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. 2019 Jan 13;9(1):19. doi: 10.3390/ani9010019

Table 1.

Effect of different maternal protein levels on early fetal muscle development. Upward-pointing arrow: “increase”; downward-pointing arrow: “decrease”; horizontal arrow: “no change”.

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]