Portal hyperglutamatemia after dietary supplementation with monosodium glutamate in pigs

被引:35
作者
Blachier, F [1 ]
Guihot-Joubrel, G
Vaugelade, P
Le Boucher, J
Bernard, F
Duée, PH
Cynober, L
机构
[1] INRA, Lab Nutr & Secur Alimentaire, F-78352 Jouy En Josas, France
[2] CHU St Antoine, INSERM, U402, Paris, France
关键词
monosodium glutamate; intestine; amino acid metabolism; pigs;
D O I
10.1159/000007682
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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 intestinal amino acid metabolism. For this purpose, pigs weighing 60 +/- 2 kg received 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 glycine together with an equal amount of sodium in the form of NaCl, the animals being their own control in all experiments. At the end of this period, pigs received a MSG or glycine-NaCl-supplemented meal and samples of portal and arterial blood were collected for amino acid analysis in plasma. The results demonstrate after MSG supplementation rapid significant increases in glutamate concentration in the portal and arterial blood plasma after a test 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-creased aspartate concentration in the portal blood plasma was observed after MSG supplementation when compared with control experiments. When enterocytes were 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 used, with glutamate and glutamine being oxidized and transaminated at a similar level. It is concluded that the portal hyperglutamatemia observed shortly after the ingestion of a MSG-supplemented meal is likely due to the saturation of the intestinal capacity to metabolize glutamate with no measurable adaptation of the metabolic pathways controlling glutamate metabolism in enterocytes.
引用
收藏
页码:349 / 357
页数:9
相关论文
共 34 条
[1]   OXIDATION OF GLUTAMIC-ACID BY THE SPLANCHNIC BED IN HUMANS [J].
BATTEZZATI, A ;
BRILLON, DJ ;
MATTHEWS, DE .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 1995, 269 (02) :E269-E276
[2]  
Bergmeyer H. U., 1974, METHODS ENZYMATIC AN, V1
[3]   ARGININE METABOLISM IN RAT ENTEROCYTES [J].
BLACHIER, F ;
DARCYVRILLON, B ;
SENER, A ;
DUEE, PH ;
MALAISSE, WJ .
BIOCHIMICA ET BIOPHYSICA ACTA, 1991, 1092 (03) :304-310
[4]   INTESTINAL ARGININE METABOLISM DURING DEVELOPMENT - EVIDENCE FOR DE-NOVO SYNTHESIS OF L-ARGININE IN NEWBORN PIG ENTEROCYTES [J].
BLACHIER, F ;
MRABETTOUIL, H ;
POSHO, L ;
DARCYVRILLON, B ;
DUEE, PH .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 1993, 216 (01) :109-117
[5]   Polyamines inhibit lipopolysaccharide-induced nitric oxide synthase activity in rat liver cytosol [J].
Blachier, F ;
Mignon, A ;
Soubrane, O .
NITRIC OXIDE-BIOLOGY AND CHEMISTRY, 1997, 1 (03) :268-272
[6]   Consumption of a high dietary dose of monosodium glutamate fails to affect extracellular glutamate levels in the hypothalamic arcuate nucleus of adult rats [J].
Bogdanov, MB ;
Tjurmina, OA ;
Wurtman, RJ .
BRAIN RESEARCH, 1996, 736 (1-2) :76-81
[7]  
Cynober L., 1993, Clinical Nutrition (Edinburgh), V12, P54, DOI 10.1016/0261-5614(93)90150-3
[8]  
DARCYVRILLON B, 1993, J NUTR, V123, P234
[9]  
Dillon J. C., 1991, Cahiers de Nutrition et de Dietetique, V26, P157
[10]   THE INDUCTION OF CITRULLINE SYNTHESIS FROM GLUTAMINE IN ENTEROCYTES OF WEANED PIGS IS NOT DUE PRIMARILY TO AGE OR CHANGE IN DIET [J].
DUGAN, MER ;
KNABE, DA ;
WU, GY .
JOURNAL OF NUTRITION, 1995, 125 (09) :2388-2393