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ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #255622
Title: SNAT2 and LAT1 transporter abundance is developmentally regulated in skeletal muscle of neonatal pigs

Author
item SURYAWAN, AGUS - Children'S Nutrition Research Center (CNRC)
item GAZZANEO, MARIA - Children'S Nutrition Research Center (CNRC)
item ALMONACI, ROSEMARIE - Children'S Nutrition Research Center (CNRC)
item NGUYEN, HANH - Children'S Nutrition Research Center (CNRC)
item MURGAS-TORRAZZA, ROBERTO - Children'S Nutrition Research Center (CNRC)
item DAVIS, TERESA - Children'S Nutrition Research Center (CNRC)

Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: 2/24/2010
Publication Date: 4/24/2010
Citation: Suryawan, A., Gazzaneo, M.C., Almonaci, R.D., Nguyen, H.V., Murgas-Torrazza, R., Davis, A. 2010. SNAT2 and LAT1 transporter abundance is developmentally regulated in skeletal muscle of neonatal pigs [abstract]. Federation of American Societies for Experimental Biology Conference, Session: Nutrient-sensing mechanisms, April 24-28, 2010, Anaheim, California. 24: 331.4.

Interpretive Summary:

Technical Abstract: Previously, we demonstrated that the insulin and amino acid–induced activation of the mammalian target of rapamycin complex 1 (mTORC1), is developmentally regulated in neonatal pigs. Recent studies have indicated an important role of the System A transporters (SNAT2 and SLC1A5) and the L transporter (LAT1) in intracellular accumulation of essential amino acids, such as, leucine and in mTORC1 activation. This study aimed to determine the effects of age and the post-prandial rise in insulin, and amino acids on the abundance, and activation of SNAT2, SLC1A5, and LAT1. Overnight fasted 6- and 26-day-old pigs were infused for 2 h with saline, insulin, or amino acids to achieve fed levels. The abundance of SNAT2 and LAT1, but not SLC1A5, was significantly higher in muscle of 6- than in 26-d-old pigs. The activation of SNAT2, determined by transporter translocation to the plasma membrane, was unaffected by 2 hr infusion of amino acids or insulin. To determine the acute effects of feeding, SNAT2 activation was determined 0, 30, and 60 min after a complete meal. Feeding had no effect on SNAT2 activation at any time point suggesting that SNAT2 activation in vivo may be short-lived. In conclusion, the elevated abundance of SNAT2 and LAT1 is likely to play a significant role in the enhanced amino acid-induced activation of mTORC1 in neonatal pigs.