Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-8-31
pubmed:abstractText
In animals receiving total parenteral nutrition (TPN), infection impairs net hepatic glucose uptake (NHGU) by 40% and induces mild hyperinsulinemia. In the normal animal, the majority of the glucose taken up by the liver is diverted to lactate, but in the infected state, lactate release is curtailed. Because of the hyperinsulinemia and reduced NHGU, more glucose is utilized by peripheral tissues. Our aims were to determine the role of infection-induced hyperinsulinemia in 1) limiting the fall in NHGU and hepatic lactate release and 2) increasing the proportion of glucose disposed of by peripheral tissues. Chronically catheterized dogs received TPN for 5 days via the inferior vena cava. On day 3, a fibrin clot with a nonlethal dose of E. coli was placed into the peritoneal cavity; sham dogs received a sterile clot. On day 5, somatostatin was infused to prevent endogenous pancreatic hormone secretion, and insulin and glucagon were replaced at rates matching incoming hormone concentrations observed previously in sham or infected dogs. The TPN-derived glucose infusion was adjusted to maintain a constant arterial plasma glucose level of approximately 120 mg/dl. after a basal blood sampling period, the insulin infusion rate was either maintained constant (infected time control, Hi-Ins, n = 6; sham time control, Sham, n = 6) or decreased (infected + reduced insulin, Lo-Ins; n = 6) for 180 min to levels seen in noninfected dogs (from 23 +/- 2 to 12 +/- 1 microU/ml). Reduction of insulin to noninfected levels decreased NHGU by 1.4 +/- 0.5 mg x kg(-1) x min(-1) (P < 0.05) and nonhepatic glucose utilization by 4.8 +/- 0.8 mg x kg(-1) x min(-1) (P < 0.01). The fall in NHGU was caused by a decline in HGU (Delta-0.6 +/- 0.4 mg x kg(-1) x min(-1)) and a concomitant increase in hepatic glucose production (HGP, Delta0.8 +/- 0.5 mg x kg(-1) x min(-1)); net hepatic lactate release was not altered. Hyperinsulinemia that accompanies infection 1) primarily diverts glucose carbon to peripheral tissues, 2) limits the fall in NHGU by enhancing HGU and suppressing HGP, and 3) does not enhance hepatic lactate release, thus favoring hepatic glucose storage. Compensatory hyperinsulinemia plays a critical role in facilitating hepatic and peripheral glucose disposal during an infection.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0193-1849
pubmed:author
pubmed:issnType
Print
pubmed:volume
279
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
E235-43
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:10913021-Animals, pubmed-meshheading:10913021-Blood Glucose, pubmed-meshheading:10913021-Catheterization, pubmed-meshheading:10913021-Dogs, pubmed-meshheading:10913021-Dose-Response Relationship, Drug, pubmed-meshheading:10913021-Energy Metabolism, pubmed-meshheading:10913021-Escherichia coli Infections, pubmed-meshheading:10913021-Fatty Acids, Nonesterified, pubmed-meshheading:10913021-Female, pubmed-meshheading:10913021-Glucagon, pubmed-meshheading:10913021-Glucose, pubmed-meshheading:10913021-Glycerol, pubmed-meshheading:10913021-Hemodynamics, pubmed-meshheading:10913021-Hindlimb, pubmed-meshheading:10913021-Hyperinsulinism, pubmed-meshheading:10913021-Infusions, Intravenous, pubmed-meshheading:10913021-Insulin, pubmed-meshheading:10913021-Lactic Acid, pubmed-meshheading:10913021-Liver, pubmed-meshheading:10913021-Parenteral Nutrition, Total, pubmed-meshheading:10913021-Somatostatin
pubmed:year
2000
pubmed:articleTitle
Hyperinsulinemia compensates for infection-induced impairment in net hepatic glucose uptake during TPN.
pubmed:affiliation
Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.