Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1
Brandon Flaig
 -- 1871 2023-01-24 01:21:48 |
2 update references and layout
Amina Yu
 -2 word(s) 1869 2023-01-29 03:19:25 |

Video Upload Options

We provide professional Video Production Services to translate complex research into visually appealing presentations. Would you like to try it?
No, upload directly Yes

Confirm

Are you sure to Delete?
Yes No
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Flaig, B.;  Garza, R.;  Singh, B.;  Hamamah, S.;  Covasa, M. Diet for Gut Microbiota and Dyslipidemia. Encyclopedia. Available online: https://encyclopedia.pub/entry/40491 (accessed on 28 November 2024).
Flaig B,  Garza R,  Singh B,  Hamamah S,  Covasa M. Diet for Gut Microbiota and Dyslipidemia. Encyclopedia. Available at: https://encyclopedia.pub/entry/40491. Accessed November 28, 2024.
Flaig, Brandon, Rachel Garza, Bhavdeep Singh, Sevag Hamamah, Mihai Covasa. "Diet for Gut Microbiota and Dyslipidemia" Encyclopedia, https://encyclopedia.pub/entry/40491 (accessed November 28, 2024).
Flaig, B.,  Garza, R.,  Singh, B.,  Hamamah, S., & Covasa, M. (2023, January 24). Diet for Gut Microbiota and Dyslipidemia. In Encyclopedia. https://encyclopedia.pub/entry/40491
Flaig, Brandon, et al. "Diet for Gut Microbiota and Dyslipidemia." Encyclopedia. Web. 24 January, 2023.
Diet for Gut Microbiota and Dyslipidemia
Edit
This entry is adapted from the peer-reviewed paper 10.3390/nu15010228

Diet is understood to be the most important determinant in shaping the microbiota ecosystem as balanced diets of fruits and vegetables are shown to increase gut bacterial richness and diversity. As such, lifestyle changes specifically through dietary interventions represent an effective therapeutic modality for dyslipidemia by creating targeted and beneficial changes in gut microbial composition. Although many dietary choices influence the composition of the gut microbiota, two particular diets have been studied extensively and can lead to significant, yet opposite effects. In this section, the metabolic changes seen in Western Diet (WD)-induced dyslipidemia followed by the role of plant-based diets was first described,  such as the Mediterranean diet (MD) play in optimizing gut microbial composition to restore defective metabolic states.

mediterranean diet prebiotics probiotics synbiotics folate fecal microbiota transplantation

1. High Fat Diet, Gut Microbiota and Dyslipidemia

High fat diets (HFD), such as the WD, are comprised by increased amounts of animal proteins, saturated fats and sugars, with low levels of fibers and phenols. Additionally, chronic HFD intake results in decreased total microbiota richness with a shift towards overgrowths of lipopolysaccharides (LPS) containing, Gram-negative enteric bacteria, which are shown to contribute to metabolic endotoxemia [1][2]. More specifically, elevated concentrations of circulating LPS induced by a chronic HFD facilitates increased binding to its receptor, Toll-like receptor 4 (TLR4), to activate innate and adaptive immunity triggering a pro-inflammatory cascade [3]. TLR4 activation has been implicated in the development of dyslipidemia and associated atherosclerosis, through enhanced release of pro-inflammatory cytokines like IL-8, IL-1beta and TNF-alpha [4]. Results here also showed TLR-4 mediated oxidation of low-density lipoproteins, which are known to accumulate in unstable plaques that deposit in the vasculature. As such, the combination of altered lipid metabolism as seen through increased LDL combined with LPS/TLR-4 mediated oxidization, worsens dyslipidemia leading to more severe associated clinical sequelae (Figure 1). It is also shown that lipoproteins, particularly HDL, has a protective effect against LPS-mediated metabolic endotoxemia by facilitating clearing of LPS from circulation [3]. Therefore, decreases in HDL and increases in relative concentrations of unfavorable Gram-negative bacteria resulting from HFD-induced dyslipidemia, further worsens hypercholesterolemic states through inability to clear excess LPS.
Nutrients 15 00228 g002 550
Figure 1. Effects of a High-Fat Diet and a Mediterranean Diet on Dyslipidemia and Atherosclerosis. (A) The High-Fat Diet is composed of large quantities of animal proteins, saturated fats and sugars with decreased fibers and phenols. HFD feeding increase Gram-negative bacteria Ruminococcus and Escherichia spp. while intestinal tight junction proteins occludin and claudin and microbial diversity are reduced. This leads to increased gut permeability, LPS enters the blood stream, resulting in metabolic endotoxemia. Lipopolysaccharides bind TLR-4 on circulating host cells to increase pro-inflammatory cytokines, increased inflammation and reactive oxygen species. Oxidized LDL builds up, causing plaques and increased risk of atherosclerosis. (B) The Mediterranean diet is rich in fibers and phenols, plant-based products, and omega-3 poly-unsaturated fatty acids. The MD increases Clostridium leptum and key genera Faecalibacterium, Lactobacillus, Dialister, Bacteroides, Dialister, Bacteroides and Blautia. It increases SCFA, while upregulating cholesterol and bile acid metabolism by increasing PPAR, CPT-1, FXR activity and decreasing SREBP-1 and FAS activity. This lead to decreased TNF-alpha, TLR4 activation, total cholesterol and LDL, increase HDL and supports intestinal barrier integrity. Less LDL builds up, lessening atherosclerosis and CAD risk. Abbreviations: LPS, Lipopolysaccharides; TLR4, Toll-like receptor 4; LDL, Low-density lipoprotein; IL, interleukin; TNF, Tumor necrosis factor; CAD, coronary artery disease; PUFA, poly-unsaturated fatty acids; PPAR, Peroxisome proliferator activated receptor; CPT-1, Carnitine palmitoyl transferase I; SREBP-1, sterol-regulatory element-binding protein 1; FAS, fatty-acid synthase; HDL, High-density lipoprotein.
Further, it has been shown that microbial species like Escherichia coli and Ruminococcus spp., that are elevated after HFD feeding, contribute to increased intestinal barrier permeability, allowing for LPS to translocate into the bloodstream and cause systemic low-grade inflammation characteristic of dyslipidemia [5]. In turn, high-fat diets and associated dyslipidemia chronically activate the NLRP3 inflammasome, which plays a role in inducing macrophage activity and release of proinflammatory cytokines like interleukin-1 (IL-1) [6]. In particular, sterol regulatory element binding protein 2 (SREBP-2), a transcription factor that facilitates lipogenesis, complexed with SREBP cleavage-activating protein (SCAP) contributes to NLRP3 inflammasome assembly [7]. This, in turn, affects cholesterol biosynthesis signaling with NLRP3 induced inflammation in macrophages. Excessive NLRP3-mediated release of proinflammatory cytokines has been associated with downregulation or decreased expression of the LDL-receptor [8]. The LDL-receptor has been shown to be downregulated in chronic high fat intake [9]. Taken together, these findings show how chronic high-fat diets can contribute to metabolic endotoxemia and dyslipidemia through upregulation of key pro-inflammatory factors including NLRP3.

2. Mediterranean Diet, Gut Microbiota and Dyslipidemia

The Mediterranean Diet (MD) consists of plant-based ingredients including wheats, cereals, nuts, fruits, vegetable, omega-3 polyunsaturated fatty acids, with high amounts of fibers and polyphenols [10]. Collectively, these ingredients have been shown to have beneficial effects on lipid imbalances through their antioxidant and anti-inflammatory effects [11][12] as shown via reduction in TNF-alpha and LPS concentrations [13][14]. Further, diets high in polyphenols, known as indigestible phytochemicals, that are abundant in plant-based foods, increase production of beneficial SCFAs because of their interaction with colonic microbiota [15]. For example, the polyphenol, resveratrol, specifically has been found to increase the SCFA-producing bacterial genera, Allobaculum, Bacterioides, and Blautia while also inhibiting TLR-4 [16][17][18]. Further, the rich plant-based MD increases fiber-derived SCFA by the gut microbiota, such as acetate, propionate, and butyrate [15] and has been shown to decrease total cholesterol and LDL cholesterol [19] (Figure 1). As described in the previous sections, SCFA exert a myriad of beneficial effects including attenuating the progression, or preventing against, the onset of dyslipidemia.
Several studies have shown that low carbohydrate (LC) diets significantly improve the Bacteroidetes/Firmicutes ratio, as well as important metabolic markers of dyslipidemia [20]. More specifically, the LC diet reduced fatty acids associated with de novo lipogenesis pathways, while increasing omega-3 PUFA that are shown to exert anti-inflammatory and anti-hypertriglyceridemia effects [21]. Importantly, microbiota changes after LC were also associated with increased HDL and decreased triglycerides. This is supported by findings showing that vegetable oils particularly omega-3 PUFA and phytonutrients, had beneficial effects on serum lipid profiles including HDL, TG, and apolipoprotein B in hypercholesterolemic patients [22]. Hypocholesterolemia has been associated with increased levels of Clostridium leptum, known to be involved in promoting increased cholesterol and bile acid metabolism [23]. Therefore, vegetable oils such as omega-3 PUFA, a key component of the MD has an important role in maintaining a healthy lipid balance.
Further, oatmeal, a food option within the umbrella of the MD, improve cardiometabolic parameters in patients with dyslipidemia through key changes in gut microbiota profile [24]. These changes include increased beneficial bacteria like Akkermansia along with SCFA-producing Faecalibacterum, Dialister, Lactobacillus, with decreases within the Rumminococcacae family. Akkermansia spp. are shown to improve metabolic parameters through reducing oxidative stress, reducing fat mass, insulin resistance and dyslipidemia in a rodent model [25][26]. Therefore, these findings of elevated Akkermansia and SCFA-producing bacterial species after oatmeal were associated with decreased total cholesterol and LDL with increased amounts of serum antioxidant capacity. Further, Sun et al. showed that oat-based foods (OF) rich in beta-glucans, when compared to high-fat diets (HFD) and control diets had significant reductions in plasma total cholesterol (TC), low-density lipoprotein (LDL), and triglycerides (TG), along with increased concentrations in several SCFAs including butyrate, propionate, and acetate [27]. Similarly, it has recently been shown that flavonoids, a component of whole-grain oat, regulates bile acid pathways to reduce hyperlipidemia induced by chronic HFD feeding [28]. Flavonoids upregulate expression of PPAR, carnitine palmitoyl transferase I (CPT-1) and FXR, while down-regulate SREBP-1 and fatty acid synthase (FAS). As mentioned, PPAR contributes to the breakdown of fatty acids via beta-oxidation by inducing CPT-1 activity while FXR regulates bile acid synthesis and transport by promoting efflux to feces to improve dyslipidemia. On the other hand, SREBP-1 induces lipogenesis in the liver and promotes fat storage in the form of triglycerides [29], therefore down-regulating this transcription factor is beneficial in states of dyslipidemia. Additionally, Akkermansia is increased in flavonoid treated mice, while unfavorable species associated with a HFD like Desulfovibrio was decreased. As such, Akkermansia can serve an important role in improving dyslipidemia not only through dietary interventions, but as a potential next-generation probiotic, discussed in a future subsection. Taken together, these findings provide strong evidence for MD as a lifestyle intervention that contributes to generalized and specific favorable changes in the gut microbiota composition to improve metabolic parameters.

3. Current Pharmacologic Treatments for Dyslipidemia and Relations to Gut Microbiota

Pharmacologic interventions of dyslipidemia may include inhibition of cholesterol synthesis, increasing use of cholesterol for bile acid production, or conversion of cholesterol in the gut to non-absorbable metabolites. Interestingly, the current pharmacological treatment modalities are associated with changes in gut microbiota, indicating the potential for synergistic effects of medications and targeted gut microbiota therapy for dyslipidemia.
Statin drugs are the first-line agents to reduce cholesterol synthesis by inhibition of HMG CoA Reductase. Use of statins has been demonstrated to improve the composition and function of gut microbiota [30] and has been associated with lower occurrence of gut microbiota dysbiosis [31]. For example, statin responsive patients showed increased concentrations of SCFA-producing genera including Lactobacillus, Eubacterium, Faecalibacterium and Bifidobacterium, all of which are characteristically decreased in dyslipidemia patients [32]. On the other hand, statin resistant patients did not exhibit similar changes. Further, other studies support the changes that statins can exert on gut microbiota, particularly elevations in Blautia and Bifidobacterium longum, which has specifically been correlated with decreased triglycerides and overall body weight [30]. As such, these combined findings suggest that response to statin treatment may, to some extent, be mediated or predicted by alterations in gut microbiota
Bile acid sequestering agents in the treatment of dyslipidemia are used to partially remove bile acids from enterohepatic cycling to increase use of cholesterol in the synthesis of new bile acids [33]. As mentioned earlier, bile acids have been shown to have favorable effects on gut microbiota. Therefore, it is possible that bile sequestering agents such as Cholestyramine, can mediate beneficial effects on dyslipidemia through changes in gut microbiota. For example, HFD and cholecystectomy mice treated with cholestyramine exhibit improved lipid profiles, beneficial effects on PPARδ and SREBP1 concentrations while concurrently elevating concentration of favorable gut bacteria including Blautia, Alistipes and Eubacterium [34]. It has also recently been shown that cholestyramine increased SCFA and enriched concentrations of SCFA-producing Lachnospiraceae spp. in treatment responsive groups [35]. More generally, cholestyramine increased the Bacteroidetes/Firmicutes ratio, indicating a shift towards a more favorable gut composition profile with overall reductions of inflammatory markers. These anti-inflammatory effects are supported by results showing that cholestyramine can reduce inflammatory signaling in HFD-induced mice [36]. Therefore, bile acid sequestrants are able to influence gut microbiota via bile acid-microbiota crosstalk to improve dyslipidemia, though more studies are needed to elucidate the specific mechanisms by which they do so.
Although not first-line for dyslipidemia treatment, metformin can also improve dyslipidemia in patients with T2DM through mechanisms that increase insulin sensitivity to reducing LDL and TG [37]. Recent findings have shown that metformin exerts favorable changes in gut microbiota, most notably through increases in Blautia and Faecalibacterium, which were associated with lipid homeostasis and improvements in serum triglyceride levels [38]. Further, metformin has been shown to increase concentrations of Akkermansia while improving total cholesterol levels in a rodent model of metabolic syndrome [39]. Therefore, these changes in gut microbiota can provide more insight into mechanisms by which pharmacological therapy can augment microbiota mediated pathways to exert their effects.

References

  1. Tomas, J.; Mulet, C.; Saffarian, A.; Cavin, J.B.; Ducroc, R.; Regnault, B.; Kun Tan, C.; Duszka, K.; Burcelin, R.; Wahli, W.; et al. High-fat diet modifies the PPAR-γ pathway leading to disruption of microbial and physiological ecosystem in murine small intestine. Proc. Natl. Acad. Sci. USA 2016, 113, E5934–E5943.
  2. Bailey, M.A.; Holscher, H.D. Microbiome-Mediated Effects of the Mediterranean Diet on Inflammation. Adv. Nutr. 2018, 9, 193–206.
  3. Määttä, A.M.; Salminen, A.; Pietiäinen, M.; Leskelä, J.; Palviainen, T.; Sattler, W.; Sinisalo, J.; Salomaa, V.; Kaprio, J.; Pussinen, P.J. Endotoxemia is associated with an adverse metabolic profile. Innate Immun. 2021, 27, 3–14.
  4. Gargiulo, S.; Gamba, P.; Testa, G.; Rossin, D.; Biasi, F.; Poli, G.; Leonarduzzi, G. Relation between TLR4/NF-κB signaling pathway activation by 27-hydroxycholesterol and 4-hydroxynonenal, and atherosclerotic plaque instability. Aging Cell 2015, 14, 569–581.
  5. Zhou, X.; Han, D.; Xu, R.; Li, S.; Wu, H.; Qu, C.; Wang, F.; Wang, X.; Zhao, Y. A model of metabolic syndrome and related diseases with intestinal endotoxemia in rats fed a high fat and high sucrose diet. PLoS ONE 2014, 9, e115148.
  6. Haneklaus, M.; O’Neill, L.A. NLRP3 at the interface of metabolism and inflammation. Immunol. Rev. 2015, 265, 53–62.
  7. Guo, C.; Chi, Z.; Jiang, D.; Xu, T.; Yu, W.; Wang, Z.; Chen, S.; Zhang, L.; Liu, Q.; Guo, X.; et al. Cholesterol Homeostatic Regulator SCAP-SREBP2 Integrates NLRP3 Inflammasome Activation and Cholesterol Biosynthetic Signaling in Macrophages. Immunity 2018, 49, 842–856.e847.
  8. Sun, R.; Peng, M.; Xu, P.; Huang, F.; Xie, Y.; Li, J.; Hong, Y.; Guo, H.; Liu, Q.; Zhu, W. Low-density lipoprotein receptor (LDLR) regulates NLRP3-mediated neuronal pyroptosis following cerebral ischemia/reperfusion injury. J. Neuroinflammation 2020, 17, 330.
  9. Chiu, S.; Williams, P.T.; Krauss, R.M. Effects of a very high saturated fat diet on LDL particles in adults with atherogenic dyslipidemia: A randomized controlled trial. PLoS ONE 2017, 12, e0170664.
  10. Hamamah, S.; Hajnal, A.; Covasa, M. Impact of Nutrition, Microbiota Transplant and Weight Loss Surgery on Dopaminergic Alterations in Parkinson’s Disease and Obesity. Int. J. Mol. Sci. 2022, 23, 7503.
  11. Rinott, E.; Meir, A.Y.; Tsaban, G.; Zelicha, H.; Kaplan, A.; Knights, D.; Tuohy, K.; Scholz, M.U.; Koren, O.; Stampfer, M.J.; et al. The effects of the Green-Mediterranean diet on cardiometabolic health are linked to gut microbiome modifications: A randomized controlled trial. Genome Med. 2022, 14, 29.
  12. Tosti, V.; Bertozzi, B.; Fontana, L. Health Benefits of the Mediterranean Diet: Metabolic and Molecular Mechanisms. J. Gerontol. A Biol. Sci. Med. Sci. 2018, 73, 318–326.
  13. Lopez-Moreno, J.; Garcia-Carpintero, S.; Gomez-Delgado, F.; Jimenez-Lucena, R.; Vals-Delgado, C.; Alcala-Diaz, J.F.; Roncero-Ramos, I.; Rangel-Zuñiga, O.A.; Yubero-Serrano, E.M.; Malagon, M.M.; et al. Endotoxemia is modulated by quantity and quality of dietary fat in older adults. Exp. Gerontol. 2018, 109, 119–125.
  14. Kenđel Jovanović, G.; Mrakovcic-Sutic, I.; Pavičić Žeželj, S.; Šuša, B.; Rahelić, D.; Klobučar Majanović, S. The Efficacy of an Energy-Restricted Anti-Inflammatory Diet for the Management of Obesity in Younger Adults. Nutrients 2020, 12, 3583.
  15. Feldman, F.; Koudoufio, M.; Desjardins, Y.; Spahis, S.; Delvin, E.; Levy, E. Efficacy of Polyphenols in the Management of Dyslipidemia: A Focus on Clinical Studies. Nutrients 2021, 13, 672.
  16. Juste, C.; Gérard, P. Cholesterol-to-Coprostanol Conversion by the Gut Microbiota: What We Know, Suspect, and Ignore. Microorganisms 2021, 9, 1881.
  17. Xue, Y.; Chen, H.; Zhang, S.; Bao, L.; Chen, B.; Gong, H.; Zhao, Y.; Qi, R. Resveratrol Confers Vascular Protection by Suppressing TLR4/Syk/NLRP3 Signaling in Oxidized Low-Density Lipoprotein-Activated Platelets. Oxid. Med. Cell. Longev. 2021, 2021, 8819231.
  18. Wang, P.; Ma, Y.; Wang, D.; Zhao, W.; Hu, X.; Chen, F.; Zhao, X. Protective Effects of Dietary Resveratrol against Chronic Low-Grade Inflammation Mediated through the Gut Microbiota in High-Fat Diet Mice. Nutrients 2022, 14, 1994.
  19. Ranaivo, H.; Thirion, F.; Béra-Maillet, C.; Guilly, S.; Simon, C.; Sothier, M.; Van Den Berghe, L.; Feugier-Favier, N.; Lambert-Porcheron, S.; Dussous, I.; et al. Increasing the diversity of dietary fibers in a daily-consumed bread modifies gut microbiota and metabolic profile in subjects at cardiometabolic risk. Gut Microbes 2022, 14, 2044722.
  20. Ma, Y.; Sun, Y.; Sun, L.; Liu, X.; Zeng, R.; Lin, X.; Li, Y. Effects of gut microbiota and fatty acid metabolism on dyslipidemia following weight-loss diets in women: Results from a randomized controlled trial. Clin. Nutr. 2021, 40, 5511–5520.
  21. Shibabaw, T. Omega-3 polyunsaturated fatty acids: Anti-inflammatory and anti-hypertriglyceridemia mechanisms in cardiovascular disease. Mol. Cell. Biochem. 2021, 476, 993–1003.
  22. Lim, R.R.X.; Park, M.A.; Wong, L.H.; Haldar, S.; Lim, K.J.; Nagarajan, N.; Henry, C.J.; Jiang, Y.R.; Moskvin, O.V. Gut microbiome responses to dietary intervention with hypocholesterolemic vegetable oils. NPJ Biofilms Microbiomes 2022, 8, 24.
  23. Raza, G.S.; Maukonen, J.; Makinen, M.; Niemi, P.; Niiranen, L.; Hibberd, A.A.; Poutanen, K.; Buchert, J.; Herzig, K.H. Hypocholesterolemic Effect of the Lignin-Rich Insoluble Residue of Brewer’s Spent Grain in Mice Fed a High-Fat Diet. J. Agric. Food Chem. 2019, 67, 1104–1114.
  24. Xu, D.; Pan, D.; Liu, H.; Yang, C.; Yang, X.; Wang, X.; Liu, F.; Feng, M.; Wu, Q.; Shen, Y.; et al. Improvement in cardiometabolic risk markers following an oatmeal diet is associated with gut microbiota in mildly hypercholesterolemic individuals. Food Res. Int. 2022, 160, 111701.
  25. Plovier, H.; Everard, A.; Druart, C.; Depommier, C.; Van Hul, M.; Geurts, L.; Chilloux, J.; Ottman, N.; Duparc, T.; Lichtenstein, L.; et al. A purified membrane protein from Akkermansia muciniphila or the pasteurized bacterium improves metabolism in obese and diabetic mice. Nat. Med. 2017, 23, 107–113.
  26. Lu, S.; Xu, S.; Chen, L.; Deng, Y.; Feng, J. Periplaneta americana Extract Pretreatment Alleviates Oxidative Stress and Inflammation and Increases the Abundance of Gut Akkermansia muciniphila in Diquat-Induced Mice. Antioxidants 2022, 11, 1806.
  27. Sun, N.X.; Tong, L.T.; Liang, T.T.; Wang, L.L.; Liu, L.Y.; Zhou, X.R.; Zhou, S.M. Effect of Oat and Tartary Buckwheat—Based Food on Cholesterol—Lowering and Gut Microbiota in Hypercholesterolemic Hamsters. J. Oleo Sci. 2019, 68, 251–259.
  28. Duan, R.; Guan, X.; Huang, K.; Zhang, Y.; Li, S.; Xia, J.; Shen, M. Flavonoids from Whole-Grain Oat Alleviated High-Fat Diet-Induced Hyperlipidemia via Regulating Bile Acid Metabolism and Gut Microbiota in Mice. J. Agric. Food Chem. 2021, 69, 7629–7640.
  29. Ito, M.; Nagasawa, M.; Omae, N.; Tsunoda, M.; Ishiyama, J.; Ide, T.; Akasaka, Y.; Murakami, K. A novel JNK2/SREBP-1c pathway involved in insulin-induced fatty acid synthesis in human adipocytes. J. Lipid Res. 2013, 54, 1531–1540.
  30. Hu, X.; Li, H.; Zhao, X.; Zhou, R.; Liu, H.; Sun, Y.; Fan, Y.; Shi, Y.; Qiao, S.; Liu, S.; et al. Multi-omics study reveals that statin therapy is associated with restoration of gut microbiota homeostasis and improvement in outcomes in patients with acute coronary syndrome. Theranostics 2021, 11, 5778–5793.
  31. Vieira-Silva, S.; Falony, G.; Belda, E.; Nielsen, T.; Aron-Wisnewsky, J.; Chakaroun, R.; Forslund, S.K.; Assmann, K.; Valles-Colomer, M.; Nguyen, T.T.D.; et al. Statin therapy is associated with lower prevalence of gut microbiota dysbiosis. Nature 2020, 581, 310–315.
  32. Sun, B.; Li, L.; Zhou, X. Comparative analysis of the gut microbiota in distinct statin response patients in East China. J. Microbiol. 2018, 56, 886–892.
  33. Jia, W.; Xie, G.; Jia, W. Bile acid-microbiota crosstalk in gastrointestinal inflammation and carcinogenesis. Nat. Rev. Gastroenterol. Hepatol. 2018, 15, 111–128.
  34. Park, S.; Zhang, T.; Yue, Y.; Wu, X. Effects of Bile Acid Modulation by Dietary Fat, Cholecystectomy, and Bile Acid Sequestrant on Energy, Glucose, and Lipid Metabolism and Gut Microbiota in Mice. Int. J. Mol. Sci. 2022, 23, 5935.
  35. Li, B.; Zhang, J.; Chen, Y.; Wang, Q.; Yan, L.; Wang, R.; Wei, Y.; You, Z.; Li, Y.; Miao, Q.; et al. Alterations in microbiota and their metabolites are associated with beneficial effects of bile acid sequestrant on icteric primary biliary Cholangitis. Gut Microbes 2021, 13, 1946366.
  36. Jena, P.K.; Setayesh, T.; Sheng, L.; Di Lucente, J.; Jin, L.W.; Wan, Y.Y. Intestinal Microbiota Remodeling Protects Mice from Western Diet-Induced Brain Inflammation and Cognitive Decline. Cells 2022, 11, 504.
  37. Lin, S.H.; Cheng, P.C.; Tu, S.T.; Hsu, S.R.; Cheng, Y.C.; Liu, Y.H. Effect of metformin monotherapy on serum lipid profile in statin-naïve individuals with newly diagnosed type 2 diabetes mellitus: A cohort study. PeerJ 2018, 6, e4578.
  38. Tong, X.; Xu, J.; Lian, F.; Yu, X.; Zhao, Y.; Xu, L.; Zhang, M.; Zhao, X.; Shen, J.; Wu , S.; et al. Structural Alteration of Gut Microbiota during the Amelioration of Human Type 2 Diabetes with Hyperlipidemia by Metformin and a Traditional Chinese Herbal Formula: A Multicenter, Randomized, Open Label Clinical Trial. mBio 2018, 9, e02392-e17.
  39. Ermolenko, E.; Simanenkova, A.; Voropaeva, L.; Lavrenova, N.; Kotyleva, M.; Minasian, S.; Chernikova, A.; Timkina, N.; Gladyshev, N.; Dmitriev, A.; et al. Metformin Influence on the Intestinal Microbiota and Organism of Rats with Metabolic Syndrome. Int. J. Mol. Sci. 2022, 23, 6837.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Upload a video for this entry
Information
Subjects: Nutrition & Dietetics
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Brandon Flaig
,
Rachel Garza
,
Bhavdeep Singh
,
Sevag Hamamah
,
Mihai Covasa
View Times: 733
Entry Collection: Gastrointestinal Disease
Revisions: 2 times (View History)
Update Date: 29 Jan 2023
Table of Contents
    1000/1000
    Hot Most Recent
    ScholarVision Creations
    Feedback