ライフサイエンスコーパス: hypertriglyceridemia

1 triglyceride hydrolysis, resulting in severe hypertriglyceridemia.

2 de accrual, VLDL-triglyceride synthesis, and hypertriglyceridemia.

3 etic polyunsaturated fatty acid that reduces hypertriglyceridemia.

4 f GPIHBP1, defective LPL binding, and severe hypertriglyceridemia.

5 NGPTL8 represents a therapeutic strategy for hypertriglyceridemia.

6 with hepatic triglyceride overproduction and hypertriglyceridemia.

7 duced bulk-adiposity, hepatic steatosis, and hypertriglyceridemia.

8 effective in the management of postprandial hypertriglyceridemia.

9 yceride concentrations only in subjects with hypertriglyceridemia.

10 ith severe hypoglycemia, lactic acidosis and hypertriglyceridemia.

11 s a lipid-lowering agent in the treatment of hypertriglyceridemia.

12 ic-range proteinuria and the pathogenesis of hypertriglyceridemia.

13 rs of WT mice promoted hepatic steatosis and hypertriglyceridemia.

14 vated insulin resistance, hyperglycemia, and hypertriglyceridemia.

15 serum iron levels in individuals at risk for hypertriglyceridemia.

16 that it would also prevent fructose-induced hypertriglyceridemia.

17 GPTL8 in Angptl3(-/-) mice failed to promote hypertriglyceridemia.

18 he fructose-induced increase in IHCL but not hypertriglyceridemia.

19 their hepatocytes and abolishes postprandial hypertriglyceridemia.

20 tions in CREB3L3 in individuals with extreme hypertriglyceridemia.

21 in the plasma, impaired VLDL catabolism, and hypertriglyceridemia.

22 e, with the development of hyperglycemia and hypertriglyceridemia.

23 VLDL levels and is used therapeutically for hypertriglyceridemia.

24 ically, mice lacking ACAT2 also exhibit mild hypertriglyceridemia.

25 for apoC-III in metabolic defects leading to hypertriglyceridemia.

26 ndrome, hypertension, abdominal obesity, and hypertriglyceridemia.

27 is, pneumothorax, haemoptysis, seizures, and hypertriglyceridemia.

28 us over 8 wk in healthy adults with moderate hypertriglyceridemia.

29 pid storage with subsequent hepatomegaly and hypertriglyceridemia.

30 vator T0901317 produces a mild and transient hypertriglyceridemia.

31 e large VLDLs accumulate and produce massive hypertriglyceridemia.

32 f apolipoprotein (apo) E are associated with hypertriglyceridemia.

33 ught to identify novel mechanisms leading to hypertriglyceridemia.

34 pe (WT) apoE4 in apoE-deficient mice induces hypertriglyceridemia.

35 other groups, especially among persons with hypertriglyceridemia.

36 of triglyceride-rich VLDL is attributable to hypertriglyceridemia.

37 F1 emerges as an important candidate gene in hypertriglyceridemia.

38 yndrome, including IR, obesity, and a marked hypertriglyceridemia.

39 e apoAIItg mice, further contributing to the hypertriglyceridemia.

40 srupt this interaction for the management of hypertriglyceridemia.

41 P-1c activity in these tissues did not cause hypertriglyceridemia.

42 rides; these agents are also widely used for hypertriglyceridemia.

43 h PPAR-gamma agonism in patients ofT2DM with hypertriglyceridemia.

44 and PD compared with untreated patients with hypertriglyceridemia.

45 ilar proportions of hypercholesterolemia and hypertriglyceridemia.

46 a have a causal role in carbohydrate-induced hypertriglyceridemia.

47 nefits and are available by prescription for hypertriglyceridemia.

48 for treating epithelial cancers and induces hypertriglyceridemia.

49 ted fatty acids on atherosclerotic events in hypertriglyceridemia.

50 reased triglyceride secretion as observed by hypertriglyceridemia.

51 nase activity levels), and 37% had grade 3/4 hypertriglyceridemia.

52 ia and colorectal neoplasia was observed for hypertriglyceridemia.

53 d prevent the onset of hepatic steatosis and hypertriglyceridemia.

54 e were most robust in individuals exhibiting hypertriglyceridemia.

55 t induces in the periphery, most prominently hypertriglyceridemia.

56 riglycerides levels in patients with primary hypertriglyceridemias.

57 d hyperlipidemia (FCHL) and primary isolated hypertriglyceridemias.

58 men and 3 postmenopausal women with moderate hypertriglyceridemia (150-500 mg/dL).

59 tio [HR] 3.73, 95% CI 1.90-7.33, P < 0.001), hypertriglyceridemia (2.91, 1.52-5.56, P = 0.001), and e

60 Hypertriglyceridemia affects more than one-third of the

61 ssociated with serum TG and with the risk of hypertriglyceridemia after 2 years (OR = 1.19; 95%CI 1.0

62 nts by the liver is a key step in preventing hypertriglyceridemia, an independent risk factor for car

63 racentrifugation in 9 patients with moderate hypertriglyceridemia and 12 normotriglyceridemic control

64 zing sequence data from 458 individuals with hypertriglyceridemia and 333 controls with normal plasma

65 enriched diet induces insulin resistance and hypertriglyceridemia and affects visceral adipose tissue

66 rome due to the serious side effects such as hypertriglyceridemia and altered thyroid hormone axis.

67 rate that contributes to insulin resistance, hypertriglyceridemia and appears to be associated with t

68 combined lipase deficiency with concomitant hypertriglyceridemia and associated disorders.

69 264A, F265A, L268A, V269A)), does not induce hypertriglyceridemia and corrects hypercholesterolemia.

70 ficient diabetic mice that displayed fasting hypertriglyceridemia and delayed clearance of dietary tr

71 4(W276A, L279A, V280A, V283A)), induces mild hypertriglyceridemia and does not correct hypercholester

72 severely obese participants with T2D display hypertriglyceridemia and excessive systemic lipolysis du

73 Hyperglycemia, hypertriglyceridemia and greater hyperinsulinemia develo

74 Excess fructose intake causes hypertriglyceridemia and hepatic insulin resistance in s

75 However, hypertriglyceridemia and hepatic steatosis are not due d

76 hepatocytes and adipocytes, is required for hypertriglyceridemia and hepatic steatosis induced by th

77 /-)) had reductions in dexamethasone-induced hypertriglyceridemia and hepatic steatosis, suggesting t

78 coid exposure causes lipid disorders such as hypertriglyceridemia and hepatic steatosis.

79 ng effect, but the relation between nuts and hypertriglyceridemia and high-density lipoprotein choles

80 Hypertriglyceridemia and higher creatinine are the key f

81 Maximum prevalence of hypertriglyceridemia and hypercholesterolemia was found

82 with hypoalbuminemia, edema, hyperlipidemia (hypertriglyceridemia and hypercholesterolemia), and lipi

83 Sirolimus causes hypertriglyceridemia and hypercholesterolemia, but it do

84 Two adverse effects of sirolimus are hypertriglyceridemia and hypercholesterolemia.

85 n of LIGHT expression on T cells resulted in hypertriglyceridemia and hypercholesterolemia.

86 Adverse metabolic changes, including hypertriglyceridemia and hyperglycemia, are common.

87 nclude that saroglitazar effectively reduces hypertriglyceridemia and improves insulin sensitivity al

88 ting LDL cholesterol in patients with severe hypertriglyceridemia and in those with mixed dyslipidemi

89 u261Ala/Trp264Ala/Phe265Ala]) did not induce hypertriglyceridemia and increased greatly the HDL chole

90 (apoE4[Leu261Ala/Trp264Ala]) induced milder hypertriglyceridemia and increased HDL cholesterol level

91 Hepatic overexpression of ANGPTL8 causes hypertriglyceridemia and increased insulin secretion.

92 CRMP treatment reversed hypertriglyceridemia and insulin resistance in liver and

93 such as hypertension, hypercholesterolemia, hypertriglyceridemia and insulin resistance, and also in

94 Rdelta has uncovered a dual benefit for both hypertriglyceridemia and insulin resistance, highlightin

95 ha and PPARgamma are therapeutic targets for hypertriglyceridemia and insulin resistance, respectivel

96 vastatin alone in participants with moderate hypertriglyceridemia and low HDL-cholesterol on major ca

97 ay reduce CVD in patients with diabetes with hypertriglyceridemia and low high-density lipoprotein ch

98 ardiovascular disease (CVD) in part owing to hypertriglyceridemia and low high-density lipoprotein ch

99 ges typically associated with NAFLD, such as hypertriglyceridemia and low high-density lipoprotein ch

100 al lipid profile (group H), 30 patients with hypertriglyceridemia and not on medication (group N), an

101 romal PD above 50% had higher frequencies of hypertriglyceridemia and prediabetes (p < 0.005, p = 0.0

102 la improves the apoE functions by preventing hypertriglyceridemia and promoting formation of spherica

103 s a genetic disorder characterized by severe hypertriglyceridemia and recurrent pancreatitis due to a

104 Marked hypertriglyceridemia and reduced levels of high-density

105 eted mitochondrial uncoupling could decrease hypertriglyceridemia and reverse NASH and diabetes in a

106 rophies are an important cause for monogenic hypertriglyceridemia and serve to highlight the role of

107 Postoperatively, the patient developed hypertriglyceridemia and systemic hypertension.

108 n medication (group N), and 30 patients with hypertriglyceridemia and taking gemfibrozil over a 3-mon

109 ation in the pathogenesis of obesity-related hypertriglyceridemia and underscore the potential effica

110 y longer in patients with bexarotene-induced hypertriglyceridemia and/or skin rash.

111 This study involved 580 patients with hypertriglyceridemias and 403 controls.

112 c and genotype frequency differences between hypertriglyceridemias and controls.

113 esented similar frequencies between isolated hypertriglyceridemias and FCHL.

114 ial and sporadic hypertriglyceridemias or to hypertriglyceridemias and hypercholesterolemia in case o

115 bution of common genetic variants in primary hypertriglyceridemias and the genetic difference between

116 ipoprotein goal but with persistent moderate hypertriglyceridemia), and off-label claim + evidence co

117 refluxed bile acids, hypercalcemia, ethanol, hypertriglyceridemia, and acidosis.

118 lerosis-hypercholesterolemia, hyperglycemia, hypertriglyceridemia, and even the process of aging-all

119 In contrast, lipogenesis, hypertriglyceridemia, and hepatic steatosis are increase

120 aused glucose intolerance, hyperinsulinemia, hypertriglyceridemia, and hepatic steatosis in mice.

121 iet-induced hyperinuslinemia, hyperglycemia, hypertriglyceridemia, and hepatic steatosis.

122 atients' baseline data on obesity, diabetes, hypertriglyceridemia, and high blood pressure to assign

123 Furthermore, associations with obesity, hypertriglyceridemia, and hyperglycemia increase with in

124 : abdominal obesity, diabetes, hypertension, hypertriglyceridemia, and hypo-alpha-lipoproteinemia.

125 ominal obesity, hyperglycemia, hypertension, hypertriglyceridemia, and hypo-high-density lipoprotein

126 key metabolic defects (e.g. hyperketonemia, hypertriglyceridemia, and increased hepatic fatty acid o

127 oligonucleotide reverses hepatic steatosis, hypertriglyceridemia, and insulin resistance in obese mi

128 reatment opposed the development of obesity, hypertriglyceridemia, and insulin resistance.

129 levated liver fat content, TG-enriched VLDL, hypertriglyceridemia, and low HDL cholesterol levels.

130 approximately 6 +/- 2%, skeletal muscle IR, hypertriglyceridemia, and low HDL-C become fully establi

131 participants with high cardiovascular risk, hypertriglyceridemia, and low levels of high-density lip

132 ulin resistance and type 2 diabetes, extreme hypertriglyceridemia, and nonalcoholic fatty liver disea

133 ed susceptibility to diet-induced steatosis, hypertriglyceridemia, and obesity.

134 S, including hyperinsulinemia, hypertension, hypertriglyceridemia, and obesity.

135 of a trial of 4 g/d prescription EPA+DHA in hypertriglyceridemia are anticipated in 2020.

136 The majority of hypertriglyceridemias are diagnosed as familial combined

137 FCHL and isolated hypertriglyceridemias are probably trace to an accumulat

138 as most effective for patients who developed hypertriglyceridemia as a side effect.

139 to TG-rich lipoprotein particles and milder hypertriglyceridemia as compared with WT apoE4.

140 Gender, diabetes, hypertension, hypertriglyceridemia, aspartate aminotransferase (AST),

141 SOCS3 is also implicated in hypertriglyceridemia associated to insulin resistance.

142 l compartment (adipose tissue and liver) and hypertriglyceridemia associated with insulin resistance.

143 lipid metabolism, as demonstrated by severe hypertriglyceridemia associated with its mutations in mi

144 e withdrawals were treatment-related (severe hypertriglyceridemia associated with rapamycin, and panc

145 ride clearance, CREB-H-deficient mice showed hypertriglyceridemia, associated with defective producti

146 containing triglyceride-rich lipoproteins in hypertriglyceridemia, associated with increased apoC-III

147 However, 11 induces hypertriglyceridemia at its effective dose.

148 Insulin-resistant apoB/BATless mice have hypertriglyceridemia because of increased assembly and s

149 herogenicity was traditionally attributed to hypertriglyceridemia because of its inhibition on the li

150 s variants were collectively associated with hypertriglyceridemia, but a range of in silico predictio

151 nd adipose tissue, subsequently resulting in hypertriglyceridemia, by inhibiting lipoprotein lipase (

152 Diabetic ketoacidosis (DKA)-induced hypertriglyceridemia causing pancreatitis is an interest

153 ion mutations in LPL or GPIHBP1 cause severe hypertriglyceridemia (chylomicronemia), but structures f

154 f fish oil-based ILE was not associated with hypertriglyceridemia, coagulopathy, or essential fatty a

155 ensity lipoprotein cholesterol, and isolated hypertriglyceridemia) compared with normolipemia, and CI

156 nditions: the presence of secondary forms of hypertriglyceridemia concurrent with genetic causes of h

157 h lower triglycerides levels, whereas severe hypertriglyceridemia denotes a population with particula

158 hereas coexpression with ANGPTL8 resulted in hypertriglyceridemia, despite a reduction in circulating

159 elop hyperinsulinemia, acanthosis nigricans, hypertriglyceridemia, diabetes mellitus, and hepatic ste

160 ion triggers undesirable liver steatosis and hypertriglyceridemia due to increased fatty acid and ste

161 ffects of genetic susceptibility variants in hypertriglyceridemia, effects that are most evident in f

162 me, which includes type 2 diabetes mellitus, hypertriglyceridemia, essential hypertension, low circul

163 n ameliorating effect on insulin resistance, hypertriglyceridemia, fatty liver, obesity, adipositis,

164 to reduce pancreatitis risk in persons with hypertriglyceridemia, fibrates may lead to the developme

165 ) B lipoprotein metabolism that characterize hypertriglyceridemia, focusing on apoC-III and apoE.

166 nia, hypophosphatemia, asthenia, anemia, and hypertriglyceridemia for all patients and those who rece

167 Hypertriglyceridemia (>200 mg/dl) also showed a similar

168 olesterol levels but persistent, significant hypertriglyceridemia (>200 mg/dl) and low high-density l

169 erienced National Cancer Institute grade 3/4 hypertriglyceridemia had significantly longer median sur

170 Patients with hypertriglyceridemia had worse periodontal status than h

171 genetic difference between FCHL and isolated hypertriglyceridemias have not been thoroughly examined.

172 weight gain, adiposity, glucose intolerance, hypertriglyceridemia, hepatic lipidosis, and hyperleptin

173 ically elevated glucocorticoid levels induce hypertriglyceridemia, hepatic steatosis, and visceral ob

174 e level (HR = 1.20, 95% CI: 1.03, 1.39), and hypertriglyceridemia (HR = 1.14, 95% CI: 1.00, 1.30).

175 However, hypertriglyceridemia (HR, 0.38; 95% CI, 0.26 to 0.55) an

176 highest quartile of DII were associated with hypertriglyceridemia (HRQ4vsQ1 = 2.28; 95% CI: 1.13, 4.5

177 ouse models and human mendelian syndromes of hypertriglyceridemia (HTG) accumulate in patients with p

178 Hypertriglyceridemia (HTG) is a heritable risk factor fo

179 in part by hypoglycemia, growth retardation, hypertriglyceridemia, hypercholesterolemia, and hepatic

180 Hypertension, renal insufficiency, hypertriglyceridemia, hypercholesterolemia, hyperuricemi

181 improves abdominal obesity, hepatosteatosis, hypertriglyceridemia, hypercholesterolemia, insulin resi

182 diovascular risk factors, including obesity, hypertriglyceridemia, hypercholesterolemia, insulin resi

183 toxicities included CNS hemorrhage (n = 1), hypertriglyceridemia/hypercholesterolemia/elevated lipas

184 coagulopathy, liver dysfunction, cytopenias, hypertriglyceridemia, hyperferritinemia, hemophagocytosi

185 s of uric acid and ameliorates hypertension, hypertriglyceridemia, hyperglycemia, and insulin resista

186 nts of the definition of metabolic syndrome (hypertriglyceridemia, hyperglycemia, and low HDL cholest

187 tabolic risk, specifically hyperinsulinemia, hypertriglyceridemia, hyperleptinemia, and hyperuricemia

188 Insulin resistance, hyperleptinemia, hypertriglyceridemia, hyperuricemia, and oxidative stres

189 tional CREB-H protein in humans with extreme hypertriglyceridemia, implying a crucial role for CREB-H

190 gulatory protein (GCKR), was associated with hypertriglyceridemia in adults.

191 acid substitution (apoE4[Phe265Ala]) induced hypertriglyceridemia in apoE-/- or apoA-I-/- mice, promo

192 xpression of apolipoprotein E (apoE) induces hypertriglyceridemia in apoE-deficient mice, which is ab

193 l study population, occurrence of high-grade hypertriglyceridemia in bexarotene-treated patients stro

194 Conversely, overexpression of Atg14 improves hypertriglyceridemia in both high fat diet-treated wild-

195 ity, is an independent risk factor of future hypertriglyceridemia in children.

196 causative factor for VLDL overproduction and hypertriglyceridemia in diabetes.

197 F1 that cause combined lipase deficiency and hypertriglyceridemia in humans.

198 In conclusion, prandial hypertriglyceridemia in men with MetS was due to an incr

199 einemia in young adulthood, hypertension and hypertriglyceridemia in middle age, and diabetes later;

200 dy dramatically improved hepatosteatosis and hypertriglyceridemia in obese mice.

201 rtriglyceridemic pancreatitis; or diagnosing hypertriglyceridemia in patients who require therapy for

202 n mice and that shedding might contribute to hypertriglyceridemia in patients with sepsis.

203 ted against the development of steatosis and hypertriglyceridemia in response to high fructose feedin

204 ntral to the pathogenesis of fatty liver and hypertriglyceridemia in these mice.

205 Moreover, DHA abrogates bexarotene-induced hypertriglyceridemia in vivo.

206 nal obesity, hypo-alpha-lipoproteinemia, and hypertriglyceridemia in young adulthood, hypertension in

207 What are the roles of n-3 fatty acids in hypertriglyceridemia, in the metabolic syndrome and type

208 glucose intolerance, hepatic steatosis, and hypertriglyceridemia induced by high-fat diet.

209 wn of TRAP80 ameliorated liver steatosis and hypertriglyceridemia induced by LXR activation and maint

210 resis is a well known treatment modality for hypertriglyceridemia-induced pancreatitis.

211 f adipose tissue often accompanied by severe hypertriglyceridemia, insulin resistance, diabetes, and

212 In rat models, CRMP reduced hypertriglyceridemia, insulin resistance, hepatic steato

213 Marked hypertriglyceridemia is a common feature of these disord

214 Hypertriglyceridemia is a consequence of increased VLDL

215 Hypertriglyceridemia is a hallmark of many disorders, in

216 Prolonged postprandial hypertriglyceridemia is a potential risk factor for card

217 Hypertriglyceridemia is a risk factor for cardiovascular

218 Hypertriglyceridemia is an independent risk factor for c

219 Hypertriglyceridemia is associated with increased cardio

220 cardiovascular disease risk in patients with hypertriglyceridemia is supported by a 25% reduction in

221 Hypertriglyceridemia is the most common lipid disorder i

222 Dyslipidemia, particularly hypertriglyceridemia, is more difficult to treat in pati

223 complex," the main features of which include hypertriglyceridemia, low HDL cholesterol levels, qualit

224 iver fat with hypertension, type 2 diabetes, hypertriglyceridemia, low HDL-cholesterol concentration,

225 idual components of MetS (abdominal obesity, hypertriglyceridemia, low high-density lipoprotein [HDL]

226 and each component, including hypertension, hypertriglyceridemia, low high-density lipoprotein chole

227 ted the TD lipid phenotype with postprandial hypertriglyceridemia, markedly decreased LDL, and near a

228 One approach for treating hypertriglyceridemia may be to increase the amount of en

229 obtained in the fasting state, postprandial hypertriglyceridemia may play an important role in ather

230 When used to treat hypertriglyceridemia, n-3 FAs with EPA+DHA or with EPA-o

231 l novel therapy for lipodystrophy-associated hypertriglyceridemia, NASH and diabetes.

232 -release mitochondrial protonophore reverses hypertriglyceridemia, nonalcoholic steatohepatitis, and

233 lin resistance, dyslipidaemia, hypertension, hypertriglyceridemia, obesity and cardiovascular disease

234 ted with reduced risk of metabolic diseases (hypertriglyceridemia, obesity, type 2 diabetes, hyperten

235 Hypertriglyceridemia occurred less in intensification co

236 eline triglycerides (P=5.5x10(-5)) and lower hypertriglyceridemia (odds ratio, 0.73; 95% confidence i

237 out the approved on-label indication (severe hypertriglyceridemia), off-label claim + pro forma discl

238 with insulin receptor mutations develop the hypertriglyceridemia or hepatic steatosis associated wit

239 riants predisposing to familial and sporadic hypertriglyceridemias or to hypertriglyceridemias and hy

240 l (OR 0.26; 95% CI: 0.09-0.71; P=0.009), and hypertriglyceridemia (OR 4.08; 95% CI: 1.45-11.50; P=0.0

241 tive BMI was a risk factor for postoperative hypertriglyceridemia (OR, 1.17).

242 d pressure (OR, 1.18; 95% CI, 0.96 to 1.44), hypertriglyceridemia (OR, 1.25; 95% CI, 1.04 to 1.51), a

243 ratio [OR]: 1.21 for SAT; OR: 1.30 for VAT), hypertriglyceridemia (OR: 1.15 for SAT; OR: 1.56 for VAT

244 lipase deficiency (cld) mutation show severe hypertriglyceridemia owing to a decrease in the activity

245 sed age (P < 0.0001), male sex (P < 0.0001), hypertriglyceridemia (P < 0.04), low high-density lipopr

246 gher endotoxin level was associated with the hypertriglyceridemia (P = 0.003) and low HDL cholesterol

247 with higher risk of overweight (p = 0.008), hypertriglyceridemia (p = 0.040) and hypercholesterolemi

248 nding of truncated apoA-V contributes to the hypertriglyceridemia phenotype associated with truncatio

249 Along with the hypertriglyceridemia phenotype, the CrebH null mice disp

250 knockdown animals developed hypoglycemia and hypertriglyceridemia, phenotypes observed in Ppara-/- mi

251 cholesterol concentration, hypertension, and hypertriglyceridemia-predict cardiovascular disease, but

252 During this period, hypertriglyceridemia prevalence decreased (33.5% to 24.3

253 hypertension, hypercholesterolemia, profound hypertriglyceridemia, proteinuria, and renal failure.

254 best with hypertension (r = 0.2, P < 0.05), hypertriglyceridemia (r = 0.37, P < 0.001), and insulin

255 s by which the lack of adipose tissue causes hypertriglyceridemia remain unknown.

256 s the leading cause of death in the USA, and hypertriglyceridemia represents an independent risk fact

257 thrombocytopenia, neutropenia, anorexia, and hypertriglyceridemia, resulting in a MTD of vorinostat 1

258 (APOC3) that are known to be associated with hypertriglyceridemia (rs2854116 [T-455C] and rs2854117 [

259 oprotein C3 (APOC3) that have been linked to hypertriglyceridemia (rs2854117 C > T and rs2854116 T >

260 CREB-H-deficient mice showed hypertriglyceridemia secondary to inefficient triglyceri

261 Patients with lipodystrophy exhibit hypertriglyceridemia, severe insulin resistance, type 2

262 n glycemic control itself, and prevention of hypertriglyceridemia should be a major focus of clinical

263 rior inhibition of atherogenesis and reduced hypertriglyceridemia side effects in comparison to the f

264 yceridemia concurrent with genetic causes of hypertriglyceridemia, termed multifactorial chylomicrone

265 g triacylglycerol and a higher prevalence of hypertriglyceridemia than did subjects in the protective

266 he265 play an important role in apoE-induced hypertriglyceridemia, the accumulation of free cholester

267 gion of residues 261-265 on the induction of hypertriglyceridemia, the esterification of cholesterol

268 ants in human subjects correlate with severe hypertriglyceridemia, the lipid binding properties of ap

269 In patients with hypertriglyceridemia, this increase in monocyte adhesion

270 ed from light and medium LDL to dense LDL in hypertriglyceridemia through a quartet of kinetic pertur

271 etin-like 4 (Angptl4) links proteinuria with hypertriglyceridemia through two negative feedback loops

272 impact of polygenic hypercholesterolemia and hypertriglyceridemia to lipid levels in 27 039 individua

273 tion of lipoprotein lipase inhibition during hypertriglyceridemia treatment.

274 Despite the frequency of hypertriglyceridemia, treatment options are primarily li

275 ia triglycerides (200-499 mg/dL); (5) severe hypertriglyceridemia triglycerides (>/=500 mg/dL).

276 riglycerides (100-149 mg/dL); (3) borderline hypertriglyceridemia triglycerides (150-199 mg/dL); (4)

277 triglycerides (150-199 mg/dL); (4) moderate hypertriglyceridemia triglycerides (200-499 mg/dL); (5)

278 Hypertriglyceridemia (triglycerides 200-499 mg/dL) is re

279 FAs include treatment of severe and moderate hypertriglyceridemia, use in statin-treated patients wit

280 Osteoporosis/osteopenia, hypertriglyceridemia, vaginal bleeding, and hypercholest

281 Hypertriglyceridemia was characterized by a 3-fold highe

282 pertriglyceridemia, we hypothesized that the hypertriglyceridemia was due largely to overproduction o

283 year mortality risk for patients with severe hypertriglyceridemia was increased by 68% when compared

284 Hypertriglyceridemia was prevented in Ldlr(-/-) recipien

285 Hypertriglyceridemia was the most notable side effect as

286 Hypertriglyceridemia was the only comorbidity whose remi

287 ce with rosiglitazone ameliorated the IR and hypertriglyceridemia, we hypothesized that the hypertrig

288 To better understand the pathophysiology of hypertriglyceridemia, we studied hepatic regulation of t

289 In addition, high education and avoidance of hypertriglyceridemia were associated with exceptional su

290 cocorticoid- initiated hepatic steatosis and hypertriglyceridemia were improved in AKO mice.

291 iants more frequently identified in isolated hypertriglyceridemias were rs7412 in APOE and rs1800795

292 Here, we show that T0901317 produces massive hypertriglyceridemia when given to mice lacking low dens

293 e hypercholanemia, hypercholesterolemia, and hypertriglyceridemia, which can result in metabolic dise

294 ng from fructose consumption is postprandial hypertriglyceridemia, which may increase visceral adipos

295 this pathology, but at the cost of inducing hypertriglyceridemia, while also suggesting a possible t

296 rterial thrombotic events, osteoporosis, and hypertriglyceridemia, while renal involvement and anti-S

297 by clinicians to treat patients with severe hypertriglyceridemia who are at risk of pancreatitis.

298 Bexarotene-treated patients with grade 3/4 hypertriglyceridemia who received the most benefit inclu

299 Here, we report a patient with severe hypertriglyceridemia who was homozygous for a GPIHBP1 po

300 Patients with hypertriglyceridemia who were taking gemfibrozil did not