Relationship of plasma apolipoprotein M with proprotein convertase subtilisin-kexin type 9 levels in non-diabetic subjects
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Relationship of plasma apolipoprotein M with proprotein convertase subtilisin-kexin type 9 levels in non-diabetic subjects. / Kappelle, Paul J W H; Lambert, Gilles; Dahlbäck, Björn; Nielsen, Lars Bo; Dullaart, Robin P F.
I: Atherosclerosis, Bind 214, Nr. 2, 2011, s. 492-494.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Relationship of plasma apolipoprotein M with proprotein convertase subtilisin-kexin type 9 levels in non-diabetic subjects
AU - Kappelle, Paul J W H
AU - Lambert, Gilles
AU - Dahlbäck, Björn
AU - Nielsen, Lars Bo
AU - Dullaart, Robin P F
N1 - Copyright © 2010. Published by Elsevier Ireland Ltd.
PY - 2011
Y1 - 2011
N2 - PURPOSE: Apolipoprotein M (apoM) retards atherosclerosis development in murine models, and may be regulated by pathways involved in LDL metabolism. Proprotein convertase subtilisin-kexin type 9 (PCSK9) plays a key role in LDL receptor processing. We determined the extent to which plasma apoM is related to PCSK9 levels in subjects with varying degrees of obesity. METHODS: We sought correlations between plasma apoM and PCSK9, measured using recently developed ELISAs, in 79 non-diabetic subjects. RESULTS: ApoM and PCSK9 levels were both correlated positively with total cholesterol, non-HDL cholesterol, LDL cholesterol and apoB (P <0.05 to P <0.001). ApoM correlated positively with PCSK9 in lean individuals (n = 37, r = 0.337, P = 0.041), but not in overweight subjects (n = 32, r = 0.125, P = 0.50) and in obese subjects (n = 10, r = -0.055, P = 0.88). CONCLUSIONS: The PCSK9 pathway may contribute to plasma apoM regulation in humans. The influence of PCSK9 on circulating apoM appears to be modified by adiposity
AB - PURPOSE: Apolipoprotein M (apoM) retards atherosclerosis development in murine models, and may be regulated by pathways involved in LDL metabolism. Proprotein convertase subtilisin-kexin type 9 (PCSK9) plays a key role in LDL receptor processing. We determined the extent to which plasma apoM is related to PCSK9 levels in subjects with varying degrees of obesity. METHODS: We sought correlations between plasma apoM and PCSK9, measured using recently developed ELISAs, in 79 non-diabetic subjects. RESULTS: ApoM and PCSK9 levels were both correlated positively with total cholesterol, non-HDL cholesterol, LDL cholesterol and apoB (P <0.05 to P <0.001). ApoM correlated positively with PCSK9 in lean individuals (n = 37, r = 0.337, P = 0.041), but not in overweight subjects (n = 32, r = 0.125, P = 0.50) and in obese subjects (n = 10, r = -0.055, P = 0.88). CONCLUSIONS: The PCSK9 pathway may contribute to plasma apoM regulation in humans. The influence of PCSK9 on circulating apoM appears to be modified by adiposity
KW - Adiposity
KW - Aged
KW - Apolipoproteins
KW - Apolipoproteins B
KW - Biological Markers
KW - Body Mass Index
KW - Cholesterol
KW - Cholesterol, LDL
KW - Enzyme-Linked Immunosorbent Assay
KW - Humans
KW - Lipocalins
KW - Middle Aged
KW - Netherlands
KW - Obesity
KW - Overweight
KW - Regression Analysis
KW - Serine Endopeptidases
U2 - 10.1016/j.atherosclerosis.2010.10.041
DO - 10.1016/j.atherosclerosis.2010.10.041
M3 - Journal article
C2 - 21122852
VL - 214
SP - 492
EP - 494
JO - Atherosclerosis
JF - Atherosclerosis
SN - 0021-9150
IS - 2
ER -
ID: 33815202