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Labile methyl group balances in the human the role of sarcosine

Labile methyl group balances in the human the role of sarcosine

Metabolism Clinical & Experimental 29(8): 707-720

Estimates of the daily rate of methionine utilization by adult humans, published previously, were underestimated because available data did not permit quantitative assessment of the rate at which the methyl moiety of methionine is oxidized. Efforts are reported to measure the rate of oxidation of methionine methyl by the 2 pathways that proceed through the intermediate N-methylglycine (sarcosine). Two sarcosinemic, sarcosinuric patients, proven or presumed to have specific genetic defects in the sarcosine-oxidizing system, were studied while maintained on constant diets containing differing amounts of methionine, choline (or choline derivatives) and glycine. The steady-state excretions of sarcosine, creatinine, creatine and other materials were determined. Sarcosine is probably formed in 2 ways: in an amount equivalent to the dietary intake of choline (or choline derivative), this pathway would make a net positive contribution to the methionine-methyl pool due to the transfer of a methyl group from betaine to homocysteine and by processes requiring net consumption of methionine methyl. For the single patient for whom reasonably complete data were attained, 2 such processes may be occurring. One proceeds at the rate (.apprx. 2 mmol/24 h) that changed little as total intake of labile methyl groups was altered. The 2nd became prominent (and accounted for the bulk of the incremental intake of labile methyl groups) when this intake exceeded the combined amounts required for the synthesis of creatine (10.2 mmol/24 h), other transmethylation reactions (1.4 mmole/24 h), polyamine synthesis (0.5 mmole/24 h) and the basal process of sarcosine formation just mentioned (2 mmole/24 h). Such basal sarcosine formation may be due to chiefly to endogenous choline synthesis, balanced by degradation, whereas the more responsive process of sarcosine formation may be due chiefly to methylation of glycine. Together with available data, these new data on methionine consumption due to sarcosine formation permit calculation of a turnover time for S-adenosylmethionine in human liver (no more than 3.5-7 min), as well as upward revision of previous minimal estimates of the rate of methylneogenesis, the number of time that the average homocysteinyl moiety cycles between methionine and homocysteine during its passage through the body and the partitioning of homocysteine between the remethylation and the transsulfuration pathways.

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Accession: 005787205

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PMID: 6157075

DOI: 10.1016/0026-0495(80)90192-4

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