CW, Freese E. Effects of fatty acids on growth and envelope proteins of Bacillus subtilis. J Bacteriol. 1972;111(2):516–24. source

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    Premisecitation

    Increased levels of B. wadsworthia were associated with a pro-inflammatory immune response and increased incidence of colitis in genetically susceptible mice.

    “The increased levels of B. wadsworthia were associated with a pro-inflammatory immune response and increased incidence of colitis in genetically susceptible mice.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [13] Devkota S, Wang Y, Musch MW, Leone V, Fehlner-Peach H, Nadimpalli A et al. Dietary-fat-induced taurocholic acid promotes pathobiont expansionand colitis in Il10-/- mice. Nature. 2012;487(7405):104-8. https://doi.org/10.1038/nature11225 . source

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  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Obesity is linked to dysregulation of lipid metabolism, which may result in abnormal levels of blood lipids, ectopic lipid deposition and associated metabolic diseases such as non-alcoholic liver disease and atherosclerosis.

    “Obesity is linked to dysregulation of lipid metabolism, which may result in abnormal levels of blood lipids, ectopic lipid deposition and associated metabolic diseases such as non-alcoholic liver disease (NAFLD) [8] and atherosclerosis [9].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [8] Katsiki N, Mikhailidis DP, Mantzoros CS. Non-alcoholic fatty liver disease and dyslipidemia: An update. Metabolism: clinical and experimental. 2016;65(8):1109–23. https://doi.org/10.1016/j.metabol.2016.05.003 . source

      Not checked in the free run.

    • cites [9] Grundy SM. Metabolic syndrome update. Trends Cardiovasc Med. 2016;26(4):364–73. https://doi.org/10.1016/j.tcm.2015.10.004 . source

      Not checked in the free run.

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    Premisecitation

    Dietary supplementation with saturated long-chain fatty acids, which were metabolized by and promoted growth of Lactobacillus, reversed alcohol-induced dysbiosis, stabilized the intestinal gut barrier, and reduced liver injury.

    “Dietary supplementation with saturated long-chain fatty acids, which were metabolized by and promoted growth of Lactobacillus, reversed alcohol-induced dysbiosis, stabilized the intestinal gut barrier, and reduced liver injury [18].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [18] Chen P, Torralba M, Tan J, Embree M, Zengler K, Starkel P, et al. Supplementation of saturated long-chain fatty acids maintains intestinal eubiosis and reduces ethanol-induced liver injury in mice. Gastroenterology. 2015;148(1):203–14.e16. https://doi.org/10.1053/j.gastro.2014.09.014 . source

      Not checked in the free run.

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    Premisecitation

    The lard diet reduced insulin sensitivity and increased inflammation in white adipose tissue through activation of Toll-like receptor 4 signaling.

    “The lard diet also reduced insulin sensitivity and increased inflammation in white adipose tissue (WAT) through activation of Toll-like receptor 4 (TLR4) signaling.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [10] Caesar R, Tremaroli V, Kovatcheva-Datchary P, Cani Patrice D, Bäckhed F. Crosstalk between Gut Microbiota and Dietary Lipids Aggravates WAT Inflammation through TLR Signaling. Cell Metabolism. 2015;22(4):658–68. https://doi.org/10.1016/j.cmet.2015.07.026 . source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisenone given

    Mechanistic links between lipid metabolism and microbial metabolites have been described in mouse models.

    “mechanistic links between lipid metabolism and microbial metabolites have been described in mouse models.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    The gut microbiota differs between mice fed diets that are high or low in fat and between diets that contain equal amounts of fat but from different sources.

    “The gut microbiota has been shown to differ between mice fed diets that are high or low in fat and between diets that contain equal amounts of fat but from different sources [10–13] (Fig. 1).”
    Quote in the paperSubstantial claim0 of 4 sources checked
    • cites [10] Caesar R, Tremaroli V, Kovatcheva-Datchary P, Cani Patrice D, Bäckhed F. Crosstalk between Gut Microbiota and Dietary Lipids Aggravates WAT Inflammation through TLR Signaling. Cell Metabolism. 2015;22(4):658–68. https://doi.org/10.1016/j.cmet.2015.07.026 . source

      Not checked in the free run.

    • cites [11] Just S, Mondot S, Ecker J, Wegner K, Rath E, Gau L, et al. The gut microbiota drives the impact of bile acids and fat source in diet on mouse metabolism. Microbiome. 2018;6(1):134. https://doi.org/10.1186/s40168-018-0510-8 . source

      Not checked in the free run.

    • cites [12] Lam YY, Ha CW, Hoffmann JM, Oscarsson J, Dinudom A, Mather TJ, et al. Effects of dietary fat profile on gut permeability and microbiota and their relationships with metabolic changes in mice. Obesity (Silver Spring). 2015;23(7):1429–39. https://doi.org/10.1002/oby.21122 . source

      Not checked in the free run.

    • cites [13] Devkota S, Wang Y, Musch MW, Leone V, Fehlner-Peach H, Nadimpalli A et al. Dietary-fat-induced taurocholic acid promotes pathobiont expansionand colitis in Il10-/- mice. Nature. 2012;487(7405):104-8. https://doi.org/10.1038/nature11225 . source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    In a study combining lard or palm oil with dietary bile acids, lard enhanced fat mass accumulation, impaired glucose tolerance, and elevated levels of hepatic triglycerides in conventionally raised but not germ-free mice when compared to palm oil.

    “In another study that combined lard or palm oil with dietary bile acids, lard enhanced fat mass accumulation, impaired glucose tolerance, and elevated levels of hepatic triglycerides in conventionally raised (CONV-R) but not in GF mice when compared to palm oil [11].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [11] Just S, Mondot S, Ecker J, Wegner K, Rath E, Gau L, et al. The gut microbiota drives the impact of bile acids and fat source in diet on mouse metabolism. Microbiome. 2018;6(1):134. https://doi.org/10.1186/s40168-018-0510-8 . source

      Not checked in the free run.

  • May combine two claims.

    Premisereasoning

    Dietary composition is central to the metabolic output of the gut microbiota because the gut microbiota processes dietary nutrients into metabolites and the diet affects the gut microbiota composition and thereby its metabolic potential and impact on the host.

    “Dietary composition is central to the metabolic output of the gut microbiota because: (1) the gut microbiota processes dietary nutrients into metabolites and (2) the diet affects the gut microbiota composition and thereby its metabolic potential and impact on the host.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    Diets with saturated fat or n-6 PUFA induced weight gain, but only saturated fat increased insulin resistance, colonic permeability, and mesenteric fat inflammation.

    “A comparison of mice on a variety of diets (low-fat diet and diets containing high levels of saturated fat, n-6 PUFA or n-3 PUFA) showed that diets with saturated fat or n-6 PUFA induced weight gain, but only saturated fat increased insulin resistance, colonic permeability, and mesenteric fat inflammation [12].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [12] Lam YY, Ha CW, Hoffmann JM, Oscarsson J, Dinudom A, Mather TJ, et al. Effects of dietary fat profile on gut permeability and microbiota and their relationships with metabolic changes in mice. Obesity (Silver Spring). 2015;23(7):1429–39. https://doi.org/10.1002/oby.21122 . source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Milk fat promoted taurine-conjugation of bile acids, which increases the availability of sulfur used by B. wadsworthia.

    “Milk fat promoted taurine-conjugation of bile acids, which increases the availability of sulfur used by B. wadsworthia.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [13] Devkota S, Wang Y, Musch MW, Leone V, Fehlner-Peach H, Nadimpalli A et al. Dietary-fat-induced taurocholic acid promotes pathobiont expansionand colitis in Il10-/- mice. Nature. 2012;487(7405):104-8. https://doi.org/10.1038/nature11225 . source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    In mice fed a high-fat high-cholesterol diet, Lactobacillus curvatus alone or together with Lactobacillus plantarum reduced cholesterol in plasma and liver and the two strains had a synergistic effect on hepatic triglycerides.

    “In mice fed a high-fat high-cholesterol diet, Lactobacillus curvatus alone or together with Lactobacillus plantarum reduced cholesterol in plasma and liver and the two strains had a synergistic effect on hepatic triglycerides [34].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [34] Yoo SR, Kim YJ, Park DY, Jung UJ, Jeon SM, Ahn YT, et al. Probiotics L. plantarum and L. curvatus in combination alter hepatic lipid metabolism and suppress diet-induced obesity. Obesity (Silver Spring). 2013;21(12):2571–8. https://doi.org/10.1002/oby.20428 . source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    The gut microbiota affects lipid composition in host tissues and serum and increases clearance of triglycerides from the circulation.

    “Furthermore, lipidomics analysis of GF and CONV-R mice fed a regular chow diet showed that the gut microbiota affects lipid composition in host tissues and serum and increases clearance of triglycerides from the circulation [30].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [30] Velagapudi VR, Hezaveh R, Reigstad CS, Gopalacharyulu P, Yetukuri L, Islam S, et al. The gut microbiota modulates host energy and lipid metabolism in mice. Journal of Lipid Research. 2010;51(5):1101–12. https://doi.org/10.1194/jlr.M002774 . source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    The gut microbiota induces hepatic production of monounsaturated fatty acids and elongation of PUFA, and acetate produced by the gut microbiota is used as precursor in hepatic fatty acid synthesis.

    “Comparisons between CONV-R and GF mice have also shown that the gut microbiota induces hepatic production of monounsaturated fatty acids and elongation of PUFA, and that acetate produced by the gut microbiota is used as precursor in hepatic fatty acid synthesis [32].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [32] Kindt A, Liebisch G, Clavel T, Haller D, Hormannsperger G, Yoon H, et al. The gut microbiota promotes hepatic fatty acid desaturation and elongation in mice. Nat Commun. 2018;9(1):3760. https://doi.org/10.1038/s41467-018-05767-4 . source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    10-hydroxy-cis-12-octadecenoic acid enhances intestinal barrier function and suppresses the development of colitis in mice in a free fatty acids 1 (FFR1/GPR40)-dependent manner.

    “10-hydroxy-cis-12-octadecenoic acid (HYA) enhances intestinal barrier function and suppresses the development of colitis in mice in a free fatty acids 1 (FFR1/GPR40)-dependent manner [27].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [27] Miyamoto J, Mizukure T, Park SB, Kishino S, Kimura I, Hirano K, et al. A gut microbial metabolite of linoleic acid, 10-hydroxy-cis-12-octadecenoic acid, ameliorates intestinal epithelial barrier impairment partially via GPR40-MEK-ERK pathway. J Biol Chem. 2015;290(5):2902–18. https://doi.org/10.1074/jbc.M114.610733 . source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    10-oxo-cis-12-octadecenoic acid increases adiponectin production and glucose uptake in a PPARγ-dependent manner, and contributes to the prevention of obesity-related metabolic perturbations.

    “Another hydroxylated CLA intermediate - 10-oxo-cis-12-octadecenoic acid (KetoA) - increases adiponectin production and glucose uptake in a PPARγ-dependent manner, and contributes to the prevention of obesity-related metabolic perturbations [28].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [28] Goto T, Kim YI, Furuzono T, Takahashi N, Yamakuni K, Yang HE, et al. 10-oxo-12(Z)-octadecenoic acid, a linoleic acid metabolite produced by gut lactic acid bacteria, potently activates PPARgamma and stimulates adipogenesis. Biochem Biophys Res Commun. 2015;459(4):597–603. https://doi.org/10.1016/j.bbrc.2015.02.154 . source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    The microbiota downregulates cholesterol biosynthesis and increased hepatic levels of cholesterol specifically in mice fed lard.

    “In another study where CONV-R and GF mice were fed lard or fish oil diet it was also found that the microbiota downregulates cholesterol biosynthesis and increased hepatic levels of cholesterol specifically in mice fed lard [33].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [33] Schedin-Weiss S, Caesar I, Winblad B, Blom H, Tjernberg LO. Super-resolution microscopy reveals gamma-secretase at both sides of the neuronal synapse. Acta Neuropathol Commun. 2016;4:29. https://doi.org/10.1186/s40478-016-0296-5 . source

      Not checked in the free run.

17 of 17

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • In dyslipidemia, there is less diversity of intestinal microbiota and a greater chance of dysbiosis, inflammation, and changes in intestinal permeability, with negative consequences for the health of the host.

    “In this sense, in the host, there is less diversity of intestinal microbiota and a greater chance of dysbiosis. That is, a greater chance of inflammation and changes in intestinal permeability is observed, with negative consequences for the health of the host (81).”

    From Kefir and Intestinal Microbiota Modulation: Implications in Human Health (2021) · cites this paper as [81]

    The section on gut microbiota and lipid metabolism links lower microbial gene richness to higher cholesterol and triglycerides, while the section on lipopolysaccharides, gut permeability and inflammation links dysbiosis, increased permeability and inflammation to high-fat-diet steatosis in mice. The paper does not establish that dyslipidemia generally entails reduced intestinal microbial diversity and an increased chance of all the stated outcomes in the host; those findings concern different measures and conditions. Page numbers were not available in our copy. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • In dyslipidemia, changes in the production of short-chain fatty acids and bile acids have been observed.

    “In dyslipidemia, changes in the production of short-chain fatty acids and bile acids have been observed.”

    From Kefir and Intestinal Microbiota Modulation: Implications in Human Health (2021) · cites this paper as [81]

    The Bile acids section (page unavailable) reports altered fecal bile acid composition in patients with NASH, a condition the paper discusses alongside dyslipidemia. The Short-chain fatty acids section describes how these acids are produced and affect lipid metabolism, but does not report observed changes in their production in dyslipidemia. Altered bile acid composition also does not establish altered bile acid production. (LLM, conf=0.78)

    Experimental — accuracy not yet measured

  • Both short-chain fatty acids and bile acids participate in lipid metabolism and intestinal microbiota change.

    “Both factors participate in lipid metabolism and intestinal microbiota change (81), indicating that modulation of intestinal microbiota may be a therapeutic alternative to prevent dyslipidemia.”

    From Kefir and Intestinal Microbiota Modulation: Implications in Human Health (2021) · cites this paper as [81]

    The Short-chain fatty acids section and Fig. 2 describe SCFAs as bacterial metabolites that regulate host lipid metabolism. The Bile acids section and the dietary-lipids interaction section link bile acids to lipid metabolism and a change in a gut bacterial population. Our copy does not establish that SCFAs themselves change intestinal microbiota composition; its discussion of fatty acids affecting that composition concerns dietary fatty acids. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

  • Modulation of intestinal microbiota may be a therapeutic alternative to prevent dyslipidemia.

    “Both factors participate in lipid metabolism and intestinal microbiota change (81), indicating that modulation of intestinal microbiota may be a therapeutic alternative to prevent dyslipidemia.”

    From Kefir and Intestinal Microbiota Modulation: Implications in Human Health (2021) · cites this paper as [81]

    The section on clinical interventions reports that microbiota-targeted approaches have improved serum lipid profiles, supporting their potential as a therapeutic approach. It discusses treatment rather than prevention of dyslipidemia, however, and says the long-term benefits of these interventions remain uncertain. The copy provides no page number for these passages. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • Short-chain fatty acids are metabolite substrates that participate in energy production, lipogenesis, gluconeogenesis, and cholesterol synthesis.

    “Short-chain fatty acids are metabolite substrates that participate in energy production, lipogenesis, gluconeogenesis, and cholesterol synthesis.”

    From Kefir and Intestinal Microbiota Modulation: Implications in Human Health (2021) · cites this paper as [81]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Reference 33 does not match the cited microbiota study

    Minor

    The text cites reference 33 for a comparison of gut microbiota and hepatic cholesterol in mice, but reference 33 is titled as a study of gamma-secretase at neuronal synapses.

  • Figure 2 misidentifies GPR41 as GPR43

    Minor

    The Figure 2 legend labels GPR41 as "GPR43(FFAR3)," while the main text identifies GPR41 as FFAR3 and GPR43 as FFAR2.

2 of 2

Cites

Flagged first, then by citations

Research works printed but not linked: 1

  1. Everard A, Geurts L, Caesar R, Van Hul M, Matamoros S, Duparc T, et al. Intestinal epithelial MyD88 is a sensor switching host metabolism towards obesity according to nutritional status. Nat Commun. 2014;5:5648. https://doi.org/10.1038/ncomms6648 . · DOI

Cited by

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Authors
Schoeler, M., & Caesar, R.
Affiliations
University of Gothenburg (SE)
Corresponding author
Caesar, Robert
ORCID
Venue
Reviews in Endocrine and Metabolic Disorders
Publisher
Springer Science and Business Media LLC
Published
2019-11-09
Volume
20
Issue
4
Pages
461-472
ISSN
  • 1389-9155 (ISSN-L)
  • 1573-2606
DOI
10.1007/s11154-019-09512-0
PMC
PMC6938793
OpenAlex
W2984669963
Semantic Scholar
33d17564819a1153e48abc717d44e12d7b246245
Cited by
1,163
References
143
Citations by year
2026: 132 · 2025: 230 · 2024: 240 · 2023: 202 · 2022: 197 · 2021: 122 · 2020: 39 · 2019: 1
FWCI
7.90
Type
journal article
Language
en
Open access
Licence
Locations
  • Reviews in Endocrine and Metabolic Disorders (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
Svenska Forskningsrådet Formas ((2017-02001)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
  • Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
  • Health Sciences › Dentistry › Periodontics › Oral microbiology and periodontitis research
Keywords
gut microbiota, dietary fat, lipid metabolism, dyslipidemia, non-alcoholic fatty liver disease, atherosclerosis, short-chain fatty acids, secondary bile acids, trimethylamine, lipopolysaccharide, bacterial metabolites, host-microbe interactions
MeSH terms
Gastrointestinal Microbiome, Animals, Bile Acids and Salts, Humans, Lipids, Methylamines, Lipid Metabolism

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