Linked Life Data

15375779

Source:http://linkedlifedata.com/resource/pubmed/id/15375779

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2004-9-17
pubmed:abstractText
The metabolism of apolipoproteins (apo)B-48, B-100, and A-I was studied with a primed constant infusion of deuterium-labeled leucine in the fed state in 3 male individuals with chronic kidney disease (CKD), a glomerular filtration rate (GFR) of 28 to 57 mL/min/1.73 m2, obesity (body mass index [BMI] 33.1), and the metabolic syndrome. Compared to 5 obese controls (BMI 30.1) and 13 non-obese controls (BMI 25.2), these CKD subjects had high plasma levels of triglycerides (TG) (343 +/- 27.5 mg/dL v 144 +/- 34.4 in the obese controls, P < .001) and low apoA-I (86.7 +/- 3.9 mg/dL). An abnormal high-density lipoprotein (HDL) particle subpopulation pattern was found, with low levels of pre beta-1 and alpha1. Compared to the obese controls, very-low-density lipoprotein (VLDL) and intermediate-density lipoprotein (IDL) apoB-100 levels were elevated 2- to 3-fold, while LDL apoB-100 levels were slightly lower (-7 %) and apoB-48 levels were comparable. The high TG levels were not associated with statistically significant changes in VLDL apoB-100 kinetics, although the production rate (PR) was higher and the fractional catabolic rate (FCR) was lower. The slightly lower LDL apoB-100 levels were accompanied by a significant 3-fold increase in the FCR and a 2.7-fold increase in the PR. The lower apoA-I levels were accompanied by a 1.6-fold increase in the FCR. Compared to the non-obese controls, the PR of apoA-I was increased by 61% and 38%, respectively (P < .001) in CKD and in obese control subjects. In the control subjects, the PR of apoA-I was significantly correlated with the BMI (r = 0.81, P < .0001). The kinetic results are consistent with these hypotheses: (1) CKD is associated with decreased clearance of the TG-rich lipoproteins (TRLs) and increased catabolism of LDL; (2) obesity increases apoB-100 and apoA-I production; and (3) in CKD, TG transfer to HDL, making HDL more susceptible to catabolism, accounts for the low apoA-I levels.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0026-0495
pubmed:author
pubmed:issnType
Print
pubmed:volume
53
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1255-61
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:15375779-Aged, pubmed-meshheading:15375779-Apolipoprotein A-I, pubmed-meshheading:15375779-Apolipoprotein B-100, pubmed-meshheading:15375779-Apolipoprotein B-48, pubmed-meshheading:15375779-Apolipoproteins B, pubmed-meshheading:15375779-Cholesterol, pubmed-meshheading:15375779-Cholesterol, HDL, pubmed-meshheading:15375779-Cholesterol, LDL, pubmed-meshheading:15375779-Chronic Disease, pubmed-meshheading:15375779-Glomerular Filtration Rate, pubmed-meshheading:15375779-Humans, pubmed-meshheading:15375779-Hyperlipidemias, pubmed-meshheading:15375779-Kidney Diseases, pubmed-meshheading:15375779-Lipids, pubmed-meshheading:15375779-Lipoproteins, pubmed-meshheading:15375779-Male, pubmed-meshheading:15375779-Metabolic Syndrome X, pubmed-meshheading:15375779-Middle Aged, pubmed-meshheading:15375779-Models, Biological, pubmed-meshheading:15375779-Obesity
pubmed:year
2004
pubmed:articleTitle
Apolipoprotein A-I, B-100, and B-48 metabolism in subjects with chronic kidney disease, obesity, and the metabolic syndrome.
pubmed:affiliation
Lipid Metabolism Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't