Evidence of decreased muscle protein turnover in gilts selected for low residual feed intake

The objective of this study was to evaluate the contribution of muscle protein turnover (synthesis and degradation) to the biological basis for genetic differences in finisher pigs selected for residual feed intake (RFI). Residual feed intake is defined as the difference between expected feed intake (based on the achieved rate of BW gain and backfat depth of individual pigs) and the observed feed intake of the individual pig. We hypothesized that protein turnover would be reduced in pigs selected for low RFI. Twelve gilts from a line selected for 7 generations for low RFI and 12 from a contemporary line selected for 2 generations for high RFI were paired by age and BW and fed a standard corn–soybean diet for 6 wk. Pigs were euthanized, muscle and liver samples were collected, and insulin signaling, protein synthesis, and protein degradation proteins were analyzed for expression and activities. Muscle from low RFI pigs tended to have less μ- and m-calpain activities (P = 0.10 and 0.09, respectively) and had significantly greater calpastatin activity and a decreased μ-calpain:calpastatin activity ratio (P \u3c 0.05). Muscle from low RFI pigs had less 20S proteasome activity compared with their high RFI counterparts (P\u3c 0.05). No differences in insulin signaling intermediates and translation initiation signaling proteins [mammalian target of rapamycin (mTOR) pathway] were observed (P \u3e 0.05). Postmortem proteolysis was determined in the LM from the eighth generation of the low RFI pigs versus their high RFI counterparts (n = 9 per line). Autolysis of μ-calpain was decreased in the low RFI pigs and less troponin-T degradation product was observed at 3 d postmortem (P \u3c 0.05), indicating slowed postmortem proteolysis during aging in the low RFI pigs. These data provide significant evidence that less protein degradation occurs in pigs selected for reduced RFI, and this may account for a significant portion of the increased efficiency observed in these animals

Rescue of Dystrophic Skeletal Muscle by PGC-1α Involves a Fast to Slow Fiber Type Shift in the mdx Mouse

Increased utrophin expression is known to reduce pathology in dystrophin-deficient skeletal muscles. Transgenic over-expression of PGC-1α has been shown to increase levels of utrophin mRNA and improve the histology of mdx muscles. Other reports have shown that PGC-1α signaling can lead to increased oxidative capacity and a fast to slow fiber type shift. Given that it has been shown that slow fibers produce and maintain more utrophin than fast skeletal muscle fibers, we hypothesized that over-expression of PGC-1α in post-natal mdx mice would increase utrophin levels via a fiber type shift, resulting in more slow, oxidative fibers that are also more resistant to contraction-induced damage. To test this hypothesis, neonatal mdx mice were injected with recombinant adeno-associated virus (AAV) driving expression of PGC-1α. PGC-1α over-expression resulted in increased utrophin and type I myosin heavy chain expression as well as elevated mitochondrial protein expression. Muscles were shown to be more resistant to contraction-induced damage and more fatigue resistant. Sirt-1 was increased while p38 activation and NRF-1 were reduced in PGC-1α over-expressing muscle when compared to control. We also evaluated if the use a pharmacological PGC-1α pathway activator, resveratrol, could drive the same physiological changes. Resveratrol administration (100 mg/kg/day) resulted in improved fatigue resistance, but did not achieve significant increases in utrophin expression. These data suggest that the PGC-1α pathway is a potential target for therapeutic intervention in dystrophic skeletal muscle

Gestational Heat Stress Alters Postnatal Offspring Body Composition Indices and Metabolic Parameters in Pigs

The study objectives were to test the hypothesis that heat stress (HS) during gestational development alters postnatal growth, body composition, and biological response to HS conditions in pigs. To investigate this, 14 first parity crossbred gilts were exposed to one of four environmental treatments (TNTN, TNHS, HSTN, or HSHS) during gestation. TNTN and HSHS dams were exposed to thermal neutral (TN, cyclical 18–22°C) or HS conditions (cyclical 28–34°C) during the entire gestation, respectively. Dams assigned to HSTN and TNHS treatments were heat-stressed for the first or second half of gestation, respectively. Postnatal offspring were exposed to one of two thermal environments for an acute (24 h) or chronic (five weeks) duration in either constant TN (21°C) or HS (35°C) environment. Exposure to chronic HS during their growth phase resulted in decreased longissimus dorsi cross-sectional area (LDA) in offspring from HSHS and HSTN treated dams whereas LDA was larger in offspring from dams in TNTN and TNHS conditions. Irrespective of HS during prepubertal postnatal growth, pigs from dams that experienced HS during the first half of gestation (HSHS and HSTN) had increased (13.9%) subcutaneous fat thickness compared to pigs from dams exposed to TN conditions during the first half of gestation. This metabolic repartitioning towards increased fat deposition in pigs from dams heat-stressed during the first half of gestation was accompanied by elevated blood insulin concentrations (33%; P = 0.01). Together, these results demonstrate HS during the first half of gestation altered metabolic and body composition parameters during future development and in biological responses to a subsequent HS challenge