ライフサイエンスコーパス: chylomicronemia

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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

10 After establishment of steady-state chylomicronemia and suppression of adipose tissue lipoly

11 linical trials for the treatment of familial chylomicronemia and TTR-mediated polyneuropathy.

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

14 Earlier studies have established that chylomicronemia can be caused by LPL mutations that inte

15 The chylomicronemia in Gpihbp1-deficient mice, the fact that

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

18 We hypothesized that some cases of chylomicronemia might be caused by LPL mutations that in

19 1, to treat three patients with the familial chylomicronemia syndrome and triglyceride levels ranging

20 The familial chylomicronemia syndrome is a genetic disorder character

21 Mice lacking GPIHBP1 manifest chylomicronemia, with plasma triglyceride levels as high

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