Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1984-7-16
pubmed:abstractText
Intragastric infusion of [1-14C]glucose into awake, fasted rats at rates that produced physiological increases in the circulating glucose concentration resulted in active glycogen deposition in liver. However, degradation of this glycogen revealed extensive randomization of the label among the carbon atoms of glucose. By contrast, muscle glycogen-glucose was labeled primarily in C-1. Treatment of rats with 3-mercaptopicolinic acid, a potent inhibitor of phosphoenol-pyruvate carboxykinase, prior to [1-14C]glucose infusion reduced hepatic glycogen synthesis by 85%; this glycogen contained most of its label in C-1 of glucose. The additional infusion of unlabeled glycerol, which enters the gluconeogenic pathway distal to the 3-mercaptopicolinic acid block, reinstated hepatic glycogen synthesis, but again the label was associated almost exclusively with C-1. In all animals treated with 3-mercaptopicolinic acid, plasma lactate concentrations rose markedly, as did the rate of hepatic lipogenesis. When [1-14C]glucose was infused into pentobarbital-treated rats or administered to awake animals as a large intragastric bolus, the degree of isotopic randomization in liver glycogen-glucose was considerably reduced when compared with that seen in the awake, infused state. The data support the concept that under normal refeeding conditions the bulk of liver glycogen is formed by an indirect pathway involving the sequence glucose ----lactate----glucose-6-P----glycogen, whereas muscle glycogen is formed by the conventional, direct pathway: glucose----glucose-6-P----glycogen. They also establish that a predominantly direct mechanism can be induced in liver, but only under artificial conditions, e.g. chemical blockade of the gluconeogenic sequence, pentobarbital anesthesia, or the administration of massive glucose loads that lead to severe hyperglycemia.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
259
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6958-63
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1984
pubmed:articleTitle
Efficient hepatic glycogen synthesis in refeeding rats requires continued carbon flow through the gluconeogenic pathway.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't