Reporting metabolomics data

Metabolomcis data should be published in a format that is reliable and useful. There are guidelines/SOPs to achieve this. Also, MetaMapp mapping and visualization essentially need data in standardized format. 

Below papers would give you an idea what must be included in the final data matrix before sending it out for publications. Check the supplement sections. 

http://www.nature.com/nbt/journal/v25/n8/full/nbt0807-846b.html MSI metabolomics standard initiative, 2007 

http://www.ncbi.nlm.nih.gov/pubmed/18269577 by O Fiehn, Quality controls in plant metabolomics. 2008

http://www.plantcell.org/content/23/7/2477.full  Recommendations for reporting metabolite profiling data. 2011. Plant Cell. 

These efforts are highly appreciated, but unless the Journal editors adopt it as an mandatory guideline, only a small number of labs will be reporting metabolomics data according to MSI guidelines. One of obstacles is having a really good mass spectrometer but not the right informatics that generate the MSI compliance data. But, MetaboAnalyst.ca and MetabolomeExpress  can significantly assist you to convert raw MS data into useful data matrices. 

Small molecule metabolome in the lung under acrolein-induced acute lung injury

Acrolein is a pulmonary irritant and its exposure can cause damage in lungs. Scientists from Pittsburgh university have published the metabolome of sensitive and resistant mice under acrolein exposure.

Abstract: 


Integrative metabolome and transcriptome profiling reveals discordant energetic stress between mouse strains with differential sensitivity to acrolein-induced acute lung injury.

Scope: This investigation sought to better understand the metabolic role of the lung and to generate insights into the pathogenesis of acrolein-induced acute lung injury. A respiratory irritant, acrolein is generated by overheating cooking oils or by domestic cooking using biomass fuels, and is in environmental tobacco smoke, a health hazard in the restaurant workplace. Methods and results: Using SM/J (sensitive) and 129X1/SvJ (resistant) inbred mouse strains, the lung metabolome was integrated with the transcriptome profile before and after acrolein exposure. A total of 280 small molecules were identified and mean values (log 2 >0.58 or <-0.58, p<0.05) were considered different for between-strain comparisons or within-strain responses to acrolein treatment. At baseline, 24 small molecules increased and 33 small molecules decreased in the SM/J mouse lung as compared to 129X1/SvJ mouse lung. Notable among the increased compounds was malonylcarnitine. Following acrolein exposure, several molecules indicative of glycolysis and branched chain amino acid metabolism increased similarly in both strains, whereas SM/J mice were less effective in generating metabolites related to fatty acid ß-oxidation. Conclusion: These findings suggest management of energetic stress varies between these strains, and that the ability to evoke auxiliary energy generating pathways rapidly and effectively may be critical in enhancing survival during acute lung injury in mice.

Comments

If you navigate through the network graphs below, the impact of acrolein can be observed on ROS scavenging mechanisms, supporting previously well established observation that acrolein causes damages in mitochonrial respiratory chain. Top network graph highlights the metabolic alterations why the mice is resistant, notice the abundance of carnitine and low level of many fatty acids. Graphs were created using 273 compounds, 7 compounds could not be mapped to any chemical structure in PubChem, database.

Metabolomic Profile of Hepatitis C Virus-Infected Hepatocytes

Abstract:- 
Hepatitis C virus (HCV) is capable of disrupting different facets of lipid metabolism and lipids have been shown to play a crucial role in the viral life cycle. The aim of this study was to examine the effect HCV infection has on the hepatocyte metabolome. Huh-7.5 cells were infected using virus produced by the HCV J6/JFH1 cell culture system and cells were harvested 24, 48, and 72-hours following infection. Metabolic profiling was performed using a non-targeted multiple platform methodology combining ultrahigh performance liquid chromatography/tandem mass spectrometry (UHPLC/MS/MS2) and gas chromatography/mass spectrometry (GC/MS). There was a significant increase in a number of metabolites involved in nucleotide synthesis and RNA replication during early HCV infection. NAD levels were also significantly increased along with several amino acids. A number of lipid metabolic pathways were disrupted by HCV infection, resulting in an increase in cholesterol and sphingolipid levels, altered phospholipid metabolism and a possible disruption in mitochondrial fatty acid transport. Fluctuations in 5'-methylthioadenosine levels were also noted, along with alterations in the glutathione synthesis pathway. These results highlight a number of previously unreported metabolic interactions and give a more in depth insight into the effect HCV has on host cell biochemical processes.

Comments:-

After mapping the data using chemical similarity distances (234 out of total 253 metabolites), it seems that on early HCV infection, the increase in many metabolites is less than 20%, which could be errors prone. There is no consistent effect on metabolome over the time series, early phase has different response than late phase. The most prevalent is decrease in organic acid and increase in fatty acids after 72 hours of infection. the highest fold change is 3.7.