Effects of low protein diet and low protein diet supplemented with synthetic essential amino acids on meat quality of broiler chickens

2012 ◽  
Vol 84 (6) ◽  
pp. 489-495 ◽  
Author(s):  
Hiroyuki Kobayashi ◽  
Kazuki Nakashima ◽  
Aiko Ishida ◽  
Akane Ashihara ◽  
Masaya Katsumata
1976 ◽  
Vol 36 (2) ◽  
pp. 219-230
Author(s):  
P. G. Lunn ◽  
R. G. Whitehead ◽  
B. A. Baker

1. Free amino acid concentrations in the plasma have been compared with those in liver and quadriceps muscle, in rats fed on diets containing 209 (control) and 31 (low-protein) g protein/kg. The effects of the low-protein diet on diurnal variations in these values were also measured.2. In the plasma, the total amino acid concentration was significantly lower in animals given the low-protein diet, at all times of day except 12.00 hours. In the liver, and to a lesser extent the muscle, total amino acid concentration was maintained.3. In the control animals, diurnal variation in the concentrations of both essential and non-essential amino acids was very similar in plasma, liver and muscle. In animals given the low-protein diet, although the same diurnal pattern was maintained for non-essential amino acids, that occurring among the essential amino acids had virtually disappeared.4. In plasma, the mean 24 h concentration of essential amino acids decreased from 24· mmol/l in control animals to only 1·29 mmol/l in the low-protein-fed animals. Concentrations in muscle and liver were reduced by a similar proportion (from 8·6 to 5·56 μmol/g and from 8·67 to 5·05 μmol/g respectively). Conversely the concentrations of non-essential amino acids in animals given the low-protein diet were increased in plasma (from 1·53 to 2·00 mmol/l), muscle (from 12·5 to 14·3 μmol/g), and liver (from 16·8 to 20·5 μmol/g), muscle showing the lowest increase.5. With the exceptions of lysine, threonine, cystine and tyrosine, the concentrations of all other essential amino acids were reduced more in liver than in muscle. The relationship between this and the failure to maintain plasma albumin concentrations is discussed.


2020 ◽  
Vol 16 (S2) ◽  
Author(s):  
Yuhei Takado ◽  
Hideaki Sato ◽  
Masako Tsukamoto‐Yasui ◽  
Keiichiro Minatohara ◽  
Manami Takahashi ◽  
...  

Diabetes ◽  
2008 ◽  
Vol 58 (3) ◽  
pp. 559-566 ◽  
Author(s):  
K. K. S. Bhasin ◽  
A. van Nas ◽  
L. J. Martin ◽  
R. C. Davis ◽  
S. U. Devaskar ◽  
...  

Nephron ◽  
1984 ◽  
Vol 38 (1) ◽  
pp. 54-56 ◽  
Author(s):  
G. Barsotti ◽  
C. Cristofano ◽  
E. Morelli ◽  
M. Meola ◽  
S. Lupetti ◽  
...  

2021 ◽  
Vol 93 (6) ◽  
pp. 729-735
Author(s):  
Nataliia A. Mikhailova

Chronic kidney disease (CKD) is characterized by high mortality from cardiovascular diseases, the development of which is facilitated by traditional risk factors (typical for the general population) and by nontraditional ones (specific to patients with CKD) as well. These factors include also uremic toxins, for which a causal relationship has been established with specific pathological processes in patients with CKD, comprising the development of vascular dysfunction and accelerated progression of atherosclerosis. Urea has long been considered not as a uremic toxin, but as a marker of metabolic imbalance or dialysis efficiency (Kt/V) in CKD patients. In recent years, more and more publications have appeared on the study of the toxic effects of urea with the development of toxic-uremic complications and the phenotype of premature aging, common in CKD. It was found that an increase in urea levels in uremic syndrome causes damage to the intestinal epithelial barrier with translocation of bacterial toxins into the bloodstream and the development of systemic inflammation, provokes apoptosis of vascular smooth muscle cells, as well as endothelial dysfunction, which directly contributes to the development of cardiovascular complications. The indirect effects of increased urea levels are associated with carbamylation reactions, when isocyanic acid (a product of urea catabolism) changes the structure and function of proteins in the body. Carbamylation of proteins in CKD patients is associated with the development of renal fibrosis, atherosclerosis and anemia. Thus, urea is now regarded as an important negative agent in the pathogenesis of complications in CKD. Studies on a low-protein diet with using ketoanalogues of essential amino acids to minimize the accumulation of urea and other uremic toxins demonstrate the clinical benefit of such an intervention in slowing the progression of CKD and the development of cardiovascular complications.


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