Linked Life Data

3109493

Source:http://linkedlifedata.com/resource/pubmed/id/3109493

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1987-8-20
pubmed:abstractText
Mechanisms responsible for hypertriglyceridemia in Tangier disease were elucidated by an analysis of the plasma post-heparin lipolytic activities and the structural and metabolic properties of very low (VLDL) and low (LDL) density lipoproteins. The levels of lipoprotein lipase activity in six Tangier patients were significantly lower (P less than 0.001) than in 40 control subjects (8.1 +/- 3.3 (+/- S.D.) vs. 14.1 +/- 3.7 units/ml). In contrast, the levels of hepatic triacylglycerol lipase were higher (P less than 0.01) than in normal controls (14.4 +/- 3.9 vs. 9.3 +/- 4.0 units/ml). Because kinetic parameters such as Km or Vmax cannot be obtained with naturally occurring triacylglycerol-rich lipoproteins, the pseudo-first-order rate constant (k1) of triacylglycerol hydrolysis was used to assess the effectiveness of triacylglycerol-rich lipoproteins as substrates for lipoprotein lipase. The k1 values for Tangier VLDL (k1 = 0.017 +/- 0.002 min-1) were significantly lower (P less than 0.001) than the k1 values (0.036 +/- 0.008 min-1) for control VLDL. Both the Tangier and control LDL2 are similar in their resistance to the action of lipoprotein lipase, as shown by their low k1 values (0.002 +/- 0.001 and 0.001 +/- 0.001 min-1, respectively). The major compositional difference between the lipoproteins of Tangier disease and normal subjects was a significant increase in the percent content of apolipoprotein A-II in all lipoprotein particles with d less than 1.063 g/ml, with the greatest increase occurring in VLDL and the lowest in LDL2. These results were interpreted as indicating that, in Tangier disease, there is a lower reactivity of VLDL with lipoprotein lipase which may in part be attributed to the abnormal apolipoprotein composition. This finding, in conjunction with the reduced levels of lipoprotein lipase activity, may explain the hypertriglyceridemia in Tangier disease.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0006-3002
pubmed:author
pubmed:issnType
Print
pubmed:day
13
pubmed:volume
920
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
9-19
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:3109493-Adult, pubmed-meshheading:3109493-Apolipoprotein A-II, pubmed-meshheading:3109493-Apolipoprotein C-III, pubmed-meshheading:3109493-Apolipoproteins, pubmed-meshheading:3109493-Apolipoproteins A, pubmed-meshheading:3109493-Apolipoproteins C, pubmed-meshheading:3109493-Cholesterol, pubmed-meshheading:3109493-Female, pubmed-meshheading:3109493-Humans, pubmed-meshheading:3109493-Hypolipoproteinemias, pubmed-meshheading:3109493-Kinetics, pubmed-meshheading:3109493-Lipolysis, pubmed-meshheading:3109493-Lipoprotein Lipase, pubmed-meshheading:3109493-Lipoproteins, pubmed-meshheading:3109493-Lipoproteins, LDL, pubmed-meshheading:3109493-Lipoproteins, VLDL, pubmed-meshheading:3109493-Male, pubmed-meshheading:3109493-Middle Aged, pubmed-meshheading:3109493-Tangier Disease, pubmed-meshheading:3109493-Triglycerides
pubmed:year
1987
pubmed:articleTitle
Studies on the mechanism of hypertriglyceridemia in Tangier disease. Determination of plasma lipolytic activities, k1 values and apolipoprotein composition of the major lipoprotein density classes.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't