Dataset Information

Determination and comparison of SCFAs in serum and colon content samples: Alzheimer's disease rat as a case study (Method validation)

ABSTRACT:

SCFAs are the main microbial fermentation products from dietary fibers in colon and play a key role in keeping healthy in the whole-body. However, differences of SCFAs concentration in the serum and colon samples collected from rats had attracted few attentions. Here, we optimized the extract and analysis methods for quantification of ten SCFAs in both serum and colon content samples. Methanol and acetonitrile were chosen for extraction of SCFAs from serum and colon content samples, respectively. Biological samples collected from Alzheimer's disease rats treated by extract of Schisandra chinensis (Turcz.) Baill (SC-extract) were taken as research objects. The results showed that, the relative peak intensities of SCFAs in colon content from all groups were quite similar, and the trend was identical in serum samples. Compared with the values in human, the ratio of ten SCFAs in rat's colon was similar, while the percent of acetate in rat's serum was significantly higher. For therapy of AD, SC-extract decreased the concentration of butyrate, 3-Methyvalerate and caproate in serum samples towards the trend of normal rats. The present study may help to understand the transport of SCFAs across colonic epithelium in healthy and diseased organisms.

Method validation is reported in the current study MTBLS2146

SCFA serum and colon content determination is reported in study MTBLS2088

INSTRUMENT(S): Liquid Chromatography Tandem MS (LC-MS/MS)

SUBMITTER: Linxiu Guo

PROVIDER: MTBLS2146 | MetaboLights | 2020-11-24

REPOSITORIES: MetaboLights

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Dataset's files

Source:

			Action	DRS
	MTBLS2146	Other
	FILES	Other
	a_MTBLS2146_alzheimer_disease_scfa_metabolite_profiling_mass_spectrometry.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS2146_alzheimer_disease_scfa_metabolite_profiling_mass_spectrometry_v2_maf.tsv	Tabular

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Project description:Neonatal hypoxic-ischemic encephalopathy (HIE) refers to nervous system damage caused by perinatal hypoxia, which is the major cause of long-term neuro-developmental disorders in surviving infants. However, the mechanisms still require further investigation. In this study, we found that the butanoate metabolism pathway exhibited significantly decreased and short chain fatty acid (SCFAs)-producing bacteria, especially butyrate-producing bacteria, were significantly decreased in fecal of neonatal hypoxic-ischemic brain damage (HIBD) rats. Surprisingly, Sodium butyrate (SB) treatment could ameliorate pathological damage both in the cerebral cortex and hippocampus and facilitate recovery of SCFAs-producing bacteria related to metabolic pathways in neonatal HIBD rats. Moreover, we found that in samples from SB treatment neonatal HIBD rats cortex with high levels of butyrate acid along with aberrant key crotonyl-CoA-producing enzymes ACADS levels was observed compared HIBD rats. We also demonstrated that a decrease in histone 3-lysine 9-crotonylation (H3K9cr) downregulated expression of the HIE-related neurotrophic genes Bdnf, Gdnf, Cdnf, and Manf in HIBD rats. Furthermore, SB restored H3K9cr binding to HIE-related neurotrophic genes. Collectively, our results indicate that SB contributes to ameliorate pathological of HIBD by altering gut microbiota and brain SCFAs levels subsequently affecting histone crotonylation-mediated neurotrophic-related genes expression. This may be a novel microbiological approach for preventing and treating HIE. Brain tissue metabolomics is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS4894' rel='noopener noreferrer' target='_blank'>MTBLS4894</a>.Feces metabolomics is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS4893' rel='noopener noreferrer' target='_blank'>MTBLS4893</a>.

Project description:Neonatal hypoxic-ischemic encephalopathy (HIE) refers to nervous system damage caused by perinatal hypoxia, which is the major cause of long-term neuro-developmental disorders in surviving infants. However, the mechanisms still require further investigation. In this study, we found that the butanoate metabolism pathway exhibited significantly decreased and short chain fatty acid (SCFAs)-producing bacteria, especially butyrate-producing bacteria, were significantly decreased in fecal of neonatal hypoxic-ischemic brain damage (HIBD) rats. Surprisingly, Sodium butyrate (SB) treatment could ameliorate pathological damage both in the cerebral cortex and hippocampus and facilitate recovery of SCFAs-producing bacteria related to metabolic pathways in neonatal HIBD rats. Moreover, we found that in samples from SB treatment neonatal HIBD rats cortex with high levels of butyrate acid along with aberrant key crotonyl-CoA-producing enzymes ACADS levels was observed compared HIBD rats. We also demonstrated that a decrease in histone 3-lysine 9-crotonylation (H3K9cr) downregulated expression of the HIE-related neurotrophic genes Bdnf, Gdnf, Cdnf and Manf in HIBD rats. Furthermore, SB restored H3K9cr binding to HIE-related neurotrophic genes. Collectively, our results indicate that SB contributes to ameliorate pathological of HIBD by altering gut microbiota and brain SCFAs levels subsequently affecting histone crotonylation-mediated neurotrophic-related genes expression. This may be a novel microbiological approach for preventing and treating HIE. Targeted SCFA brain metabolomics is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS4933' rel='noopener noreferrer' target='_blank'>MTBLS4933</a>.Untargeted fecal metabolomics is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS4932' rel='noopener noreferrer' target='_blank'>MTBLS4932</a>.

Dataset Information

Determination and comparison of SCFAs in serum and colon content samples: Alzheimer's disease rat as a case study (Method validation)

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