Low-protein diet improves meat quality of growing and finishing pigs through changing lipid metabolism, fiber characteristics, and free amino acid profile of the muscle.

The objective of the study was to investigate the effect of feeding reduced CP, AA-supplemented diets on meat quality in growing and finishing pigs as well as the related mechanism. In experiment 1, 18 growing pigs (36.5 kg BW) were assigned randomly and fed 1 of 3 corn-soybean meal diets containing either 18% CP (normal protein, NP), 15% CP (low protein, LP), or 12% CP (very low protein, VLP). In experiment 2, 18 finishing pigs (62.3 kg BW) were allotted randomly into 1 of the following diets: 16% CP (NP), 13% CP (LP), or 10% CP (VLP). In both experiments, the LP and VLP diets were supplemented with crystalline AA to achieve equal content of standardized ileal digestible lysine, methionine, threonine, and tryptophan. At the end of each experiment, all pigs were slaughtered to collect longissimus dorsi muscle (LM) samples. Samples were used for determining meat quality, intramuscular fat (IMF) content, fatty acid composition, free AA profile, and expression of genes for myosin heavy chain isoforms. Results showed that growing and finishing pigs fed the LP diets increased (P < 0.05) redness value of LM, while finishing pigs fed the LP and VLP diets decreased (P < 0.05) the shear force values. Compared with the NP diet, growing and finishing pigs fed lower CP diets had higher (P < 0.05) contents of IMF and MUFA, and lower (P < 0.05) contents of PUFA. Besides, higher (P < 0.05) expression levels of type I and/or IIa muscle fibers were observed in LP diet-fed growing and finishing pigs, and greater concentrations of taurine and tasty AA in VLP diet-fed growing and finishing pigs. Taken together, our results indicate that low-protein diets could positively affect meat quality of growing and finishing pigs, and likely through regulation of IMF content and fatty acid composition, fiber characteristics, and free AA profile in the muscle.

Branched-chain amino acid ratios in low-protein diets regulate the free amino acid profile and the expression of hepatic fatty acid metabolism-related genes in growing pigs.

Liver metabolism is affected by nutrients. The aim of this study was to explore the effects of low-protein diets (17% crude protein, CP) supplemented with branched-chain amino acids (BCAAs), including leucine (Leu), isoleucine (Ile) and valine (Val), on hepatic amino acid profile and lipid metabolism in growing pigs. The ratio of Leu : Ile : Val in all groups was 1 : 0.51 : 0.63 (20% crude protein, CP), 1 : 1 : 1 (17% CP), 1 : 0.75 : 0.75 (17% CP), 1 : 0.51 : 0.63 (17% CP) and 1 : 0.25 : 0.25 (17% CP) respectively. Results revealed that compared to the positive control group (1 : 0.51 : 0.63, 20% CP), the low-protein diets significantly augmented the concentrations of most essential amino acids and non-essential amino acids (p < .05), with the greatest values observed in the 1 : 0.25 : 0.25 group. Moreover, relative to the control, the low-protein diets with the Leu : Ile : Val ratio ranging from 1 : 0.75 : 0.75 to 1 : 0.25 : 0.25 markedly downregulated the mRNA abundance of acetyl-CoA carboxylase (ACC), lipoprotein lipase (LPL) and fatty acid-binding protein 4 (FABP-4) (p < .05), and upregulated the mRNA expression of hormone-sensitive lipase (HSL), peroxisome proliferator-activated receptor-g coactivator-1α (PGC-1α), uncoupling protein 3 (UCP3) and liver carnitine palmitoyltransferase 1 (L-CPT-1) (p < .05). Therefore, our data suggest that protein-restricted diets supplemented with optimal BCAA ratio, that is, 1 : 0.75 : 0.75-1 : 0.25 : 0.25, induce a shift from fatty acid synthesis to fatty acid oxidation in the liver of growing pigs. These effects may be associated with increased mitochondrial biogenesis.

Regulation in free amino acid profile and protein synthesis pathway of growing pig skeletal muscles by low-protein diets for different time periods.

The objective of the study was to explore the extent to which the dietary CP level can be reduced for maintaining muscle protein deposition in growing pigs as well as the related mechanism and whether the response to dietary protein restriction is diversely modified throughout the 2 trial periods. A total of 36 pigs (9.57 ± 0.64 kg initial BW) were individually penned and fed 1 of 3 diets for 10 or 25 d. During each period, the diets contained 20, 17, and 14% CP, respectively. Both the 17% CP diet and the 14% CP diet were supplemented with Lys, Met, Thr, and Trp to provide the same total concentrations as those in the 20% CP diet. Results showed that feeding the 14% CP diet for 10 or 25 d seriously impaired ( < 0.05) growth performance of the pigs compared with those fed the 20 or 17% CP diets. Pigs fed the 20% CP diet for 25 d had a higher ( < 0.05) serum content of urea nitrogen than those fed the 17 and 14% CP diets. In addition, the free AA (FAA) profile in skeletal muscle of the pigs was evidently changed ( < 0.05) by the low-protein diets for 25 d; of note, the 14% CP diet increased ( < 0.05) the size of muscle FAA pool compared with the 20% CP diet. Meanwhile, on d 25, reducing dietary CP levels also influenced ( < 0.05) mRNA levels of specific AA transceptors expressed in skeletal muscle, especially revealing the striking differences between the 14 and 20% CP diet-fed pigs. Most importantly, we observed a globally decreased ( < 0.05) activation of the mammalian target of rapamycin complex 1 (mTORC1) pathway in skeletal muscle of pigs fed the 14% CP diet, whereas only partial inhibition was observed for those fed the 17% CP diet compared with those fed the 20% CP diet. However, feeding the low-protein diets for 10 d had minimal effects on serum parameters, muscle FAA profile, and muscle mTORC1 pathway of the pigs. Taken together, our results indicate that supplementing with limiting AA to the 14% CP diet is not highly effective for the pigs in restoring protein synthesis and muscle growth, whereas the 17% CP diet likely maintains the pigs' muscle mass, which were regulated, at least in part, by mediating AA transceptors expression, FAA profile, and activation of the mTORC1 pathway.