Portal hyperglutamatemia after dietary supplementation with monosodium glutamate in pigs

Citation
F. Blachier et al., Portal hyperglutamatemia after dietary supplementation with monosodium glutamate in pigs, DIGESTION, 60(4), 1999, pp. 349-357
Citations number
34
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
DIGESTION
ISSN journal
00122823 → ACNP
Volume
60
Issue
4
Year of publication
1999
Pages
349 - 357
Database
ISI
SICI code
0012-2823(199907/08)60:4<349:PHADSW>2.0.ZU;2-M
Abstract
The aim of the present work was to examine in pigs the effect of a dietary supplementation with the flavor enhancer monosodium glutamate (MSG) on inte stinal amino acid metabolism. For this purpose, pigs weighing 60 +/- 2 kg r eceived a standard meal twice a day for 1 week, supplemented with either 10 g MSG per meal or, as control experiments, an isonitrogenous amount of gly cine together with an equal amount of sodium in the form of NaCl, the anima ls being their own control in all experiments. At the end of this period, p igs received a MSG or glycine-NaCl-supplemented meal and samples of portal and arterial blood were collected for amino acid analysis in plasma. The re sults demonstrate after MSG supplementation rapid significant increases in glutamate concentration in the portal and arterial blood plasma after a tes t meal which resulted in a positive portoarterial difference. In comparison , after glycine-NaCl supplementation, glutamate concentrations were almost identical in portal and arterial plasma. Furthermore, significant in-crease d aspartate concentration in the portal blood plasma was observed after MSG supplementation when compared with control experiments. When enterocytes w ere isolated at the end of the supplementation period from the jejunum and examined for their metabolic capacities towards L-glutamate and L-glutamine , it was found that metabolism did not differ according to the supplement u sed, with glutamate and glutamine being oxidized and transaminated at a sim ilar level. It is concluded that the portal hyperglutamatemia observed shor tly after the ingestion of a MSG-supplemented meal is likely due to the sat uration of the intestinal capacity to metabolize glutamate with no measurab le adaptation of the metabolic pathways controlling glutamate metabolism in enterocytes.