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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1995-10-4
pubmed:abstractText
In a randomized crossover study, we measured the hepatic secretion rate of very-low-density lipoprotein (VLDL) apolipoprotein B-100 (apoB) in seven patients with well-controlled non-insulin-dependent diabetes mellitus (NIDDM) (HbA1 8.4 +/- 0.4% [mean +/- SE]) on two occasions: during a 13-h hyperinsulinemic (plasma insulin concentration 586 +/- 9.7 pmol/l) euglycemic (plasma glucose concentration 5.2 +/- 0.1 mmol/l) clamp; and during a 13-h saline (control) infusion. After 5 h of the hyperinsulinemic euglycemic clamp (or saline infusion) when a new steady state of apoB turnover was reached, [1-(13)C]leucine was administered by a primed (1 mg/kg), constant 8-h infusion (1 mg.kg-1. h-1). VLDL apoB isotopic enrichment was determined with gas chromatography-mass spectrometry, and a monoexponential model was used to calculate the fractional secretion rate of VLDL apoB. VLDL apoB secretion rate was significantly reduced during the hyperinsulinemic euglycemic clamp compared with the saline study (12.2 +/- 3.6 vs. 24.5 +/- 7.1 mg.kg-1.day-1, P = 0.001), but there was no change in the fractional catabolic rate of VLDL apoB. Concomitantly, plasma concentrations of nonesterified fatty acids (NEFAs), glycerol, and triglycerides (TGs) were significantly lower during the hyperinsulinemic euglycemic clamp compared with the saline study (NEFAs, P < 0.001; glycerol, P = 0.005; TGs P = 0.004). We conclude that acute hyperinsulinemia decreases the hepatic secretion rate of VLDL apoB in NIDDM, probably in part due to reduction in the delivery of NEFA and glycerol substrate to the liver.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
44
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1059-65
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:7657029-Apolipoprotein B-100, pubmed-meshheading:7657029-Apolipoproteins B, pubmed-meshheading:7657029-Apolipoproteins E, pubmed-meshheading:7657029-C-Peptide, pubmed-meshheading:7657029-Cross-Over Studies, pubmed-meshheading:7657029-Diabetes Mellitus, Type 2, pubmed-meshheading:7657029-Female, pubmed-meshheading:7657029-Glucose Clamp Technique, pubmed-meshheading:7657029-Humans, pubmed-meshheading:7657029-Hyperinsulinism, pubmed-meshheading:7657029-Infusions, Intravenous, pubmed-meshheading:7657029-Insulin, pubmed-meshheading:7657029-Kinetics, pubmed-meshheading:7657029-Lipoproteins, VLDL, pubmed-meshheading:7657029-Liver, pubmed-meshheading:7657029-Male, pubmed-meshheading:7657029-Middle Aged, pubmed-meshheading:7657029-Phenotype, pubmed-meshheading:7657029-Time Factors
pubmed:year
1995
pubmed:articleTitle
Acute hyperinsulinemia decreases the hepatic secretion of very-low-density lipoprotein apolipoprotein B-100 in NIDDM.
pubmed:affiliation
Department of Medicine, St. Thomas' Hospital, United Medical and Dental School of Guys Hospital, London, U.K.
pubmed:publicationType
Journal Article, Clinical Trial, Comparative Study, Randomized Controlled Trial, Research Support, Non-U.S. Gov't