Table 2. Summary of publications about bioavailability of L-Met compared with DL-Met


Paper


Baker 1992 Htoo 2016 Htoo 2015 Kong 2016 Kong 2016


Average daily gain


100 99.6 89


Gain to Feed 100


Nitrogen utilization


fed piglets had the highest body weight (Rasch et al. 2016). Overall, it shows that L-Met is more efficiently used in different sulfur amino acid demanding physiological processes.


114 and 111 114 and 112


Lim 2015 (1) 368.4 and 111.1 Lim 2015 (2)


61.8 and 63 73.2 and 75.3


Lim 2015 (3) 95.9 and 100.4 104.6 and 147.3 Lim 2015 (4) Shen 2014 Average


88.9 and 92.9 135.3 and 139.6 144 and 159 121


123 and 139 115


Gut morphology and oxidative status: Additional to the better performance results with L-Met, gut morphology and oxidative status of pigs fed with L-Met are also improved as compared with DL-Met (Shen et al. 2014). Conversion of D-Met to L-Met is possible because D-Amino Acid Oxidase (DAAO) does exist in the peroxisomes (a cell organelle responsible for fat oxidation) in order to oxidize D-amino acids. DAAO has a high affinity for D-proline followed by hydrophobic amino acids and neutral amino acids. DAAO oxidation of D-Met is a hydrogen peroxide (H2 reaction (Appendino et al. 2010; Equation 1). H2


O2 113 Controversy in results is also happening in more recent data.


Even a lower RBA value is claimed for L-Met compared with D-Met irrespective of how questionable such data are, claiming a D isomer being better than the natural L form. Herein, the published data in pigs are summarized (Table 2) and on average RBA of L-Met is 113%, 115%, and 121% compared with DL-Met in pigs for nitrogen utilization, gain to feed, and average daily gain, respectively. Remus et al. (2015) also made a meta-analysis on data from 4406 weaning pigs and found that performance is always at a higher level with L-Met compared to the other Met sources (Figure 2).


) producing enzymatic O2


reactive oxygen species (ROS) can damage the peroxisomes. H2 can also damage the other organelles within cells because H2


O2


as an oxidant or O2


is the


only oxidant which can flow even out of the cells and move through the body fluids into other tissues and organs.


Moreover, the entire conversion of the ingested D-Met needs to


be done within the peroxisomes. Peroxisomes are well prepared to fight back against oxidants (H2


O2 or free radicals) because fat oxidation


which is the major function of peroxisomes would create a lot of ROS compounds. There are different enzymatic and non-enzymatic pathways to neutralize ROS within peroxisomes. However, it is not well investigated if peroxisomes are able to tolerate extra load of ROS which is produced via D-Met conversion into L-Met. With L-Met as a supplemental source of Met, one can avoid the extra load of ROS to this small organelle.


Conclusion DL-HMTBA and DL-Met could be easily replaced with lower amount of L-Met without compromising performance of animals. L-Met also creates a better redox condition for the pigs. Thus, customers can save money by using L-Met as their supplemental source of methionine and can support their pigs with a healthier and a more sustainable solution.


Figure 2. L-Met outperformed DL-Met and DL-HMTBA (adapted from Remus et al. 2015)


Cho (1980) measured the appearance of D-Met in urine and found


that 63% of Met excreted in urine is in D form. Thus, the ingested D-Met which is absorbed in the intestine but not transformed into L-Met is not utilized and consequently excreted in urine. Rasch et al. (2019) demonstrated that L-Met is better (56%)


converted to L-cysteine (transsulfuration) as compared with DL-Met and DL-HMTBA (44% and 46%, respectively) and DL-HMTBA resembles a Met deficient condition. Moreover, the highest rate of transmethylation (62%) was in L-Met fed piglets as compared with DL-Met and DL- HMTBA fed piglets (59% and 42%, respectively). L-Met enrichment in liver tissue was also higher than DL-Met and DL-HMTBA. L-Met


References


Baker, D.H. 1994. Utilization of precursors for L-amino acids. In: D’Mello, J.P.F. (ed.) Amino Acids in Farm Animal Nutrition. CAB International, Wallingford, UK, pp. 37–61.


Baker, D.H. 2006. J. Nutr. 136: 1670S–1675S. Bauchart-Thevret et al. 2009. Am J Physiol Endocrinol Metab 296: E1239– E1250.


Cho. 1980. J Parenter Enteral Nutr. 4(6):544-7. Chun and Baker. 1992. Can. J. Anim. Sci. 72: 185-188. Appendino, G., Fontana, G. and F. Pollastro. In Comprehensive Natural Products II Chemistry and Biology; Mander, L., Lui, H.-W., Eds.; Elsevier: Oxford, 2010; volume 3, pp.205–236.


Htoo and Moraless. 2016. J. Anim. Sci. 94:249–252. Katz R.S. and D.H. Baker. 1975. Poul. Sci. 54:1667-1674. Rasch et al. 2016. 17th Day of the Doctoral Student. ZB MED Informationszentrum Lebenswissenschaften. urn:nbn:de:hbz:38m:1-60797. Rasch et al. 2019. J Nutr. 149:1–9.


Remus et al. 2015. Livestock Science 181:96–102. Riedijk et al. 2007. PNAS. 104(9)3408-3413. Shen et al. 2014. J Anim Sci. 92:5530-5539. Zhang et al. 2018. Poul. Sci. 97:2053–2063.


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