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1 LpL knockout mice; however, these mice were hypertriglyceridemic.
2 , hyperleptinemic, hypercholesterolemic, and hypertriglyceridemic.
6 cterized by hyperglycemic, hyperinsulinemic, hypertriglyceridemic, and enhanced noradrenergic indexes
8 ess mice became obese, hypercholesterolemic, hypertriglyceridemic, and hyperinsulinemic compared with
11 In addition, SCD1 deficiency prevented the hypertriglyceridemic effect and reduced hepatic triglyce
13 creased in both the hypercholesterolemic and hypertriglyceridemic groups (298 +/- 29 and 342 +/- 31 n
16 [NL]) and those with moderately elevated TG (hypertriglyceridemic [HTG]) were studied on both a contr
17 ism by which statins lower VLDL (and LDL) in hypertriglyceridemic individuals is by stimulation of li
18 litate the development of atherosclerosis in hypertriglyceridemic individuals, we used in situ hybrid
20 gnosing and treating patients with suspected hypertriglyceridemic pancreatitis; or diagnosing hypertr
21 n of lipoproteins is increased when familial hypertriglyceridemic patients are treated with drugs tha
22 n of VLDL to an apoC-III-dominated system in hypertriglyceridemic patients characterized by reduced c
27 ce received an adenovirus encoding Pltp, the hypertriglyceridemic response to T0901317 was partially
32 asted VLDLr knockout (VLDLr0) mice were more hypertriglyceridemic than controls (2-fold greater trigl
33 istics seem to be common to postprandial and hypertriglyceridemic very low density lipoproteins as we
34 vivo to examine the capacity of fasting vs. hypertriglyceridemic whole blood to attenuate the effect
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