Stachyose combined with tea polyphenols mitigated metabolic disorders in high fructose diet-fed mice as studied by GC-MS metabolomics approach

Abstract

(2018) Stachyose combined with tea polyphenols mitigated metabolic disorders in high fructose diet-fed mice as studied by GC-MS metabolomics approach, CyTA -Journal of Food, 16:1,[516][517][518][519][520][521][522][523][524] To link to this article: https://doi.org/10. 1080/19476337.2017 High fructose (HF) ingestion is a common risk factor for the development of nonalcoholic fatty liver disease (NAFLD), which has become a serious health problem. The underlying mechanism of HFinduced NAFLD needs to be further understood and an effective prevention needs to be established urgently. Gas chromatography-mass spectrometer-based metabonomic method was employed to characterize the serum metabolic profile of HF-induced NAFLD in mice. β-Hydroxybutyric acid, elaidic acid and oleic acid that contributed to energy and lipid metabolism were confirmed as potential biomarkers for HF-induced NAFLD. With these changed metabolic pathways as possible drug targets, different administrations revealed that co-administration of stachyose and tea polyphenols was a more effective method than treatment of stachyose or tea polyphenols alone for preventing HF-induced negative changes of metabolic pathways in mice. These findings suggest that β-hydroxybutyric acid, elaidic acid and oleic acid are potential biomarkers in HF-induced NAFLD, and co-administration is a novel preventive strategy.Estaquiosa combinada con polifenoles de té para mitigar los trastornos metabólicos en ratones alimentados con una dieta alta en fructosa, estudio realizado mediante un enfoque metabolómico GC-MS RESUMEN La ingesta elevada de fructosa (HF) constituye un factor de riesgo común en el desarrollo de esteatohepatitis no alcohólica (NAFLD), padecimiento que se ha convertido en un problema de salud serio. El mecanismo subyacente de la NAFLD inducida por HF debe ser mejor comprendido, al tiempo que urge establecer mecanismos de prevención que resulten efectivos. En este sentido, para caracterizar el perfil metabólico del suero de ratones con NAFLD inducida por HF se utilizó el método metabolómico basado en GC-MS. Ello permitió constatar que los ácidos betahidroxibutírico, elaídico y oleico, que contribuyen al metabolismo energético y lipídico, son biomarcadores potenciales para la NAFLD inducida por el HF. A partir de la identificación de estas vías metabólicas alteradas como posibles dianas de los medicamentos, la administración diferenciada de sustancias (combinadas o por separado) reveló que, para prevenir los cambios negativos inducidos por la HF en las vías metabólicas de ratones, la coadministración de estaquiosa y polifenoles de té resultó ser un método más efectivo que el tratamiento con estaquiosa o con polifenoles de té por separado. Estos hallazgos sugieren que los ácidos betahidroxibutírico, elaídico y oleico son biomarcadores potenciales para la NAFLD inducida por HF y que la coadministración constituye una estrategia preventiva innovadora. ARTICLE HISTORY

Impact of a long‐term high‐fructose diet on systemic metabolic profiles of mice

“…Previous studies have shown that high fructose mainly affects lipid peroxidation, butanoate metabolism, and fatty acid biosynthesis and metabolism. 17,18 Although the regulatory roles of amino acids as important substrates involved in metabolic pathways have been reported previously, [23][24][25] the amino acid components found by these studies were inconsistent. In the present study, high fructose led to dramatic alterations in l-serine, glycine, threonine, l-valine, l-aspartic acid, l-glutamic acid, pyroglutamic acid, tyrosine, and l-phenylalanine, suggesting that high fructose intake promoted changes in amino acids components.…”

“…Under conditions of high fructose and increased maltose in starch and sucrose metabolism, d ‐glucose may facilitate the activation of glycine, serine, and threonine metabolism, before entering the TCA cycle via acetyl‐CoA. Previous studies have shown that high fructose mainly affects lipid peroxidation, butanoate metabolism, and fatty acid biosynthesis and metabolism 17,18 . Although the regulatory roles of amino acids as important substrates involved in metabolic pathways have been reported previously, 23–25 the amino acid components found by these studies were inconsistent.…”

“…The results suggested that β‐hydroxybutyric acid, elaidic acid, and oleic acid were underlying metabolites of high fructose‐induced NAFLD; thus, this combination treatment represented a promising strategy. 17 Moreover, targeted metabolomics analysis of serum samples from women consuming a high‐fructose diet revealed that high fructose intake in healthy women might lead to metabolic alterations in acylcarnitine and lysophosphatidylcholine via interruption of mitochondrial β‐oxidation and lipid peroxidation. 18 To the best of our knowledge, the majority of metabolomics studies on the effects of HFrD have focused on the analysis of urine and serum samples.…”

“…A previous study employed GC–MS metabolomics to identify the underlying metabolites of stachyose combined with tea polyphenols administrated as a treatment for HFrD‐induced NAFLD. The results suggested that β‐hydroxybutyric acid, elaidic acid, and oleic acid were underlying metabolites of high fructose‐induced NAFLD; thus, this combination treatment represented a promising strategy 17 . Moreover, targeted metabolomics analysis of serum samples from women consuming a high‐fructose diet revealed that high fructose intake in healthy women might lead to metabolic alterations in acylcarnitine and lysophosphatidylcholine via interruption of mitochondrial β‐oxidation and lipid peroxidation 18 .…”

Elaidic acid leads to mitochondrial dysfunction via mitochondria-associated membranes triggers disruption of mitochondrial calcium fluxes

“…Consumption of EA exacerbates hyperlipidemia and fatty liver change in zebrafish [6]. EA contributes to energy and lipid metabolism, and was confirmed as a potential biomarker for high fructose-induced nonalcoholic fatty liver disease (NAFLD) [7]. Studies have shown that EA causes apoptosis in a variety of cells [8][9][10], increased endoplasmic reticulum stress (ERS) and OS in diabetic mice [11], and activated NLRP3 inflammasome in macrophages [12], but its specific pathogenic mechanism in chronic diseases remains to be further studied.…”