As an important contributor to  dietary protein, meat intake in human has a significant impact on a large  number of nutritional and health outcomes. The high consumption of meat in the  developed world is an important contributor to cardiovascular disease (CVD)  risk because of the large content of saturated fats and cholesterol in meat.  However, no association between dietary saturated fat intake and CVD was shown  in recent meta-analysis of prospective cohort studies. Therefore, it is  suggested that the cholesterol and saturated fat content of red meat may not be  sufficient to responsible for the increased CVD risk. This suspicion has  stimulated investigation of high salt content, or heterocyclic compounds  generated during cooking, which are alternative disease-promoting exposures responsible  for increased CVD risk. As a result numerous studies throughout the years, the  following metabolites are regarded as biomarkers of meat intake: creatinine,  creatine, carnitine, carnosine, taurine, 1-methylhistidine and  3-methylhistidine and TMAO. A recent study showed that in conjunction with  taurine and creatinine, 3-methylhistidine and 1-methylhistidine are also  regarded as biomarkers of meat intake.

As a trimethylamine and part of the  head group of phosphatidylcholine, metabolized by gut microbiota, choline converts  to trimethylamine (TMA). Catalyzed by hepatic flavinmonooxygenases, TMA is  rapidly oxidized to generate trimethylamine-N-oxide (TMAO), which is proatherogenic  and associated with cardiovascular risks. It is confirmed in a large cohort  that TMAO is a predictor of cardiovascular risk. It is also supposed that other  dietary nutrients with a trimethylamine structure may also generate TMAO from  gut microbiota and accelerate atherosclerosis. As a compound with trimethylamine  structure abundant in red meat, L-carnitine is another excellent substrate for  gut flora to produce TMA and then converts to TMAO. However, the specific  microbial species responsible for TMAO formation and mechanism of accelerated  atherosclerosis by TMAO remains unknown. The mechanism maybe that, by  increasing the expression of proatherogenic scavenger receptors CD36 and  scavenger receptor A on macrophage cell surface, TMAO inhibits reverse  cholesterol transport and induces foam cell formation. Two main bacterial phyla  among intestinal flora, Bacteroidetes and Firmicutes may  be associated with TMA formation. Therefore, alteration of gut flora  composition with microbial faecal transplantation may be an appealing approach  to prevent or inhibit atherosclerosis. In some studies, oral broad-spectrum  antibiotics are also administered in mice and humans have been investigated for  the same purpose to alter gut flora composition.

Creative Proteomics has established a  robust, reproducible and highly sensitive HPLC-MS platform for the simultaneous  quantification of meat markers.

Platform

• HPLC-MS

Summary

• Identification and  quantification of meat markers by HPLC-MS

Sample Requirement

• Normal Volume:  200ul plasma, 200 mg tissue, 2e7 cells
• Minimal Volume:  50ul plasma, 50 mg tissue, 5e6 cells

Report

• A detailed  technical report will be provided at the end of the whole project, including  the experiment procedure, MS/MS instrument parameters.
• Analytes are  reported as uM or ug/mg (tissue), and CV's are generally <10%.
• The name of the  analytes, abbreviation, formula, molecular weight and CAS# would also be  included in the report.

With integrated set of separation,  characterization, identification and quantification systems featured with  excellent robustness & reproducibility, high and ultra-sensitivity,  Creative Proteomics provides reliable, rapid and cost-effective Meat Markers targeted metabolomics services.