Dietary intake of fructose increases purine de novo synthesis: A crucial mechanism for hyperuricemia

BackgroundFructose consumption is a potential risk factor for hyperuricemia because uric acid (UA) is a byproduct of fructose metabolism caused by the rapid consumption of adenosine triphosphate and accumulation of adenosine monophosphate (AMP) and other purine nucleotides. Additionally, a clinical experiment with four gout patients demonstrated that intravenous infusion of fructose increased the purine de novo synthesis rate, which implied fructose-induced hyperuricemia might be related to purine nucleotide synthesis. Moreover, the mechanistic (mammalian) target of rapamycin (mTOR) is a key protein both involved in fructose metabolism and purine de novo synthesis. The present study was conducted to elucidate how fructose influences mTOR and purine de novo synthesis in a hepatic cell line and livers of mice.Materials and methodsRNA-sequencing in NCTC 1469 cells treated with 0- and 25-mM fructose for 24 h and metabolomics analysis on the livers of mice fed with 0- and 30-g/kg fructose for 2 weeks were assessed. Gene and protein expression of phosphoribosyl pyrophosphate synthase (PRPSAP1), Glutamine PRPP aminotransferase (PPAT), adenyl succinate lyase (ADSL), adenyl succinate synthetase isozyme-1 (Adss1), inosine-5’-monophosphate dehydrogenase (IMPDH), and guanine monophosphate synthetase (GMPS) was measured. The location of PRPSAP1 and PPAT in the liver was assessed by an immunofluorescence assay.ResultsMetabolite profiling showed that the level of AMP, adenine, adenosine, hypoxanthine, and guanine was increased significantly. RNA-sequencing showed that gene expression of phosphoribosyl pyrophosphate synthase (PRPS2), phosphoribosyl glycinamide formyl transferase (GART), AICAR transformylase (ATIC), ADSL, Adss1, and IMPDH were raised, and gene expression of adenosine monophosphate deaminase 3 (AMPD3), adenosine deaminase (ADA), 5’,3’-nucleotidase, cytosolic (NT5C), and xanthine oxidoreductase (XOR) was also increased significantly. Fructose increased the gene expression, protein expression, and fluorescence intensity of PRPSAP1 and PPAT in mice livers by increasing mTOR expression. Fructose increased the expression and activity of XOR, decreased the expression of uricase, and increased the serum level of UA.ConclusionThis study demonstrated that the increased purine de novo synthesis may be a crucial mechanism for fructose-induced hyperuricemia. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Pengfei Zhang [verfasserIn] Huimin Sun [verfasserIn] Xinyu Cheng [verfasserIn] Yajing Li [verfasserIn] Yanli Zhao [verfasserIn] Wuxuan Mei [verfasserIn] Xing Wei [verfasserIn] Hairong Zhou [verfasserIn] Yunbo Du [verfasserIn] Changchun Zeng [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	purine de novo synthesis fructose hyperuricemia metabolomic analysis RNA-seq analysis

Übergeordnetes Werk:	In: Frontiers in Nutrition - Frontiers Media S.A., 2014, 9(2022)
Übergeordnetes Werk:	volume:9 ; year:2022

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fnut.2022.1045805

Katalog-ID:	DOAJ085139912

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520			\|a BackgroundFructose consumption is a potential risk factor for hyperuricemia because uric acid (UA) is a byproduct of fructose metabolism caused by the rapid consumption of adenosine triphosphate and accumulation of adenosine monophosphate (AMP) and other purine nucleotides. Additionally, a clinical experiment with four gout patients demonstrated that intravenous infusion of fructose increased the purine de novo synthesis rate, which implied fructose-induced hyperuricemia might be related to purine nucleotide synthesis. Moreover, the mechanistic (mammalian) target of rapamycin (mTOR) is a key protein both involved in fructose metabolism and purine de novo synthesis. The present study was conducted to elucidate how fructose influences mTOR and purine de novo synthesis in a hepatic cell line and livers of mice.Materials and methodsRNA-sequencing in NCTC 1469 cells treated with 0- and 25-mM fructose for 24 h and metabolomics analysis on the livers of mice fed with 0- and 30-g/kg fructose for 2 weeks were assessed. Gene and protein expression of phosphoribosyl pyrophosphate synthase (PRPSAP1), Glutamine PRPP aminotransferase (PPAT), adenyl succinate lyase (ADSL), adenyl succinate synthetase isozyme-1 (Adss1), inosine-5’-monophosphate dehydrogenase (IMPDH), and guanine monophosphate synthetase (GMPS) was measured. The location of PRPSAP1 and PPAT in the liver was assessed by an immunofluorescence assay.ResultsMetabolite profiling showed that the level of AMP, adenine, adenosine, hypoxanthine, and guanine was increased significantly. RNA-sequencing showed that gene expression of phosphoribosyl pyrophosphate synthase (PRPS2), phosphoribosyl glycinamide formyl transferase (GART), AICAR transformylase (ATIC), ADSL, Adss1, and IMPDH were raised, and gene expression of adenosine monophosphate deaminase 3 (AMPD3), adenosine deaminase (ADA), 5’,3’-nucleotidase, cytosolic (NT5C), and xanthine oxidoreductase (XOR) was also increased significantly. Fructose increased the gene expression, protein expression, and fluorescence intensity of PRPSAP1 and PPAT in mice livers by increasing mTOR expression. Fructose increased the expression and activity of XOR, decreased the expression of uricase, and increased the serum level of UA.ConclusionThis study demonstrated that the increased purine de novo synthesis may be a crucial mechanism for fructose-induced hyperuricemia.
650		4	\|a purine de novo synthesis
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allfields	10.3389/fnut.2022.1045805 doi (DE-627)DOAJ085139912 (DE-599)DOAJ4f6dec3072714fc7985b1c53b3c88767 DE-627 ger DE-627 rakwb eng TX341-641 Pengfei Zhang verfasserin aut Dietary intake of fructose increases purine de novo synthesis: A crucial mechanism for hyperuricemia 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier BackgroundFructose consumption is a potential risk factor for hyperuricemia because uric acid (UA) is a byproduct of fructose metabolism caused by the rapid consumption of adenosine triphosphate and accumulation of adenosine monophosphate (AMP) and other purine nucleotides. Additionally, a clinical experiment with four gout patients demonstrated that intravenous infusion of fructose increased the purine de novo synthesis rate, which implied fructose-induced hyperuricemia might be related to purine nucleotide synthesis. Moreover, the mechanistic (mammalian) target of rapamycin (mTOR) is a key protein both involved in fructose metabolism and purine de novo synthesis. The present study was conducted to elucidate how fructose influences mTOR and purine de novo synthesis in a hepatic cell line and livers of mice.Materials and methodsRNA-sequencing in NCTC 1469 cells treated with 0- and 25-mM fructose for 24 h and metabolomics analysis on the livers of mice fed with 0- and 30-g/kg fructose for 2 weeks were assessed. Gene and protein expression of phosphoribosyl pyrophosphate synthase (PRPSAP1), Glutamine PRPP aminotransferase (PPAT), adenyl succinate lyase (ADSL), adenyl succinate synthetase isozyme-1 (Adss1), inosine-5’-monophosphate dehydrogenase (IMPDH), and guanine monophosphate synthetase (GMPS) was measured. The location of PRPSAP1 and PPAT in the liver was assessed by an immunofluorescence assay.ResultsMetabolite profiling showed that the level of AMP, adenine, adenosine, hypoxanthine, and guanine was increased significantly. RNA-sequencing showed that gene expression of phosphoribosyl pyrophosphate synthase (PRPS2), phosphoribosyl glycinamide formyl transferase (GART), AICAR transformylase (ATIC), ADSL, Adss1, and IMPDH were raised, and gene expression of adenosine monophosphate deaminase 3 (AMPD3), adenosine deaminase (ADA), 5’,3’-nucleotidase, cytosolic (NT5C), and xanthine oxidoreductase (XOR) was also increased significantly. Fructose increased the gene expression, protein expression, and fluorescence intensity of PRPSAP1 and PPAT in mice livers by increasing mTOR expression. Fructose increased the expression and activity of XOR, decreased the expression of uricase, and increased the serum level of UA.ConclusionThis study demonstrated that the increased purine de novo synthesis may be a crucial mechanism for fructose-induced hyperuricemia. purine de novo synthesis fructose hyperuricemia metabolomic analysis RNA-seq analysis Nutrition. Foods and food supply Pengfei Zhang verfasserin aut Huimin Sun verfasserin aut Xinyu Cheng verfasserin aut Yajing Li verfasserin aut Yanli Zhao verfasserin aut Wuxuan Mei verfasserin aut Xing Wei verfasserin aut Hairong Zhou verfasserin aut Yunbo Du verfasserin aut Changchun Zeng verfasserin aut In Frontiers in Nutrition Frontiers Media S.A., 2014 9(2022) (DE-627)790231158 (DE-600)2776676-7 2296861X nnns volume:9 year:2022 https://doi.org/10.3389/fnut.2022.1045805 kostenfrei https://doaj.org/article/4f6dec3072714fc7985b1c53b3c88767 kostenfrei https://www.frontiersin.org/articles/10.3389/fnut.2022.1045805/full kostenfrei https://doaj.org/toc/2296-861X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4367 GBV_ILN_4700 AR 9 2022
spelling	10.3389/fnut.2022.1045805 doi (DE-627)DOAJ085139912 (DE-599)DOAJ4f6dec3072714fc7985b1c53b3c88767 DE-627 ger DE-627 rakwb eng TX341-641 Pengfei Zhang verfasserin aut Dietary intake of fructose increases purine de novo synthesis: A crucial mechanism for hyperuricemia 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier BackgroundFructose consumption is a potential risk factor for hyperuricemia because uric acid (UA) is a byproduct of fructose metabolism caused by the rapid consumption of adenosine triphosphate and accumulation of adenosine monophosphate (AMP) and other purine nucleotides. Additionally, a clinical experiment with four gout patients demonstrated that intravenous infusion of fructose increased the purine de novo synthesis rate, which implied fructose-induced hyperuricemia might be related to purine nucleotide synthesis. Moreover, the mechanistic (mammalian) target of rapamycin (mTOR) is a key protein both involved in fructose metabolism and purine de novo synthesis. The present study was conducted to elucidate how fructose influences mTOR and purine de novo synthesis in a hepatic cell line and livers of mice.Materials and methodsRNA-sequencing in NCTC 1469 cells treated with 0- and 25-mM fructose for 24 h and metabolomics analysis on the livers of mice fed with 0- and 30-g/kg fructose for 2 weeks were assessed. Gene and protein expression of phosphoribosyl pyrophosphate synthase (PRPSAP1), Glutamine PRPP aminotransferase (PPAT), adenyl succinate lyase (ADSL), adenyl succinate synthetase isozyme-1 (Adss1), inosine-5’-monophosphate dehydrogenase (IMPDH), and guanine monophosphate synthetase (GMPS) was measured. The location of PRPSAP1 and PPAT in the liver was assessed by an immunofluorescence assay.ResultsMetabolite profiling showed that the level of AMP, adenine, adenosine, hypoxanthine, and guanine was increased significantly. RNA-sequencing showed that gene expression of phosphoribosyl pyrophosphate synthase (PRPS2), phosphoribosyl glycinamide formyl transferase (GART), AICAR transformylase (ATIC), ADSL, Adss1, and IMPDH were raised, and gene expression of adenosine monophosphate deaminase 3 (AMPD3), adenosine deaminase (ADA), 5’,3’-nucleotidase, cytosolic (NT5C), and xanthine oxidoreductase (XOR) was also increased significantly. Fructose increased the gene expression, protein expression, and fluorescence intensity of PRPSAP1 and PPAT in mice livers by increasing mTOR expression. Fructose increased the expression and activity of XOR, decreased the expression of uricase, and increased the serum level of UA.ConclusionThis study demonstrated that the increased purine de novo synthesis may be a crucial mechanism for fructose-induced hyperuricemia. purine de novo synthesis fructose hyperuricemia metabolomic analysis RNA-seq analysis Nutrition. Foods and food supply Pengfei Zhang verfasserin aut Huimin Sun verfasserin aut Xinyu Cheng verfasserin aut Yajing Li verfasserin aut Yanli Zhao verfasserin aut Wuxuan Mei verfasserin aut Xing Wei verfasserin aut Hairong Zhou verfasserin aut Yunbo Du verfasserin aut Changchun Zeng verfasserin aut In Frontiers in Nutrition Frontiers Media S.A., 2014 9(2022) (DE-627)790231158 (DE-600)2776676-7 2296861X nnns volume:9 year:2022 https://doi.org/10.3389/fnut.2022.1045805 kostenfrei https://doaj.org/article/4f6dec3072714fc7985b1c53b3c88767 kostenfrei https://www.frontiersin.org/articles/10.3389/fnut.2022.1045805/full kostenfrei https://doaj.org/toc/2296-861X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4367 GBV_ILN_4700 AR 9 2022
allfields_unstemmed	10.3389/fnut.2022.1045805 doi (DE-627)DOAJ085139912 (DE-599)DOAJ4f6dec3072714fc7985b1c53b3c88767 DE-627 ger DE-627 rakwb eng TX341-641 Pengfei Zhang verfasserin aut Dietary intake of fructose increases purine de novo synthesis: A crucial mechanism for hyperuricemia 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier BackgroundFructose consumption is a potential risk factor for hyperuricemia because uric acid (UA) is a byproduct of fructose metabolism caused by the rapid consumption of adenosine triphosphate and accumulation of adenosine monophosphate (AMP) and other purine nucleotides. Additionally, a clinical experiment with four gout patients demonstrated that intravenous infusion of fructose increased the purine de novo synthesis rate, which implied fructose-induced hyperuricemia might be related to purine nucleotide synthesis. Moreover, the mechanistic (mammalian) target of rapamycin (mTOR) is a key protein both involved in fructose metabolism and purine de novo synthesis. The present study was conducted to elucidate how fructose influences mTOR and purine de novo synthesis in a hepatic cell line and livers of mice.Materials and methodsRNA-sequencing in NCTC 1469 cells treated with 0- and 25-mM fructose for 24 h and metabolomics analysis on the livers of mice fed with 0- and 30-g/kg fructose for 2 weeks were assessed. Gene and protein expression of phosphoribosyl pyrophosphate synthase (PRPSAP1), Glutamine PRPP aminotransferase (PPAT), adenyl succinate lyase (ADSL), adenyl succinate synthetase isozyme-1 (Adss1), inosine-5’-monophosphate dehydrogenase (IMPDH), and guanine monophosphate synthetase (GMPS) was measured. The location of PRPSAP1 and PPAT in the liver was assessed by an immunofluorescence assay.ResultsMetabolite profiling showed that the level of AMP, adenine, adenosine, hypoxanthine, and guanine was increased significantly. RNA-sequencing showed that gene expression of phosphoribosyl pyrophosphate synthase (PRPS2), phosphoribosyl glycinamide formyl transferase (GART), AICAR transformylase (ATIC), ADSL, Adss1, and IMPDH were raised, and gene expression of adenosine monophosphate deaminase 3 (AMPD3), adenosine deaminase (ADA), 5’,3’-nucleotidase, cytosolic (NT5C), and xanthine oxidoreductase (XOR) was also increased significantly. Fructose increased the gene expression, protein expression, and fluorescence intensity of PRPSAP1 and PPAT in mice livers by increasing mTOR expression. Fructose increased the expression and activity of XOR, decreased the expression of uricase, and increased the serum level of UA.ConclusionThis study demonstrated that the increased purine de novo synthesis may be a crucial mechanism for fructose-induced hyperuricemia. purine de novo synthesis fructose hyperuricemia metabolomic analysis RNA-seq analysis Nutrition. Foods and food supply Pengfei Zhang verfasserin aut Huimin Sun verfasserin aut Xinyu Cheng verfasserin aut Yajing Li verfasserin aut Yanli Zhao verfasserin aut Wuxuan Mei verfasserin aut Xing Wei verfasserin aut Hairong Zhou verfasserin aut Yunbo Du verfasserin aut Changchun Zeng verfasserin aut In Frontiers in Nutrition Frontiers Media S.A., 2014 9(2022) (DE-627)790231158 (DE-600)2776676-7 2296861X nnns volume:9 year:2022 https://doi.org/10.3389/fnut.2022.1045805 kostenfrei https://doaj.org/article/4f6dec3072714fc7985b1c53b3c88767 kostenfrei https://www.frontiersin.org/articles/10.3389/fnut.2022.1045805/full kostenfrei https://doaj.org/toc/2296-861X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4367 GBV_ILN_4700 AR 9 2022
allfieldsGer	10.3389/fnut.2022.1045805 doi (DE-627)DOAJ085139912 (DE-599)DOAJ4f6dec3072714fc7985b1c53b3c88767 DE-627 ger DE-627 rakwb eng TX341-641 Pengfei Zhang verfasserin aut Dietary intake of fructose increases purine de novo synthesis: A crucial mechanism for hyperuricemia 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier BackgroundFructose consumption is a potential risk factor for hyperuricemia because uric acid (UA) is a byproduct of fructose metabolism caused by the rapid consumption of adenosine triphosphate and accumulation of adenosine monophosphate (AMP) and other purine nucleotides. Additionally, a clinical experiment with four gout patients demonstrated that intravenous infusion of fructose increased the purine de novo synthesis rate, which implied fructose-induced hyperuricemia might be related to purine nucleotide synthesis. Moreover, the mechanistic (mammalian) target of rapamycin (mTOR) is a key protein both involved in fructose metabolism and purine de novo synthesis. The present study was conducted to elucidate how fructose influences mTOR and purine de novo synthesis in a hepatic cell line and livers of mice.Materials and methodsRNA-sequencing in NCTC 1469 cells treated with 0- and 25-mM fructose for 24 h and metabolomics analysis on the livers of mice fed with 0- and 30-g/kg fructose for 2 weeks were assessed. Gene and protein expression of phosphoribosyl pyrophosphate synthase (PRPSAP1), Glutamine PRPP aminotransferase (PPAT), adenyl succinate lyase (ADSL), adenyl succinate synthetase isozyme-1 (Adss1), inosine-5’-monophosphate dehydrogenase (IMPDH), and guanine monophosphate synthetase (GMPS) was measured. The location of PRPSAP1 and PPAT in the liver was assessed by an immunofluorescence assay.ResultsMetabolite profiling showed that the level of AMP, adenine, adenosine, hypoxanthine, and guanine was increased significantly. RNA-sequencing showed that gene expression of phosphoribosyl pyrophosphate synthase (PRPS2), phosphoribosyl glycinamide formyl transferase (GART), AICAR transformylase (ATIC), ADSL, Adss1, and IMPDH were raised, and gene expression of adenosine monophosphate deaminase 3 (AMPD3), adenosine deaminase (ADA), 5’,3’-nucleotidase, cytosolic (NT5C), and xanthine oxidoreductase (XOR) was also increased significantly. Fructose increased the gene expression, protein expression, and fluorescence intensity of PRPSAP1 and PPAT in mice livers by increasing mTOR expression. Fructose increased the expression and activity of XOR, decreased the expression of uricase, and increased the serum level of UA.ConclusionThis study demonstrated that the increased purine de novo synthesis may be a crucial mechanism for fructose-induced hyperuricemia. purine de novo synthesis fructose hyperuricemia metabolomic analysis RNA-seq analysis Nutrition. Foods and food supply Pengfei Zhang verfasserin aut Huimin Sun verfasserin aut Xinyu Cheng verfasserin aut Yajing Li verfasserin aut Yanli Zhao verfasserin aut Wuxuan Mei verfasserin aut Xing Wei verfasserin aut Hairong Zhou verfasserin aut Yunbo Du verfasserin aut Changchun Zeng verfasserin aut In Frontiers in Nutrition Frontiers Media S.A., 2014 9(2022) (DE-627)790231158 (DE-600)2776676-7 2296861X nnns volume:9 year:2022 https://doi.org/10.3389/fnut.2022.1045805 kostenfrei https://doaj.org/article/4f6dec3072714fc7985b1c53b3c88767 kostenfrei https://www.frontiersin.org/articles/10.3389/fnut.2022.1045805/full kostenfrei https://doaj.org/toc/2296-861X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4367 GBV_ILN_4700 AR 9 2022
allfieldsSound	10.3389/fnut.2022.1045805 doi (DE-627)DOAJ085139912 (DE-599)DOAJ4f6dec3072714fc7985b1c53b3c88767 DE-627 ger DE-627 rakwb eng TX341-641 Pengfei Zhang verfasserin aut Dietary intake of fructose increases purine de novo synthesis: A crucial mechanism for hyperuricemia 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier BackgroundFructose consumption is a potential risk factor for hyperuricemia because uric acid (UA) is a byproduct of fructose metabolism caused by the rapid consumption of adenosine triphosphate and accumulation of adenosine monophosphate (AMP) and other purine nucleotides. Additionally, a clinical experiment with four gout patients demonstrated that intravenous infusion of fructose increased the purine de novo synthesis rate, which implied fructose-induced hyperuricemia might be related to purine nucleotide synthesis. Moreover, the mechanistic (mammalian) target of rapamycin (mTOR) is a key protein both involved in fructose metabolism and purine de novo synthesis. The present study was conducted to elucidate how fructose influences mTOR and purine de novo synthesis in a hepatic cell line and livers of mice.Materials and methodsRNA-sequencing in NCTC 1469 cells treated with 0- and 25-mM fructose for 24 h and metabolomics analysis on the livers of mice fed with 0- and 30-g/kg fructose for 2 weeks were assessed. Gene and protein expression of phosphoribosyl pyrophosphate synthase (PRPSAP1), Glutamine PRPP aminotransferase (PPAT), adenyl succinate lyase (ADSL), adenyl succinate synthetase isozyme-1 (Adss1), inosine-5’-monophosphate dehydrogenase (IMPDH), and guanine monophosphate synthetase (GMPS) was measured. The location of PRPSAP1 and PPAT in the liver was assessed by an immunofluorescence assay.ResultsMetabolite profiling showed that the level of AMP, adenine, adenosine, hypoxanthine, and guanine was increased significantly. RNA-sequencing showed that gene expression of phosphoribosyl pyrophosphate synthase (PRPS2), phosphoribosyl glycinamide formyl transferase (GART), AICAR transformylase (ATIC), ADSL, Adss1, and IMPDH were raised, and gene expression of adenosine monophosphate deaminase 3 (AMPD3), adenosine deaminase (ADA), 5’,3’-nucleotidase, cytosolic (NT5C), and xanthine oxidoreductase (XOR) was also increased significantly. Fructose increased the gene expression, protein expression, and fluorescence intensity of PRPSAP1 and PPAT in mice livers by increasing mTOR expression. Fructose increased the expression and activity of XOR, decreased the expression of uricase, and increased the serum level of UA.ConclusionThis study demonstrated that the increased purine de novo synthesis may be a crucial mechanism for fructose-induced hyperuricemia. purine de novo synthesis fructose hyperuricemia metabolomic analysis RNA-seq analysis Nutrition. Foods and food supply Pengfei Zhang verfasserin aut Huimin Sun verfasserin aut Xinyu Cheng verfasserin aut Yajing Li verfasserin aut Yanli Zhao verfasserin aut Wuxuan Mei verfasserin aut Xing Wei verfasserin aut Hairong Zhou verfasserin aut Yunbo Du verfasserin aut Changchun Zeng verfasserin aut In Frontiers in Nutrition Frontiers Media S.A., 2014 9(2022) (DE-627)790231158 (DE-600)2776676-7 2296861X nnns volume:9 year:2022 https://doi.org/10.3389/fnut.2022.1045805 kostenfrei https://doaj.org/article/4f6dec3072714fc7985b1c53b3c88767 kostenfrei https://www.frontiersin.org/articles/10.3389/fnut.2022.1045805/full kostenfrei https://doaj.org/toc/2296-861X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4367 GBV_ILN_4700 AR 9 2022
language	English
source	In Frontiers in Nutrition 9(2022) volume:9 year:2022
sourceStr	In Frontiers in Nutrition 9(2022) volume:9 year:2022
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	purine de novo synthesis fructose hyperuricemia metabolomic analysis RNA-seq analysis Nutrition. Foods and food supply
isfreeaccess_bool	true
container_title	Frontiers in Nutrition
authorswithroles_txt_mv	Pengfei Zhang @@aut@@ Huimin Sun @@aut@@ Xinyu Cheng @@aut@@ Yajing Li @@aut@@ Yanli Zhao @@aut@@ Wuxuan Mei @@aut@@ Xing Wei @@aut@@ Hairong Zhou @@aut@@ Yunbo Du @@aut@@ Changchun Zeng @@aut@@
publishDateDaySort_date	2022-01-01T00:00:00Z
hierarchy_top_id	790231158
id	DOAJ085139912
language_de	englisch
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Additionally, a clinical experiment with four gout patients demonstrated that intravenous infusion of fructose increased the purine de novo synthesis rate, which implied fructose-induced hyperuricemia might be related to purine nucleotide synthesis. Moreover, the mechanistic (mammalian) target of rapamycin (mTOR) is a key protein both involved in fructose metabolism and purine de novo synthesis. The present study was conducted to elucidate how fructose influences mTOR and purine de novo synthesis in a hepatic cell line and livers of mice.Materials and methodsRNA-sequencing in NCTC 1469 cells treated with 0- and 25-mM fructose for 24 h and metabolomics analysis on the livers of mice fed with 0- and 30-g/kg fructose for 2 weeks were assessed. Gene and protein expression of phosphoribosyl pyrophosphate synthase (PRPSAP1), Glutamine PRPP aminotransferase (PPAT), adenyl succinate lyase (ADSL), adenyl succinate synthetase isozyme-1 (Adss1), inosine-5’-monophosphate dehydrogenase (IMPDH), and guanine monophosphate synthetase (GMPS) was measured. The location of PRPSAP1 and PPAT in the liver was assessed by an immunofluorescence assay.ResultsMetabolite profiling showed that the level of AMP, adenine, adenosine, hypoxanthine, and guanine was increased significantly. RNA-sequencing showed that gene expression of phosphoribosyl pyrophosphate synthase (PRPS2), phosphoribosyl glycinamide formyl transferase (GART), AICAR transformylase (ATIC), ADSL, Adss1, and IMPDH were raised, and gene expression of adenosine monophosphate deaminase 3 (AMPD3), adenosine deaminase (ADA), 5’,3’-nucleotidase, cytosolic (NT5C), and xanthine oxidoreductase (XOR) was also increased significantly. Fructose increased the gene expression, protein expression, and fluorescence intensity of PRPSAP1 and PPAT in mice livers by increasing mTOR expression. Fructose increased the expression and activity of XOR, decreased the expression of uricase, and increased the serum level of UA.ConclusionThis study demonstrated that the increased purine de novo synthesis may be a crucial mechanism for fructose-induced hyperuricemia.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">purine de novo synthesis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">fructose</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">hyperuricemia</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">metabolomic analysis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">RNA-seq analysis</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Nutrition. 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callnumber-first	T - Technology
author	Pengfei Zhang
spellingShingle	Pengfei Zhang misc TX341-641 misc purine de novo synthesis misc fructose misc hyperuricemia misc metabolomic analysis misc RNA-seq analysis misc Nutrition. Foods and food supply Dietary intake of fructose increases purine de novo synthesis: A crucial mechanism for hyperuricemia
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topic_title	TX341-641 Dietary intake of fructose increases purine de novo synthesis: A crucial mechanism for hyperuricemia purine de novo synthesis fructose hyperuricemia metabolomic analysis RNA-seq analysis
topic	misc TX341-641 misc purine de novo synthesis misc fructose misc hyperuricemia misc metabolomic analysis misc RNA-seq analysis misc Nutrition. Foods and food supply
topic_unstemmed	misc TX341-641 misc purine de novo synthesis misc fructose misc hyperuricemia misc metabolomic analysis misc RNA-seq analysis misc Nutrition. Foods and food supply
topic_browse	misc TX341-641 misc purine de novo synthesis misc fructose misc hyperuricemia misc metabolomic analysis misc RNA-seq analysis misc Nutrition. Foods and food supply
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title	Dietary intake of fructose increases purine de novo synthesis: A crucial mechanism for hyperuricemia
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title_full	Dietary intake of fructose increases purine de novo synthesis: A crucial mechanism for hyperuricemia
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author_browse	Pengfei Zhang Huimin Sun Xinyu Cheng Yajing Li Yanli Zhao Wuxuan Mei Xing Wei Hairong Zhou Yunbo Du Changchun Zeng
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title_sort	dietary intake of fructose increases purine de novo synthesis: a crucial mechanism for hyperuricemia
callnumber	TX341-641
title_auth	Dietary intake of fructose increases purine de novo synthesis: A crucial mechanism for hyperuricemia
abstract	BackgroundFructose consumption is a potential risk factor for hyperuricemia because uric acid (UA) is a byproduct of fructose metabolism caused by the rapid consumption of adenosine triphosphate and accumulation of adenosine monophosphate (AMP) and other purine nucleotides. Additionally, a clinical experiment with four gout patients demonstrated that intravenous infusion of fructose increased the purine de novo synthesis rate, which implied fructose-induced hyperuricemia might be related to purine nucleotide synthesis. Moreover, the mechanistic (mammalian) target of rapamycin (mTOR) is a key protein both involved in fructose metabolism and purine de novo synthesis. The present study was conducted to elucidate how fructose influences mTOR and purine de novo synthesis in a hepatic cell line and livers of mice.Materials and methodsRNA-sequencing in NCTC 1469 cells treated with 0- and 25-mM fructose for 24 h and metabolomics analysis on the livers of mice fed with 0- and 30-g/kg fructose for 2 weeks were assessed. Gene and protein expression of phosphoribosyl pyrophosphate synthase (PRPSAP1), Glutamine PRPP aminotransferase (PPAT), adenyl succinate lyase (ADSL), adenyl succinate synthetase isozyme-1 (Adss1), inosine-5’-monophosphate dehydrogenase (IMPDH), and guanine monophosphate synthetase (GMPS) was measured. The location of PRPSAP1 and PPAT in the liver was assessed by an immunofluorescence assay.ResultsMetabolite profiling showed that the level of AMP, adenine, adenosine, hypoxanthine, and guanine was increased significantly. RNA-sequencing showed that gene expression of phosphoribosyl pyrophosphate synthase (PRPS2), phosphoribosyl glycinamide formyl transferase (GART), AICAR transformylase (ATIC), ADSL, Adss1, and IMPDH were raised, and gene expression of adenosine monophosphate deaminase 3 (AMPD3), adenosine deaminase (ADA), 5’,3’-nucleotidase, cytosolic (NT5C), and xanthine oxidoreductase (XOR) was also increased significantly. Fructose increased the gene expression, protein expression, and fluorescence intensity of PRPSAP1 and PPAT in mice livers by increasing mTOR expression. Fructose increased the expression and activity of XOR, decreased the expression of uricase, and increased the serum level of UA.ConclusionThis study demonstrated that the increased purine de novo synthesis may be a crucial mechanism for fructose-induced hyperuricemia.
abstractGer	BackgroundFructose consumption is a potential risk factor for hyperuricemia because uric acid (UA) is a byproduct of fructose metabolism caused by the rapid consumption of adenosine triphosphate and accumulation of adenosine monophosphate (AMP) and other purine nucleotides. Additionally, a clinical experiment with four gout patients demonstrated that intravenous infusion of fructose increased the purine de novo synthesis rate, which implied fructose-induced hyperuricemia might be related to purine nucleotide synthesis. Moreover, the mechanistic (mammalian) target of rapamycin (mTOR) is a key protein both involved in fructose metabolism and purine de novo synthesis. The present study was conducted to elucidate how fructose influences mTOR and purine de novo synthesis in a hepatic cell line and livers of mice.Materials and methodsRNA-sequencing in NCTC 1469 cells treated with 0- and 25-mM fructose for 24 h and metabolomics analysis on the livers of mice fed with 0- and 30-g/kg fructose for 2 weeks were assessed. Gene and protein expression of phosphoribosyl pyrophosphate synthase (PRPSAP1), Glutamine PRPP aminotransferase (PPAT), adenyl succinate lyase (ADSL), adenyl succinate synthetase isozyme-1 (Adss1), inosine-5’-monophosphate dehydrogenase (IMPDH), and guanine monophosphate synthetase (GMPS) was measured. The location of PRPSAP1 and PPAT in the liver was assessed by an immunofluorescence assay.ResultsMetabolite profiling showed that the level of AMP, adenine, adenosine, hypoxanthine, and guanine was increased significantly. RNA-sequencing showed that gene expression of phosphoribosyl pyrophosphate synthase (PRPS2), phosphoribosyl glycinamide formyl transferase (GART), AICAR transformylase (ATIC), ADSL, Adss1, and IMPDH were raised, and gene expression of adenosine monophosphate deaminase 3 (AMPD3), adenosine deaminase (ADA), 5’,3’-nucleotidase, cytosolic (NT5C), and xanthine oxidoreductase (XOR) was also increased significantly. Fructose increased the gene expression, protein expression, and fluorescence intensity of PRPSAP1 and PPAT in mice livers by increasing mTOR expression. Fructose increased the expression and activity of XOR, decreased the expression of uricase, and increased the serum level of UA.ConclusionThis study demonstrated that the increased purine de novo synthesis may be a crucial mechanism for fructose-induced hyperuricemia.
abstract_unstemmed	BackgroundFructose consumption is a potential risk factor for hyperuricemia because uric acid (UA) is a byproduct of fructose metabolism caused by the rapid consumption of adenosine triphosphate and accumulation of adenosine monophosphate (AMP) and other purine nucleotides. Additionally, a clinical experiment with four gout patients demonstrated that intravenous infusion of fructose increased the purine de novo synthesis rate, which implied fructose-induced hyperuricemia might be related to purine nucleotide synthesis. Moreover, the mechanistic (mammalian) target of rapamycin (mTOR) is a key protein both involved in fructose metabolism and purine de novo synthesis. The present study was conducted to elucidate how fructose influences mTOR and purine de novo synthesis in a hepatic cell line and livers of mice.Materials and methodsRNA-sequencing in NCTC 1469 cells treated with 0- and 25-mM fructose for 24 h and metabolomics analysis on the livers of mice fed with 0- and 30-g/kg fructose for 2 weeks were assessed. Gene and protein expression of phosphoribosyl pyrophosphate synthase (PRPSAP1), Glutamine PRPP aminotransferase (PPAT), adenyl succinate lyase (ADSL), adenyl succinate synthetase isozyme-1 (Adss1), inosine-5’-monophosphate dehydrogenase (IMPDH), and guanine monophosphate synthetase (GMPS) was measured. The location of PRPSAP1 and PPAT in the liver was assessed by an immunofluorescence assay.ResultsMetabolite profiling showed that the level of AMP, adenine, adenosine, hypoxanthine, and guanine was increased significantly. RNA-sequencing showed that gene expression of phosphoribosyl pyrophosphate synthase (PRPS2), phosphoribosyl glycinamide formyl transferase (GART), AICAR transformylase (ATIC), ADSL, Adss1, and IMPDH were raised, and gene expression of adenosine monophosphate deaminase 3 (AMPD3), adenosine deaminase (ADA), 5’,3’-nucleotidase, cytosolic (NT5C), and xanthine oxidoreductase (XOR) was also increased significantly. Fructose increased the gene expression, protein expression, and fluorescence intensity of PRPSAP1 and PPAT in mice livers by increasing mTOR expression. Fructose increased the expression and activity of XOR, decreased the expression of uricase, and increased the serum level of UA.ConclusionThis study demonstrated that the increased purine de novo synthesis may be a crucial mechanism for fructose-induced hyperuricemia.
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title_short	Dietary intake of fructose increases purine de novo synthesis: A crucial mechanism for hyperuricemia
url	https://doi.org/10.3389/fnut.2022.1045805 https://doaj.org/article/4f6dec3072714fc7985b1c53b3c88767 https://www.frontiersin.org/articles/10.3389/fnut.2022.1045805/full https://doaj.org/toc/2296-861X
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