Long-chain n-3 fatty acids enhance neonatal insulin-regulated protein metabolism in piglets by differentially altering muscle lipid composition
Identifieur interne : 002461 ( Main/Curation ); précédent : 002460; suivant : 002462Long-chain n-3 fatty acids enhance neonatal insulin-regulated protein metabolism in piglets by differentially altering muscle lipid composition
Auteurs : Karen Bergeron [Canada] ; Pierre Julien [Canada] ; Teresa A. Davis [États-Unis] ; Alexandre Myre [Canada] ; M. Carole Thivierge [Canada, Royaume-Uni]Source :
- Journal of lipid research [ 0022-2275 ] ; 2007.
Abstract
This study investigated the role of long-chain n-3 polyunsaturated fatty acids (LCn-3PUFAs) of muscle phospholipids in the regulation of neonatal metabolism. Twenty-eight piglets were weaned at 2 days of age and raised on one of two milk formulas that consisted of either a control formula supplying 0% or a formula containing 3.5% LCn-3PUFAs until 10 or 28 days of age. There was a developmental decline in the insulin sensitivity of amino acid disposal in control pigs during the first month of life, with a slope of −2.24 μmol·kg−1·h−1 (
Url:
DOI: 10.1194/jlr.M700166-JLR200
PubMed: 17673528
PubMed Central: 2668875
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<front><div type="abstract" xml:lang="en"><p id="P1">This study investigated the role of long-chain n-3 polyunsaturated fatty acids (LCn-3PUFAs) of muscle phospholipids in the regulation of neonatal metabolism. Twenty-eight piglets were weaned at 2 days of age and raised on one of two milk formulas that consisted of either a control formula supplying 0% or a formula containing 3.5% LCn-3PUFAs until 10 or 28 days of age. There was a developmental decline in the insulin sensitivity of amino acid disposal in control pigs during the first month of life, with a slope of −2.24 μmol·kg<sup>−1</sup>
·h<sup>−1</sup>
(<italic>P</italic>
= 0.01) per unit of insulin increment, as assessed using hyperinsulinemic-euglycemic-euaminoacidemic clamps. LCn-3PUFA feeding blunted this developmental decline, resulting in differing insulin sensitivities (<italic>P</italic>
< 0.001). When protein metabolism was assessed under parenteral feeding-induced hyperinsulinemia, LCn-3PUFAs reduced by 16% whole body oxidative losses of amino acids (from 238 to 231 μmol·kg<sup>−1</sup>
·h<sup>−1</sup>
; <italic>P</italic>
= 0.06), allowing 41% more amino acids to accrete into body proteins (from 90 to 127 μmol·kg<sup>−1</sup>
·h<sup>−1</sup>
; <italic>P</italic>
= 0.06). The fractional synthetic rate of muscle mixed proteins remained unaltered by the LCn-3PUFA feeding. However, LCn-3PUFAs retarded a developmental increase in the essential-to-nonessential amino acid ratio of the muscle intracellular free pool (<italic>P</italic>
= 0.05). Overall, alterations in metabolism were concomitant with a preferential incorporation of LCn-3PUFAs into muscle total membrane phospholipids (<italic>P</italic>
< 0.001), in contrast to intramuscular triglycerides. These results underscore the potential role of LCn-3PUFAs as regulators of different aspects of protein metabolism in the neonate.</p>
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