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Metabolic analysis and database mining strategy. A total of 324 metabolic genes were chosen from three systems: Hcy (119), glucose-related (95), and Lipid (66 for triglyceride and 44 for cholesterol metabolism) from the <t>NCBI</t> database. The mRNA expression patterns of these genes were analyzed across 21 human and 20 mouse organs using the NCBI Unigene <t>EST</t> database. Organs were categorized based on gene enrichment levels. Hcy metabolites were measured in 6 mouse organs (heart, liver, lung, kidney, spleen, and brain) using LC-ESI-MS/MS. Simple linear regression analysis was conducted to identify genes responsive to Hcy metabolites. The responsive genes were then utilized to identify corresponsive metabolic changes, construct protein-protein interaction networks, and identify organ-specific metabolic features related to Hcy metabolites. Finally, genetic-metabolic models were established for how Hcy metabolites contribute to metabolic reprogramming, crosstalk, and oxidative stress. Abbreviations: Hcy, homocysteine; SAH, S-adenosylhomocysteine; SAM, S-adenosylmethionine; HM, homocysteine-methionine; CH, cholesterol; TG, triglyceride.
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Metabolic analysis and database mining strategy. A total of 324 metabolic genes were chosen from three systems: Hcy (119), glucose-related (95), and Lipid (66 for triglyceride and 44 for cholesterol metabolism) from the NCBI database. The mRNA expression patterns of these genes were analyzed across 21 human and 20 mouse organs using the NCBI Unigene EST database. Organs were categorized based on gene enrichment levels. Hcy metabolites were measured in 6 mouse organs (heart, liver, lung, kidney, spleen, and brain) using LC-ESI-MS/MS. Simple linear regression analysis was conducted to identify genes responsive to Hcy metabolites. The responsive genes were then utilized to identify corresponsive metabolic changes, construct protein-protein interaction networks, and identify organ-specific metabolic features related to Hcy metabolites. Finally, genetic-metabolic models were established for how Hcy metabolites contribute to metabolic reprogramming, crosstalk, and oxidative stress. Abbreviations: Hcy, homocysteine; SAH, S-adenosylhomocysteine; SAM, S-adenosylmethionine; HM, homocysteine-methionine; CH, cholesterol; TG, triglyceride.

Journal: Redox Biology

Article Title: SAH is a major metabolic sensor mediating worsening metabolic crosstalk in metabolic syndrome

doi: 10.1016/j.redox.2024.103139

Figure Lengend Snippet: Metabolic analysis and database mining strategy. A total of 324 metabolic genes were chosen from three systems: Hcy (119), glucose-related (95), and Lipid (66 for triglyceride and 44 for cholesterol metabolism) from the NCBI database. The mRNA expression patterns of these genes were analyzed across 21 human and 20 mouse organs using the NCBI Unigene EST database. Organs were categorized based on gene enrichment levels. Hcy metabolites were measured in 6 mouse organs (heart, liver, lung, kidney, spleen, and brain) using LC-ESI-MS/MS. Simple linear regression analysis was conducted to identify genes responsive to Hcy metabolites. The responsive genes were then utilized to identify corresponsive metabolic changes, construct protein-protein interaction networks, and identify organ-specific metabolic features related to Hcy metabolites. Finally, genetic-metabolic models were established for how Hcy metabolites contribute to metabolic reprogramming, crosstalk, and oxidative stress. Abbreviations: Hcy, homocysteine; SAH, S-adenosylhomocysteine; SAM, S-adenosylmethionine; HM, homocysteine-methionine; CH, cholesterol; TG, triglyceride.

Article Snippet: The mRNA expression patterns of these genes were analyzed across 21 human and 20 mouse organs using the NCBI Unigene EST database.

Techniques: Expressing, Tandem Mass Spectroscopy, Construct