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Alleviation of high-fat diet-induced lipid metabolism disorders: Role of quinoa peptides in inhibiting high-activity BSH-producing gut microbiota and modulating of BA-FXR/TGR5 signaling

ABSTRACT: Abstract Background: Lipid metabolism disorders contribute significantly to various metabolic diseases and are closely related to gut microbiota dysbiosis. Our previous study showed that oral gavage of quinoa peptides (QPep) restored gut microbiota composition and alleviated liver lipid metabolism disorders in high-fat diet (HFD)-induced obese mice. Nevertheless, the precise mechanisms are still not fully understood. This study aimed to clarify how QPep improve lipid metabolism disorders in HFD mice. Results: Oral gavage of QPep significantly attenuated HFD-induced metabolic disorders in mice, as evidenced by reduced body weight gain and adipose mass, improved serum lipid profiles, decreased hepatic lipid accumulation, and ameliorated impaired glucose homeostasis. The microbiota clearance and fecal microbiota transplantation experiments demonstrated that the beneficial effect of QPep on lipid metabolism disorders depends on the gut microbiota. QPep selectively suppressed gut bacteria that encode bile salt hydrolase (BSH), with high enzymatic activity, reducing intestinal BSH activity while preserving conjugated bile acids (BAs). These accumulated conjugated BAs served as natural FXR antagonists, inhibiting the ileal FXR-FGF15 signaling pathway and stimulating hepatic BAs synthesis by upregulating CYP7A1/CYP27A1. Concurrently, the altered BAs profile strongly activated TGR5 in epididymal white adipose and ileum tissues, reprogramming systemic lipid metabolism and alleviating metabolic disorders. Conclusions: This study reveals a novel mechanism by which bioactive peptides derived from quinoa protein ameliorate lipid metabolism disorders via gut microbiota-BAs crosstalk. These findings demonstrate the potential of quinoa peptides as functional ingredients for metabolic syndrome management and suggest a strategy for precise gut microbiota regulation through dietary interventions.

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse phase, Liquid Chromatography MS - positive - reverse phase

PROVIDER: MTBLS12584 | MetaboLights | 2025-06-16

REPOSITORIES: MetaboLights

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Project description:BACKGROUND: Intestinal bacteria are known to regulate the bile acid (BA) homeostasis via intestinal biotransformation of BAs and stimulating the expression of fibroblast growth factor 19 through intestinal nuclear farnesoid X receptor (FXR). On the other hand, BAs directly regulate the gut microbiota with their strong antimicrobial activities. It remains unclear, however, how mammalian BAs cross-talk with gut microbiome and shape microbial composition in a dynamic and interactive way.RESULTS: We quantitatively profiled small molecule metabolites derived from host-microbial co-metabolism in mice, demonstrating that Bas were the most significant factor correlated with microbial alterations among all types of endogenous metabolites. HFD intervention resulted in a rapid and significant increase in intestinal BA pool within 12 hrs followed by alteration in microbial composition at 24 hrs, providing supporting evidence that BAs are major dietary factors regulating gut microbiota. Feeding mice with BAs along with normal diet induced obese phenotype and obesity-associated gut microbial composition, similar to HFD fed mice. Finally, inhibition of hepatic BA biosynthesis under HFD conditions attenuated the HFD-induced gut microbiome alterations. Inhibition of BAs and direct suppression of micriobiota improved obese phenotypes.CONCLUSIONS: Our study highlights a liver - BAs - gut microbiome metabolic axis that drives significant modifications of BA and microbiota compositions capable of triggering metabolic disorders, suggesting new therapeutic strategies targeting BA metabolism for metabolic diseases. The untargeted metabolome profile assay for this study can be found in the MetaboLights study <a href='https://www.ebi.ac.uk/metabolights/MTBLS545' rel='noopener noreferrer' target='_blank'>MTBLS545</a>.The targeted bile acid analysis assay for this study can be found in the MetaboLights study <a href='https://www.ebi.ac.uk/metabolights/MTBLS547' rel='noopener noreferrer' target='_blank'>MTBLS547</a>.The targeted fatty acid analysis assay for this study can be found in the MetaboLights study <a href='https://www.ebi.ac.uk/metabolights/MTBLS548' rel='noopener noreferrer' target='_blank'>MTBLS548</a>.

Project description:BACKGROUND: Intestinal bacteria are known to regulate the bile acid (BA) homeostasis via intestinal biotransformation of BAs and stimulating the expression of fibroblast growth factor 19 through intestinal nuclear farnesoid X receptor (FXR). On the other hand, BAs directly regulate the gut microbiota with their strong antimicrobial activities. It remains unclear, however, how mammalian BAs cross-talk with gut microbiome and shape microbial composition in a dynamic and interactive way.RESULTS: We quantitatively profiled small molecule metabolites derived from host-microbial co-metabolism in mice, demonstrating that Bas were the most significant factor correlated with microbial alterations among all types of endogenous metabolites. HFD intervention resulted in a rapid and significant increase in intestinal BA pool within 12 hrs followed by alteration in microbial composition at 24 hrs, providing supporting evidence that BAs are major dietary factors regulating gut microbiota. Feeding mice with BAs along with normal diet induced obese phenotype and obesity-associated gut microbial composition, similar to HFD fed mice. Finally, inhibition of hepatic BA biosynthesis under HFD conditions attenuated the HFD-induced gut microbiome alterations. Inhibition of BAs and direct suppression of micriobiota improved obese phenotypes.CONCLUSIONS: Our study highlights a liver - BAs - gut microbiome metabolic axis that drives significant modifications of BA and microbiota compositions capable of triggering metabolic disorders, suggesting new therapeutic strategies targeting BA metabolism for metabolic diseases. The targeted short chain fatty acid analysis assay for this study can be found in the MetaboLights study <a href='https://www.ebi.ac.uk/metabolights/MTBLS546' rel='noopener noreferrer' target='_blank'>MTBLS546</a>.The targeted bile acid analysis assay for this study can be found in the MetaboLights study <a href='https://www.ebi.ac.uk/metabolights/MTBLS547' rel='noopener noreferrer' target='_blank'>MTBLS547</a>.The targeted fatty acid analysis assay for this study can be found in the MetaboLights study <a href='https://www.ebi.ac.uk/metabolights/MTBLS548' rel='noopener noreferrer' target='_blank'>MTBLS548</a>.

Project description:BACKGROUND: Intestinal bacteria are known to regulate the bile acid (BA) homeostasis via intestinal biotransformation of BAs and stimulating the expression of fibroblast growth factor 19 through intestinal nuclear farnesoid X receptor (FXR). On the other hand, BAs directly regulate the gut microbiota with their strong antimicrobial activities. It remains unclear, however, how mammalian BAs cross-talk with gut microbiome and shape microbial composition in a dynamic and interactive way.RESULTS: We quantitatively profiled small molecule metabolites derived from host-microbial co-metabolism in mice, demonstrating that Bas were the most significant factor correlated with microbial alterations among all types of endogenous metabolites. HFD intervention resulted in a rapid and significant increase in intestinal BA pool within 12 hrs followed by alteration in microbial composition at 24 hrs, providing supporting evidence that BAs are major dietary factors regulating gut microbiota. Feeding mice with BAs along with normal diet induced obese phenotype and obesity-associated gut microbial composition, similar to HFD fed mice. Finally, inhibition of hepatic BA biosynthesis under HFD conditions attenuated the HFD-induced gut microbiome alterations. Inhibition of BAs and direct suppression of micriobiota improved obese phenotypes.CONCLUSIONS: Our study highlights a liver - BAs - gut microbiome metabolic axis that drives significant modifications of BA and microbiota compositions capable of triggering metabolic disorders, suggesting new therapeutic strategies targeting BA metabolism for metabolic diseases. The untargeted metabolome profile assay for this study can be found in the MetaboLights study <a href='https://www.ebi.ac.uk/metabolights/MTBLS545' rel='noopener noreferrer' target='_blank'>MTBLS545</a>.The targeted short chain fatty acid analysis assay for this study can be found in the MetaboLights study <a href='https://www.ebi.ac.uk/metabolights/MTBLS546' rel='noopener noreferrer' target='_blank'>MTBLS546</a>.The targeted fatty acid analysis assay for this study can be found in the MetaboLights study <a href='https://www.ebi.ac.uk/metabolights/MTBLS548' rel='noopener noreferrer' target='_blank'>MTBLS548</a>.

Project description:BACKGROUND: Intestinal bacteria are known to regulate the bile acid (BA) homeostasis via intestinal biotransformation of BAs and stimulating the expression of fibroblast growth factor 19 through intestinal nuclear farnesoid X receptor (FXR). On the other hand, BAs directly regulate the gut microbiota with their strong antimicrobial activities. It remains unclear, however, how mammalian BAs cross-talk with gut microbiome and shape microbial composition in a dynamic and interactive way.RESULTS: We quantitatively profiled small molecule metabolites derived from host-microbial co-metabolism in mice, demonstrating that Bas were the most significant factor correlated with microbial alterations among all types of endogenous metabolites. HFD intervention resulted in a rapid and significant increase in intestinal BA pool within 12 hrs followed by alteration in microbial composition at 24 hrs, providing supporting evidence that BAs are major dietary factors regulating gut microbiota. Feeding mice with BAs along with normal diet induced obese phenotype and obesity-associated gut microbial composition, similar to HFD fed mice. Finally, inhibition of hepatic BA biosynthesis under HFD conditions attenuated the HFD-induced gut microbiome alterations. Inhibition of BAs and direct suppression of micriobiota improved obese phenotypes.CONCLUSIONS: Our study highlights a liver - BAs - gut microbiome metabolic axis that drives significant modifications of BA and microbiota compositions capable of triggering metabolic disorders, suggesting new therapeutic strategies targeting BA metabolism for metabolic diseases. The untargeted metabolome profile assay for this study can be found in the MetaboLights study <a href='https://www.ebi.ac.uk/metabolights/MTBLS545' rel='noopener noreferrer' target='_blank'>MTBLS545</a>.The targeted short chain fatty acid analysis assay for this study can be found in the MetaboLights study <a href='https://www.ebi.ac.uk/metabolights/MTBLS546' rel='noopener noreferrer' target='_blank'>MTBLS546</a>.The targeted bile acid analysis assay for this study can be found in the MetaboLights study <a href='https://www.ebi.ac.uk/metabolights/MTBLS547' rel='noopener noreferrer' target='_blank'>MTBLS547</a>.

			Action	DRS
	NEG.xlsx	Xlsx
	POS.xlsx	Xlsx
	negHFD1.raw	Raw
	negHFD2.raw	Raw
	negHFD3.raw	Raw

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Alleviation of high-fat diet-induced lipid metabolism disorders: Role of quinoa peptides in inhibiting high-activity BSH-producing gut microbiota and modulating of BA-FXR/TGR5 signaling

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