scholarly journals Protein sparing effect and amino acid digestibilities of supplemental lysine and methionine in weanling pigs

1995 ◽  
Vol 8 (4) ◽  
pp. 393-402 ◽  
Author(s):  
I. K. Han ◽  
K. N. Heo ◽  
I. S. Shin ◽  
H. Lee
1980 ◽  
Vol 58 (6) ◽  
pp. 507-515 ◽  
Author(s):  
K. J. Foster ◽  
K. G. M. M. Alberti ◽  
C. Binder ◽  
Leslie Hinks ◽  
S. Karran ◽  
...  

1. The mechanism of the purported protein-sparing effects of different postoperative intravenous regimens still remains controversial. We have therefore measured circulating concentrations of metabolites and hormones in blood and urine nitrogen excretion in patients receiving (a) sodium chloride solution (saline), (b) 1.5 g of glucose day−1 kg−1 body weight, (c) 1.5 g of glucose day−1 kg−1 with insulin (0.56 unit day−1 kg−1) or (d) mixed amino acids (1.5 g day−1 kg−1) after abdominal operation. 2. Compared with results for saline-treated patients, glucose infusion resulted in raised glucose and insulin concentrations and lowered ketone body and non-esterified fatty acid concentrations but did not influence protein catabolism. 3. Addition of insulin lowered blood glucose by approximately 1 mmol/l. Total nitrogen excretion during glucose/insulin infusion was significantly less than during saline infusion. 4. Infusion of amino acids, compared with saline infusion, resulted in raised blood glucose, alanine, serum insulin and plasma glucagon concentrations but lower concentrations of plasma non-esterified fatty acids and blood ketone bodies. Insulin concentrations, however, were similar in both amino acid- and glucose-treated groups. 5. Amino acid infusion increased urea and total nitrogen excretion but net nitrogen loss was only 1.9 mmol of nitrogen day−1 kg−1 compared with 12.7 mmol day−1 kg−1 in the saline-treated group and 11.0 mmol day−1 kg−1 in the glucose-treated group. 6. Glucose (and insulin) infusion appeared to inhibit gluconeogenesis, and amino acids to enhance it. The nitrogen-sparing effect of amino acids appears largely related to their mass and is apparently unrelated to changes in ketone bodies and insulin.


1996 ◽  
Vol 62 (4) ◽  
pp. 624-628 ◽  
Author(s):  
José Manuel Vergara ◽  
Lidia Robainà ◽  
Marisol Izquierdo ◽  
Manuel De La Higuera

2011 ◽  
Vol 300 (1) ◽  
pp. G137-G145 ◽  
Author(s):  
Claire Boutry ◽  
Hideki Matsumoto ◽  
Gheorghe Airinei ◽  
Robert Benamouzig ◽  
Daniel Tomé ◽  
...  

The consumption of monosodium glutamate (MSG) is advocated to elicit physiological and metabolic effects, yet these effects have been poorly investigated directly in humans and in particular in the postprandial phase. Thirteen healthy adults were supplemented for 6 days with a nutritional dose of MSG (2 g) or sodium chloride (NaCl) as control, following a crossover design. On the 7th day, they underwent a complete postprandial examination for the 6 h following the ingestion of the same liquid standard meal (700 kcal, 20% of energy as [15N]protein, 50% as carbohydrate, and 30% as fat) supplemented with MSG or NaCl. Real-ultrasound measures of antral area indicated a significant increased distension for the 2 h following the meal supplemented with MSG vs. NaCl. This early postprandial phase was also associated with significantly increased levels of circulating leucine, isoleucine, valine, lysine, cysteine, alanine, tyrosine, and tryptophan after MSG compared with NaCl. No changes to the postprandial glucose, insulin, glucagon-like peptide (GLP)-1, and ghrelin were noted between MSG- and NaCl-supplemented meals. Subjective assessments of hunger and fullness were neither affected by MSG supplementation. Finally, the postprandial fate of dietary N was identical between dietary conditions. Our findings indicate that nutritional dose of MSG promoted greater postprandial elevations of several indispensable amino acids in plasma and induced gastric distension. Further work to elucidate the possible sparing effect of MSG on indispensable amino acid first-pass uptake in humans is warranted. This trial was registered at clinicaltrials.gov as NCT00862017.


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