Linked Life Data

20237302

Source:http://linkedlifedata.com/resource/pubmed/id/20237302

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2010-8-17
pubmed:abstractText
To examine the regulation of hepatic acetogenesis in neonatal swine, carnitine palmitoyltransferase I (CPT I) activity was measured in the presence of varying palmitoyl-CoA (substrate) and malonyl-CoA (inhibitor) concentrations, and [1-(14)C]-palmitate oxidation was simultaneously measured. Accumulation rates of (14)C-labeled acetate, ketone bodies, and citric acid cycle intermediates within the acid-soluble products were determined using radio-HPLC. Measurements were conducted in mitochondria isolated from newborn, 24-h (fed or fasted), and 5-mo-old pigs. Acetate rather than ketone bodies was the predominant radiolabeled product, and its production increased twofold with increasing fatty acid oxidation during the first 24-h suckling period. The rate of acetogenesis was directly proportional to CPT I activity. The high activity of CPT I in 24-h-suckling piglets was not attributable to an increase in CPT I gene expression, but rather to a large decrease in the sensitivity of CPT I to malonyl-CoA inhibition, which offset a developmental decrease in affinity of CPT I for palmitoyl-CoA. Specifically, the IC(50) for malonyl-CoA inhibition and K(m) value for palmitoyl-CoA measured in 24-h-suckling pigs were 1.8- and 2.7-fold higher than measured in newborn pigs. The addition of anaplerotic carbon from malate (10 mM) significantly reduced (14)C accumulation in acetate (P < 0.003); moreover, the reduction was much greater in newborn (80%) than in 24-h-fed (72%) and 5-mo-old pigs (55%). The results demonstrate that acetate is the primary product of hepatic mitochondrial beta-oxidation in Sus scrofa and that regulation during early development is mediated primarily via kinetic modulation of CPT I.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1522-1490
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
298
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
R1435-43
pubmed:meshHeading
pubmed-meshheading:20237302-Acetates, pubmed-meshheading:20237302-Acetyl-CoA Hydrolase, pubmed-meshheading:20237302-Age Factors, pubmed-meshheading:20237302-Animals, pubmed-meshheading:20237302-Animals, Suckling, pubmed-meshheading:20237302-Carbon Radioisotopes, pubmed-meshheading:20237302-Carnitine O-Palmitoyltransferase, pubmed-meshheading:20237302-Citric Acid, pubmed-meshheading:20237302-Citric Acid Cycle, pubmed-meshheading:20237302-Enzyme Activation, pubmed-meshheading:20237302-Fatty Acids, pubmed-meshheading:20237302-Gene Expression Regulation, Enzymologic, pubmed-meshheading:20237302-Ketone Bodies, pubmed-meshheading:20237302-Liver, pubmed-meshheading:20237302-Malonyl Coenzyme A, pubmed-meshheading:20237302-Mitochondria, pubmed-meshheading:20237302-Mitochondria, Liver, pubmed-meshheading:20237302-Oxidation-Reduction, pubmed-meshheading:20237302-Palmitates, pubmed-meshheading:20237302-Palmitoyl Coenzyme A, pubmed-meshheading:20237302-RNA, Messenger, pubmed-meshheading:20237302-Sus scrofa
pubmed:year
2010
pubmed:articleTitle
Carnitine palmitoyltransferase I control of acetogenesis, the major pathway of fatty acid {beta}-oxidation in liver of neonatal swine.
pubmed:affiliation
Laboratory of Developmental Nutrition, Department of Animal Science, North Carolina State University, Raleigh, NC 27695, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.