Table 1.
Animals | Experimental Design | Results | Conclusion | References |
---|---|---|---|---|
14 primiparous pure-bred Meishan gilt sbody weight: 36.1 ± 1.8 kg |
Digestible energy 13 MJ/kg Control treatment: 12.2% crude protein (CP) (gestation) and 14% CP (lactation) Low protein treatment: 6.1% CP (gestation) and 6.9% CP (lactation) |
Muscle protein synthesis: p70S6K and eIF4E ↓ Negative regulator of skeletal muscle development and growth ↑ Muscle weight: Longissimus dorsi muscles ↓ |
Maternal low protein diet throughout gestation and lactation causes retardation in muscle hypertrophy and protein synthesis | [28] |
16 Landrace × Yorkshire crossbred sows in the second parity | Digestible energy:13 MJ/kg (gestation),14.39 MJ/kg (lactation) Control treatment: 15% (CP, gestation) and 18% CP (lactation) Low protein treatment: 7.5% (CP, gestation) and 9% CP (lactation) |
Back fat thickness ↓ Restricted amino acid response (AAR) pathway: CHOP, IRE1α, PERK, ATF-6, XBP-1 and Bip, ATF4, and EIF2α↑ Autophagy-related genes: ATG7 and LC3 ↑ |
Maternal low protein diet throughout gestation and lactation causes offspring reduced adipogenesis and increased lipolysis | [33] |
56 German Landrace gilts | Metabolic energy: 13.7 MJ/kg Adequate protein treatment: 12.1% CP High protein treatment: 30% CP; Low protein treatment, 6.5% CP |
Total number of myofibers ↔ Myogenic regulatory factors in low protein treatment: MYOG, MRF4, IGF1, IGF1R ↓ Myogenic regulatory factors in high protein treatment: MYOD, MYOG, IGF1R, and IGFBP5 ↑ |
Moderate high or low maternal protein diets change gene expression but not the phenotype of skeletal muscle from porcine fetuses | [32] |
47 pure German Landrace gilts | Metabolic energy: 13.7 ME/kg Adequate protein treatment: 12.1% CP High protein treatment: 30% CP; Low protein treatment, 6.5% CP |
Percentage of muscle tissue in in HP in high protein treatment ↑ Primary and secondary myofibers in low protein diet treatment ↓ Subcutaneous adipose tissue mass in low protein diet treatment and high protein diet treatment ↓ |
Both limited and excess protein supply retards fetal growth, but only limited protein supply impairs myogenesis, persistently restricts muscle growth potential, and favors obesity at infancy. | [30] |
24 primiparous German Landrace sows | Metabolic energy: 13.7 ME/kg Adequate protein treatment: 12.1% CP High protein treatment: 30% CP; Low protein treatment, 6.5% CP |
Candidate genes of nutrient- dependent pre- and postnatal development: muscular expression of NCAPD2 (LP ↓), NCAPG (↔), NCAPH (LP ↓) Key genes of methionine metabolism: both HP and LP diet significant influence DNMT1 (HP ↑), DNMT3a (LP ↓) and MAT2B (HP ↑) |
Maternal protein supply regulate condensin I subunit gene expression by methylation process and in turn may affect cell division in skeletal muscle tissue | [34] |