These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Influences of somatotropin on Na(+)-K(+)-ATPase, Mg(2+)-ATPase and Ca(2+)-ATPases of Porcine visceral tissues.
    Author: Caperna TJ, Gavelek D.
    Journal: Comp Biochem Physiol B Biochem Mol Biol; 1996 Sep; 115(1):13-8. PubMed ID: 8896328.
    Abstract:
    Two experiments were conducted to determine the overall influence of porcine somatotropin (pST) administration on the specific activity of visceral tissue ATPases. Pigs were fed a corn-soybean meal-skim milk-based diet approximately 85% of ad libitum, such that for each experiment, control and pST-treated pigs consumed similar amounts of feed. As observed for pigs chronically treated with pST, enhanced growth of visceral tissues was evident in pigs treated for 6 and 14 days (d) with pST. The specific activity of detergent-activated Na(+)-K(+)-ATPase (ouabain-sensitive adenosine triphosphatase activity) was determined in fresh tissue homogenates prepared from liver, heart, kidney and duodenum. Treatment with pST was associated with a 19% increase in Na(+)-K(+)-ATPase-specific activity in the liver; specific activity of Mg(2+)-ATPase was not influenced by pST. Whole liver Na(+)-K(+)-ATPase and Mg(2+)-ATPase activities were 35% and 25% greater, respectively, in somatotropin-treated pigs. The specific activities of Na(+)-K(+)-ATPase in heart, kidney and duodenum were similar for controls and pigs treated for 14 d with pST. The specific activities of high- and low-affinity Ca(2+)-ATPase in kidney medulla were 20 and 26% lower, respectively, in pigs treated for 14 d with pST compared with controls. In contrast, Ca(2+)-ATPases in other tissues, including kidney cortex, were not influenced by pST treatment. These data indicate that some of the observed increase in energy expenditure associated with pST treatment may be attributable to increased organ size as well as to enhanced hepatic Na+ and K+ flux. While Na(+)-K(+)-ATPase activity is specifically enhanced in the liver, pST does not appear to be a general Na(+)-K(+)-ATPase activator in all tissues and may be associated with depressed activity of Ca(2+)-ATPases in the kidney.
    [Abstract] [Full Text] [Related] [New Search]