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Neonatal phosphate nutrition alters in vivo and in vitro satellite cell activity in pigs
Lindsey S Alexander1, Brynn S Seabolt, Robert P Rhoads
1Laboratory of Developmental Nutrition, Department of Animal Science, North Carolina State University, Raleigh, NC 27695, USA. lindsey.alexander1@gmail.com
Insights
Neonatal phosphate (PO(4)) deficiency impairs skeletal muscle growth by reducing satellite cell proliferation. Optimizing early PO(4) nutrition may enhance lean growth potential.
Area of Science:
- Muscle biology
- Nutritional science
- Skeletal muscle development
Background:
- Satellite cell activity is crucial for postnatal skeletal muscle growth.
- The impact of early nutrition on satellite cell biology requires further investigation.
Purpose of the Study:
- To investigate the role of neonatal dietary phosphate (PO(4)) on satellite cell activity and myogenic potential in piglets.
- To determine if altered PO(4) nutrition affects satellite cell proliferation and differentiation.
Main Methods:
- Piglets were fed diets with adequate, supra-adequate, or deficient PO(4) levels for 12 days.
- Satellite cell proliferation was assessed in vivo using BrdU incorporation.
- In vitro cell culture was used to evaluate satellite cell myogenic progression markers.
Main Results:
- Dietary PO(4) deficiency reduced serum PO(4) and parathyroid hormone (PTH) levels.
- PO(4) deficiency led to decreased in vivo satellite cell proliferation.
- Satellite cells from deficient piglets showed altered in vitro expression of myogenic markers.
Conclusions:
- Neonatal phosphate deficiency negatively impacts satellite cell function, potentially hindering muscle growth.
- Early nutritional programming, specifically adequate PO(4) intake, may be important for optimizing long-term muscle development and lean growth.
Abstract:
Satellite cell activity is necessary for postnatal skeletal muscle growth. Severe phosphate (PO(4)) deficiency can alter satellite cell activity, however the role of neonatal PO(4) nutrition on satellite cell biology remains obscure. Twenty-one piglets (1 day of age, 1.8 ± 0.2 kg BW) were pair-fed liquid diets that were either PO(4) adequate (0.9% total P), supra-adequate (1.2% total P) in PO(4) requirement or deficient (0.7% total P) in PO(4) content for 12 days. Body weight was recorded daily and blood samples collected every 6 days. At day 12, pigs were orally dosed with BrdU and 12 h later, satellite cells were isolated. Satellite cells were also cultured in vitro for 7 days to determine if PO(4) nutrition alters their ability to proceed through their myogenic lineage. Dietary PO(4) deficiency resulted in reduced (P < 0.05) sera PO(4) and parathyroid hormone (PTH) concentrations, while supra-adequate dietary PO(4) improved (P < 0.05) feed conversion efficiency as compared to the PO(4) adequate group. In vivo satellite cell proliferation was reduced (P < 0.05) among the PO(4) deficient pigs, and these cells had altered in vitro expression of markers of myogenic progression. Further work to better understand early nutritional programming of satellite cells and the potential benefits of emphasizing early PO(4) nutrition for future lean growth potential is warranted.
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