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1 ted triglyceride levels in the plasma (i.e., chylomicronemia).
2 d GPIHBP1 and LPL mutations causing familial chylomicronemia.
3 P1 mutations prevent LPL binding and lead to chylomicronemia.
4 ients with an orphan indication for familial chylomicronemia.
5 deficient mice (Gpihbp1(-/-)) exhibit severe chylomicronemia.
6 at interfere with LPL binding cause familial chylomicronemia.
7 y reducing and GLP-2 increasing postprandial chylomicronemia.
8 , Dgat1(-/-) mice had reduced postabsorptive chylomicronemia (1 h after a high fat challenge) and acc
9 residues, including several associated with chylomicronemia, also led to protein dimerization/multim
12 monomers is relevant to the pathogenesis of chylomicronemia because only GPIHBP1 monomers-and not di
13 ations initially identified in patients with chylomicronemia, C418Y and E421K, abolish LPL's ability
16 nted to support the concept that a sustained chylomicronemia is the primary factor in the production
17 ncluding mutants identified in patients with chylomicronemia) led to the formation of disulfide-linke
19 1, to treat three patients with the familial chylomicronemia syndrome and triglyceride levels ranging
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