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1 ted triglyceride levels in the plasma (i.e., chylomicronemia).
2 ure provides insights into mutations causing chylomicronemia.
3 d GPIHBP1 and LPL mutations causing familial chylomicronemia.
4 P1 mutations prevent LPL binding and lead to chylomicronemia.
5 at interfere with LPL binding cause familial chylomicronemia.
6 y reducing and GLP-2 increasing postprandial chylomicronemia.
7 ients with an orphan indication for familial chylomicronemia.
8 deficient mice (Gpihbp1(-/-)) exhibit severe chylomicronemia.
9 , Dgat1(-/-) mice had reduced postabsorptive chylomicronemia (1 h after a high fat challenge) and acc
10  636 UK Biobank participants: 63 (0.01%) had chylomicronemia; 40 005 (8.9%) had hypercholesterolemia;
11  residues, including several associated with chylomicronemia, also led to protein dimerization/multim
12 protein lipase activity and characterized by chylomicronemia and recurrent episodes of pancreatitis.
13          After establishment of steady-state chylomicronemia and suppression of adipose tissue lipoly
14 linical trials for the treatment of familial chylomicronemia and TTR-mediated polyneuropathy.
15  monomers is relevant to the pathogenesis of chylomicronemia because only GPIHBP1 monomers-and not di
16 r GPIHBP1 cause severe hypertriglyceridemia (chylomicronemia), but structures for LPL and GPIHBP1 hav
17 ations initially identified in patients with chylomicronemia, C418Y and E421K, abolish LPL's ability
18        Earlier studies have established that chylomicronemia can be caused by LPL mutations that inte
19                                          The chylomicronemia in Gpihbp1-deficient mice, the fact that
20                                   Persistent chylomicronemia is a genetic recessive disorder that is
21 nted to support the concept that a sustained chylomicronemia is the primary factor in the production
22 ncluding mutants identified in patients with chylomicronemia) led to the formation of disulfide-linke
23           We hypothesized that some cases of chylomicronemia might be caused by LPL mutations that in
24 order that is classically caused by familial chylomicronemia syndrome (FCS), but it also has multifac
25 ely compromised LPL activity causes familial chylomicronemia syndrome (FCS), which is associated with
26 nd some associated proteins, termed familial chylomicronemia syndrome (FCS); or familial partial lipo
27  hypertriglyceridemia, termed multifactorial chylomicronemia syndrome (MFCS); a deficiency in the enz
28 1, to treat three patients with the familial chylomicronemia syndrome and triglyceride levels ranging
29                                         Most chylomicronemia syndrome cases are the result of MFCS; F
30                                     Familial chylomicronemia syndrome is a genetic disorder associate
31                                 The familial chylomicronemia syndrome is a genetic disorder character
32                                     Familial chylomicronemia syndrome is a rare genetic disorder that
33                                          The chylomicronemia syndrome occurs when triglyceride levels
34 atients with genetically identified familial chylomicronemia syndrome to receive olezarsen at a dose
35 ts of patients with sHTG: cohort 1, familial chylomicronemia syndrome with bi-allelic loss-of-functio
36 mutations (n = 17); cohort 2, multifactorial chylomicronemia syndrome with heterozygous loss-of-funct
37 tions (n = 15); and cohort 3, multifactorial chylomicronemia syndrome without LPL pathway mutations (
38 lemia, elevated lipoprotein(a), and familial chylomicronemia syndrome, and discusses the genetic-base
39                    In patients with familial chylomicronemia syndrome, olezarsen may represent a new
40 ring triglycerides in patients with familial chylomicronemia syndrome.
41 r deciliter in 77% of patients with familial chylomicronemia syndrome.
42 of volanesorsen in 66 patients with familial chylomicronemia syndrome.
43 s review describes the 3 major causes of the chylomicronemia syndrome; their consequences; and the ap
44                     Patients with persistent chylomicronemia who received plozasiran had significantl
45 andomly assigned 75 patients with persistent chylomicronemia (with or without a genetic diagnosis) to
46                Mice lacking GPIHBP1 manifest chylomicronemia, with plasma triglyceride levels as high