Thermal stress and selection for growth affect myogenic satellite cell lipid accumulation and adipogenic gene expression through mechanistic target of rapamycin pathway.

Abstract

Satellite cells (SCs) are multipotential stem cells having the plasticity to convert to an adipogenic lineage in response to thermal stress during the period of peak mitotic activity (the first week after hatch in poultry). The mechanistic target of rapamycin (mTOR) pathway, which regulates cellular function and fate of SCs, is greatly altered by thermal stress in turkey pectoralis major muscle SCs. The objective of the present study was to determine the effects of thermal stress, selection for growth, and the role of the mTOR pathway on SC intracellular lipid accumulation and expression of adipogenic regulatory genes. These effects were analyzed using SCs isolated from the pectoralis major muscle of 1-wk-old modern faster-growing commercial turkey line (NC) selected for increased growth and breast muscle yield as compared with SCs of a historic slower-growing Randombred Control Line 2 (RBC2) turkey. Heat stress (43 °C) of SCs during proliferation increased intracellular lipid accumulation (P < 0.001), whereas cold stress (33 °C) showed an inhibitory effect (P < 0.001) in both lines. Knockdown of mTOR reduced the intracellular lipid accumulation (P < 0.001) and suppressed the expression of several adipogenic regulatory genes: peroxisome proliferator-activated receptor-γ (PPARγ; P < 0.001), CCAAT/enhancer-binding protein-β (C/EBPβ; P < 0.001), and neuropeptide-Y (NPY; P < 0.001) during both proliferation and differentiation. The NC line SCs showed fewer reductions in lipid accumulation compared with the RBC2 line independent of temperature. Both intracellular lipid accumulation (P < 0.001) and PPARγ expression (P < 0.001) were greater at 72 h of proliferation than at 48 h of differentiation in both the RBC2 and NC lines independent of temperature. Thus, hot and cold thermal stress affected intracellular lipid accumulation in the pectoralis major muscle SCs, in part, through the mTOR pathway in wea growth-dependent manner. Altered intracellular lipid accumulation could eventually affect intramuscular fat deposition, resulting in a long-lasting effect on the structure and protein to fat ratio of the poultry pectoralis major muscle.