Melatonin supplementation to sows in mid to late gestation affects offspring circadian, myogenic, and growth factors in pre and postnatal skeletal muscle.

Abstract

The neuroendocrine hormone melatonin is associated with circadian rhythms and has antioxidant and vasodilative properties. In cattle, melatonin rescues fetal growth during maternal nutrient restriction in a seasonally dependent manner, but melatonin research in swine is limited. The objective of this study was to evaluate effects of dietary melatonin supplementation during mid to late gestation on circadian rhythm and muscle growth and development of the longissimus dorsi in utero and postnatally. Sows received 20mg dietary melatonin daily (MEL) or no melatonin supplement (CON). Experiment 1 supplemented sows from gestational age (dGA) 38 ± 1 to 99 ± 1, experiment 2 supplemented sows from 41 to 106 ± 1 dGA, and experiment 3 supplemented sows from 60 dGA to farrowing. At harvest, morphometric measurements of all fetuses were taken, while the small (SM), medium (MED), and large (LG) piglet from each litter were used for further analysis. Prenatal data were analyzed using the MIXED procedure of SAS, and postnatal data were analyzed using the GLIMMIX procedure. Fetal morphometrics were analyzed for fixed effect of treatment, and transcript abundance was analyzed for treatment, time, and size. Postnatal parameters were analyzed for fixed effects of treatment, size, and production stage. In Exp. 1, MEL increased (P = 0.016) Period 1 (PER1) transcript abundance in the evening (PM) compared to the morning (AM). In Exp. 1, myogenin (MYOG) transcript abundance was increased (P = 0.033) in MEL fetuses in the AM compared to MEL in the PM. Myogenic factor 5 (MYF5) and paired box 7 (PAX7) were increased (P = 0.016) in the PM. Fetuses from MEL treated sows had increased (P < 0.05) BW, curve crown rump length, and head circumference in Exp. 2. In Exp. 2, MEL increased (P = 0.012) PER1 and Period 2 (PER2) transcript abundance in the PM. In Exp. 2, myoblast differentiation 1 (MYOD) was increased (P = 0.016) in SM and MED fetuses, while MYF5 and PAX7 were increased (P = 0.019) in SM fetuses. Postnatal BW was increased (P = 0.025) in MED and LG MEL treated offspring compared to CON. Insulin-like growth factor 1 (IGF1) was downregulated (P = 0.050) in MEL treated offspring, while insulin-like growth factor 1 receptor (IGF1R) was upregulated (P = 0.009) in MEL offspring. These results indicate that maternal melatonin supplementation during gestation modulates fetal circadian regulatory genes and alters myogenic genes during growth.