Mammary Protein Synthesis upon Long-Term Nutritional Restriction Was Attenuated by Oxidative-Stress-Induced Inhibition of Vacuolar H+-Adenosine Triphosphatase/Mechanistic Target of Rapamycin Complex 1 Signaling.

Abstract

To determine how nutritional restriction compromised milk synthesis, sows were fed 100% (control) or76% (restricted) of the recommended feed allowance from postpartum day (PD)-1 to PD-28. In comparison to the control, more body reserves loss, increased plasma triglyceride and high-density lipoprotein cholesterol levels, and decreased plasma methionine concentrations were observed in the restricted group at PD-21. The increased plasma malondialdehyde level, decreased plasma histidine and taurine concentrations, and decreased glutathione peroxidase activity were observed at PD-28 when backfat loss further increased in the restricted group. In mammary glands, vacuolar H+-adenosine triphosphatase (v-ATPase), as the upstream of the mechanistic target of rapamycin (mTOR) signaling, showed decreased activity, while phosphorylation of mTOR, S6 kinase, and eukaryotic translation initiation factor 4E-binding protein 1 and β-casein abundance all decreased following feed restriction. Altogether, long-term nutrition restriction could induce progressively aggravated oxidative stress and compromise mammary protein synthesis through repression of v-ATPase/mTORC1 signaling.