Physicochemical Considerations of Protein Utilization

Author(s):  
P.A. Finot
Keyword(s):  
Genes ◽  
2021 ◽  
Vol 12 (3) ◽  
pp. 456
Author(s):  
Hewa Bahithige Pavithra Chathurangi Ariyarathne ◽  
Martin Correa-Luna ◽  
Hugh Thomas Blair ◽  
Dorian John Garrick ◽  
Nicolas Lopez-Villalobos

The objective of this study was to identify genomic regions associated with milk fat percentage (FP), crude protein percentage (CPP), urea concentration (MU) and efficiency of crude protein utilization (ECPU: ratio between crude protein yield in milk and dietary crude protein intake) using grazing, mixed-breed, dairy cows in New Zealand. Phenotypes from 634 Holstein Friesian, Jersey or crossbred cows were obtained from two herds at Massey University. A subset of 490 of these cows was genotyped using Bovine Illumina 50K SNP-chips. Two genome-wise association approaches were used, a single-locus model fitted to data from 490 cows and a single-step Bayes C model fitted to data from all 634 cows. The single-locus analysis was performed with the Efficient Mixed-Model Association eXpedited model as implemented in the SVS package. Single nucleotide polymorphisms (SNPs) with genome-wide association p-values ≤ 1.11 × 10−6 were considered as putative quantitative trait loci (QTL). The Bayes C analysis was performed with the JWAS package and 1-Mb genomic windows containing SNPs that explained > 0.37% of the genetic variance were considered as putative QTL. Candidate genes within 100 kb from the identified SNPs in single-locus GWAS or the 1-Mb windows were identified using gene ontology, as implemented in the Ensembl Genome Browser. The genes detected in association with FP (MGST1, DGAT1, CEBPD, SLC52A2, GPAT4, and ACOX3) and CPP (DGAT1, CSN1S1, GOSR2, HERC6, and IGF1R) were identified as candidates. Gene ontology revealed six novel candidate genes (GMDS, E2F7, SIAH1, SLC24A4, LGMN, and ASS1) significantly associated with MU whose functions were in protein catabolism, urea cycle, ion transportation and N excretion. One novel candidate gene was identified in association with ECPU (MAP3K1) that is involved in post-transcriptional modification of proteins. The findings should be validated using a larger population of New Zealand grazing dairy cows.


1997 ◽  
Vol 77 (2) ◽  
pp. 197-212 ◽  
Author(s):  
Jens Kondrup ◽  
Klaus Nielsen ◽  
Anders Juul

Patients with cirrhosis of the liver require an increased amount of protein to achieve N balance. However, the utilization of protein with increased protein intake, i.e. the slope from regression analysis of N balance v. intake, is highly efficient (Nielsen et al. 1995). In the present study, protein requirement and protein utilization were investigated further by measuring protein synthesis and degradation. In two separate studies, five or six patients with cirrhosis of the liver were refed on a balanced diet for an average of 2 or 4 weeks. Protein and energy intakes were doubled in both studies. Initial and final whole-body protein metabolism was measured in the fed state by primed continous [15N]glycine infusion. Refeeding caused a statistically significant increase of about 30% in protein synthesis in both studies while protein degradation was only slightly affected. The increase in protein synthesis was associated with significant increases in plasma concentrations of total amino acids (25%), leucine (58%), isoleucine (82%), valine (72%), proline (48%) and triiodothyronine (27%) while insulin, growth hormone, insulin-like growth factor (IGF)-I and IGF-binding protein-3 were not changed significantly. The results indicate that the efficient protein utilization is due to increased protein synthesis, rather than decreased protein degradation, and suggest that increases in plasma amino acids may be responsible for the increased protein synthesis. A comparison of the patients who had a normal protein requirement with the patients who had an increased protein requirement suggests that the increased protein requirement is due to a primary increase in protein degradation. It is speculated that this is due to low levels of IGF-I secondary to impaired liver function, since initial plasma concentration of IGF-I was about 25% of control values and remained low during refeeding.


1984 ◽  
Vol 51 (02) ◽  
pp. 171 ◽  
Author(s):  
Gail E. Butterfield ◽  
Doris H. Calloway

1992 ◽  
Vol 38 (5) ◽  
pp. 493-499
Author(s):  
Sadaichi SAKAMOTO ◽  
Masahiro MORI ◽  
Masaharu OHNAKA ◽  
Yoshiaki NIIYAMA

1988 ◽  
Vol 64 (2) ◽  
pp. 550-555 ◽  
Author(s):  
D. G. Dolny ◽  
P. W. Lemon

Male subjects (n = 8) cycled for 90 min in 5, 20, and 30 degrees C environments. Rectal (Tre), chest, and thigh temperatures, O2 consumption (VO2), respiratory exchange ratio (R), and venous concentrations of glucose, free fatty acids (FFA), urea N, lactic acid (LA), norepinephrine (NE), epinephrine (E), and cortisol (C) were measured before, during, and after exercise. Urea N excretion was measured in 72 h of nonexercise, in 72 h of exercise (exercise day + 2 post-exercise days) urine samples, and in exercise sweat. Calculated 72-h protein utilization (means +/- SE) was significantly greater (P less than 0.05) for the 5 (86.9 +/- 27.1 g) and 20 (82.9 +/- 22.7 g) compared with 30 degrees C (34.01 +/- 19.1 g) trial. Regardless of ambient temperature exercise increased the venous concentration of C, E, and NE. These catabolic hormones were greatest in 5, lowest in 20, and intermediate in 30 degrees C. Exercise Tre and VO2 were greatest in the 30 degrees C environment. Venous FFA concentration was significantly higher and R significantly lower in 5 vs. 20 or 30 degrees C, and venous LA concentration was significantly greater in 30 vs. 20 or 5 degrees C. Although these results indicate that exercise protein breakdown is affected by ambient temperatures, the mechanism of action is not due solely to circulating NE, E, and C. Differences in venous FFA and LA across environmental temperatures suggest that alterations in carbohydrate and fat metabolism may have contributed to the observed variable protein utilization.


1996 ◽  
Vol 75 (2) ◽  
pp. 237-248 ◽  
Author(s):  
Christiani Jeyakumar Henry ◽  
Amal Ghusain-Choueiri ◽  
Philip R. Payne

AbstractThe relationship between essential fatty acids (EFA) deficiency and the utilization of dietary protein, growth rate and survival of offspring was investigated in rats during development and reproduction. EFA deficiency was induced by feeding a 200 g casein/kg-based diet containing 70 g hydrogenated coconut oil (HCO)/lkg as the only source of fat. The conversion efficiency of dietary protein was assessed as net protein utilization (NPU), using a 10 d comparative carcass technique. Consumption of the deficient diet during the 10 d assay period induced biochemical changes characteristic of mild EFA deficiency in humans (triene:tetraene 0·27 (SD 0·04) compared with 0·026 (SD 0·004) for wn-deficient controls), but there were no significant changes in growth rate or protein utilization. These variables were also unchanged when the deficient diet was fed for an additional 7 d before the assay, although triene: tetraene increased to 0.8 (SD 0·02). Feeding the deficient diet for 63 d before assay produced severe EFA deficiency (triene:tetraene 1.4 (SD 0·3) v. 0·036 (SD 0·005) for controls), a fall in growth rate (25% during assay period), and NPU (31.5 (SD 0·63) v. 39.0 (SD 0·93) for controls). These severely-EFA-deficient animals had a 30% higher fasting-resting rate of energy metabolism than that of age-matched controls. However, there was no change in the rate of endogenous N loss. Voluntary energy consumption was increased in animals fed on deficient diets, either with 200 g protein/kg, or protein free. The reduced efficiency of protein utilization could be entirely accounted for by the restricted amount of energy available for growth and protein deposition. Consumption of an EFA-deficient diet during pregnancy and lactation resulted in high mortality (11% survival rate at weaning compared with 79% for controls) and retarded growth in the preweaning offspring. It is concluded that animals are particularly sensitive to EFA deficiency during reproduction and pre- and post-natal stages of development. However, after weaning only severe EFA deficiency retarded growth, primarily through changes in energy balance.


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