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1 and PD compared with untreated patients with hypertriglyceridemia.
2 ic-range proteinuria and the pathogenesis of hypertriglyceridemia.
3 rs of WT mice promoted hepatic steatosis and hypertriglyceridemia.
4 vated insulin resistance, hyperglycemia, and hypertriglyceridemia.
5 serum iron levels in individuals at risk for hypertriglyceridemia.
6 that it would also prevent fructose-induced hypertriglyceridemia.
7 GPTL8 in Angptl3(-/-) mice failed to promote hypertriglyceridemia.
8 he fructose-induced increase in IHCL but not hypertriglyceridemia.
9 their hepatocytes and abolishes postprandial hypertriglyceridemia.
10 tions in CREB3L3 in individuals with extreme hypertriglyceridemia.
11 in the plasma, impaired VLDL catabolism, and hypertriglyceridemia.
12 e, with the development of hyperglycemia and hypertriglyceridemia.
13 nefits and are available by prescription for hypertriglyceridemia.
14 VLDL levels and is used therapeutically for hypertriglyceridemia.
15 ically, mice lacking ACAT2 also exhibit mild hypertriglyceridemia.
16 for apoC-III in metabolic defects leading to hypertriglyceridemia.
17 us over 8 wk in healthy adults with moderate hypertriglyceridemia.
18 pid storage with subsequent hepatomegaly and hypertriglyceridemia.
19 vator T0901317 produces a mild and transient hypertriglyceridemia.
20 e large VLDLs accumulate and produce massive hypertriglyceridemia.
21 f apolipoprotein (apo) E are associated with hypertriglyceridemia.
22 ught to identify novel mechanisms leading to hypertriglyceridemia.
23 pe (WT) apoE4 in apoE-deficient mice induces hypertriglyceridemia.
24 other groups, especially among persons with hypertriglyceridemia.
25 of triglyceride-rich VLDL is attributable to hypertriglyceridemia.
26 F1 emerges as an important candidate gene in hypertriglyceridemia.
27 yndrome, including IR, obesity, and a marked hypertriglyceridemia.
28 e apoAIItg mice, further contributing to the hypertriglyceridemia.
29 P-1c activity in these tissues did not cause hypertriglyceridemia.
30 ch very low density lipoprotein resulting in hypertriglyceridemia.
31 peutic regimen was well tolerated except for hypertriglyceridemia.
32 ided that there is aggressive prophylaxis of hypertriglyceridemia.
33 ted fatty acids on atherosclerotic events in hypertriglyceridemia.
34 to be ineffective in the presence of severe hypertriglyceridemia.
35 orrect hypercholesterolemia and induced mild hypertriglyceridemia.
36 reased triglyceride secretion as observed by hypertriglyceridemia.
37 t track history as oral agents used to treat hypertriglyceridemia.
38 nd after a 20% intralipid infusion to induce hypertriglyceridemia.
39 n glucose intolerance, hyperinsulinemia, and hypertriglyceridemia.
40 constitutively active Foxo1 allele exhibited hypertriglyceridemia.
41 ation at baseline to vasoconstriction during hypertriglyceridemia.
42 I production in the pathogenesis of diabetic hypertriglyceridemia.
43 plasma cholesterol levels and did not cause hypertriglyceridemia.
44 high-density lipoprotein (HDL) and may cause hypertriglyceridemia.
45 ilar proportions of hypercholesterolemia and hypertriglyceridemia.
46 ia and colorectal neoplasia was observed for hypertriglyceridemia.
47 d prevent the onset of hepatic steatosis and hypertriglyceridemia.
48 a have a causal role in carbohydrate-induced hypertriglyceridemia.
49 e were most robust in individuals exhibiting hypertriglyceridemia.
50 t induces in the periphery, most prominently hypertriglyceridemia.
51 de accrual, VLDL-triglyceride synthesis, and hypertriglyceridemia.
52 etic polyunsaturated fatty acid that reduces hypertriglyceridemia.
53 f GPIHBP1, defective LPL binding, and severe hypertriglyceridemia.
54 NGPTL8 represents a therapeutic strategy for hypertriglyceridemia.
55 with hepatic triglyceride overproduction and hypertriglyceridemia.
56 duced bulk-adiposity, hepatic steatosis, and hypertriglyceridemia.
57 effective in the management of postprandial hypertriglyceridemia.
58 yceride concentrations only in subjects with hypertriglyceridemia.
59 s a lipid-lowering agent in the treatment of hypertriglyceridemia.
60 riglycerides levels in patients with primary hypertriglyceridemias.
61 d hyperlipidemia (FCHL) and primary isolated hypertriglyceridemias.
63 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
65 rome, 43% increased waist circumference, 31% hypertriglyceridemia, 69% low HDL cholesterol, 31% incre
68 ssociated with serum TG and with the risk of hypertriglyceridemia after 2 years (OR = 1.19; 95%CI 1.0
70 nts by the liver is a key step in preventing hypertriglyceridemia, an independent risk factor for car
71 racentrifugation in 9 patients with moderate hypertriglyceridemia and 12 normotriglyceridemic control
72 zing sequence data from 458 individuals with hypertriglyceridemia and 333 controls with normal plasma
73 iets, on the other hand, they develop severe hypertriglyceridemia and advanced lesions, characterized
74 enriched diet induces insulin resistance and hypertriglyceridemia and affects visceral adipose tissue
75 rate that contributes to insulin resistance, hypertriglyceridemia and appears to be associated with t
77 264A, F265A, L268A, V269A)), does not induce hypertriglyceridemia and corrects hypercholesterolemia.
78 ficient diabetic mice that displayed fasting hypertriglyceridemia and delayed clearance of dietary tr
79 4(W276A, L279A, V280A, V283A)), induces mild hypertriglyceridemia and does not correct hypercholester
80 severely obese participants with T2D display hypertriglyceridemia and excessive systemic lipolysis du
84 /-)) had reductions in dexamethasone-induced hypertriglyceridemia and hepatic steatosis, suggesting t
85 ng effect, but the relation between nuts and hypertriglyceridemia and high-density lipoprotein choles
88 with hypoalbuminemia, edema, hyperlipidemia (hypertriglyceridemia and hypercholesterolemia), and lipi
95 ting LDL cholesterol in patients with severe hypertriglyceridemia and in those with mixed dyslipidemi
96 u261Ala/Trp264Ala/Phe265Ala]) did not induce hypertriglyceridemia and increased greatly the HDL chole
97 (apoE4[Leu261Ala/Trp264Ala]) induced milder hypertriglyceridemia and increased HDL cholesterol level
100 such as hypertension, hypercholesterolemia, hypertriglyceridemia and insulin resistance, and also in
101 Rdelta has uncovered a dual benefit for both hypertriglyceridemia and insulin resistance, highlightin
102 ha and PPARgamma are therapeutic targets for hypertriglyceridemia and insulin resistance, respectivel
103 intolerance, hypertension, and dyslipidemia (hypertriglyceridemia and low HDL cholesterol levels).
104 vastatin alone in participants with moderate hypertriglyceridemia and low HDL-cholesterol on major ca
105 ges typically associated with NAFLD, such as hypertriglyceridemia and low high-density lipoprotein ch
106 ay reduce CVD in patients with diabetes with hypertriglyceridemia and low high-density lipoprotein ch
107 ardiovascular disease (CVD) in part owing to hypertriglyceridemia and low high-density lipoprotein ch
108 dyslipidemias, mainly hypercholesterolemia, hypertriglyceridemia and low-plasma HDL cholesterol, amo
109 al lipid profile (group H), 30 patients with hypertriglyceridemia and not on medication (group N), an
110 la improves the apoE functions by preventing hypertriglyceridemia and promoting formation of spherica
111 s a genetic disorder characterized by severe hypertriglyceridemia and recurrent pancreatitis due to a
113 eted mitochondrial uncoupling could decrease hypertriglyceridemia and reverse NASH and diabetes in a
114 rophies are an important cause for monogenic hypertriglyceridemia and serve to highlight the role of
116 n medication (group N), and 30 patients with hypertriglyceridemia and taking gemfibrozil over a 3-mon
117 ed approach to study the association between hypertriglyceridemia and the apolipoprotein A5 gene.
118 ation in the pathogenesis of obesity-related hypertriglyceridemia and underscore the potential effica
123 ial and sporadic hypertriglyceridemias or to hypertriglyceridemias and hypercholesterolemia in case o
124 bution of common genetic variants in primary hypertriglyceridemias and the genetic difference between
126 lerosis-hypercholesterolemia, hyperglycemia, hypertriglyceridemia, and even the process of aging-all
128 aused glucose intolerance, hyperinsulinemia, hypertriglyceridemia, and hepatic steatosis in mice.
130 atients' baseline data on obesity, diabetes, hypertriglyceridemia, and high blood pressure to assign
131 Furthermore, associations with obesity, hypertriglyceridemia, and hyperglycemia increase with in
132 : abdominal obesity, diabetes, hypertension, hypertriglyceridemia, and hypo-alpha-lipoproteinemia.
133 ominal obesity, hyperglycemia, hypertension, hypertriglyceridemia, and hypo-high-density lipoprotein
134 oligonucleotide reverses hepatic steatosis, hypertriglyceridemia, and insulin resistance in obese mi
136 levated liver fat content, TG-enriched VLDL, hypertriglyceridemia, and low HDL cholesterol levels.
137 approximately 6 +/- 2%, skeletal muscle IR, hypertriglyceridemia, and low HDL-C become fully establi
138 ulin resistance and type 2 diabetes, extreme hypertriglyceridemia, and nonalcoholic fatty liver disea
139 ypertension, diabetes, hypercholesterolemia, hypertriglyceridemia, and obesity) were assessed from 19
144 tion of dyslipidemia characterized by severe hypertriglyceridemia as a result of point mutations in h
149 l compartment (adipose tissue and liver) and hypertriglyceridemia associated with insulin resistance.
150 lipid metabolism, as demonstrated by severe hypertriglyceridemia associated with its mutations in mi
151 e withdrawals were treatment-related (severe hypertriglyceridemia associated with rapamycin, and panc
152 ride clearance, CREB-H-deficient mice showed hypertriglyceridemia, associated with defective producti
153 containing triglyceride-rich lipoproteins in hypertriglyceridemia, associated with increased apoC-III
155 Insulin-resistant apoB/BATless mice have hypertriglyceridemia because of increased assembly and s
156 herogenicity was traditionally attributed to hypertriglyceridemia because of its inhibition on the li
157 oxyl-terminal 261-299 domain of apoE induces hypertriglyceridemia, because of increased VLDL secretio
159 s variants were collectively associated with hypertriglyceridemia, but a range of in silico predictio
160 nd adipose tissue, subsequently resulting in hypertriglyceridemia, by inhibiting lipoprotein lipase (
162 f fish oil-based ILE was not associated with hypertriglyceridemia, coagulopathy, or essential fatty a
163 ensity lipoprotein cholesterol, and isolated hypertriglyceridemia) compared with normolipemia, and CI
164 h lower triglycerides levels, whereas severe hypertriglyceridemia denotes a population with particula
165 hereas coexpression with ANGPTL8 resulted in hypertriglyceridemia, despite a reduction in circulating
166 elop hyperinsulinemia, acanthosis nigricans, hypertriglyceridemia, diabetes mellitus, and hepatic ste
167 ffects of genetic susceptibility variants in hypertriglyceridemia, effects that are most evident in f
168 me, which includes type 2 diabetes mellitus, hypertriglyceridemia, essential hypertension, low circul
169 n ameliorating effect on insulin resistance, hypertriglyceridemia, fatty liver, obesity, adipositis,
170 to reduce pancreatitis risk in persons with hypertriglyceridemia, fibrates may lead to the developme
171 ) B lipoprotein metabolism that characterize hypertriglyceridemia, focusing on apoC-III and apoE.
172 nia, hypophosphatemia, asthenia, anemia, and hypertriglyceridemia for all patients and those who rece
175 olesterol levels but persistent, significant hypertriglyceridemia (>200 mg/dl) and low high-density l
176 erienced National Cancer Institute grade 3/4 hypertriglyceridemia had significantly longer median sur
178 genetic difference between FCHL and isolated hypertriglyceridemias have not been thoroughly examined.
179 ically elevated glucocorticoid levels induce hypertriglyceridemia, hepatic steatosis, and visceral ob
180 e level (HR = 1.20, 95% CI: 1.03, 1.39), and hypertriglyceridemia (HR = 1.14, 95% CI: 1.00, 1.30).
182 ouse models and human mendelian syndromes of hypertriglyceridemia (HTG) accumulate in patients with p
185 in part by hypoglycemia, growth retardation, hypertriglyceridemia, hypercholesterolemia, and hepatic
187 improves abdominal obesity, hepatosteatosis, hypertriglyceridemia, hypercholesterolemia, insulin resi
188 diovascular risk factors, including obesity, hypertriglyceridemia, hypercholesterolemia, insulin resi
189 expressivity include dilated cardiomyopathy, hypertriglyceridemia, hypercholesterolemia, scoliosis, d
190 toxicities included CNS hemorrhage (n = 1), hypertriglyceridemia/hypercholesterolemia/elevated lipas
191 coagulopathy, liver dysfunction, cytopenias, hypertriglyceridemia, hyperferritinemia, hemophagocytosi
192 s of uric acid and ameliorates hypertension, hypertriglyceridemia, hyperglycemia, and insulin resista
193 nts of the definition of metabolic syndrome (hypertriglyceridemia, hyperglycemia, and low HDL cholest
194 tabolic risk, specifically hyperinsulinemia, hypertriglyceridemia, hyperleptinemia, and hyperuricemia
196 of low high-density lipoprotein cholesterol, hypertriglyceridemia/hypertransaminasemia/hypertension,
198 esented with high fever, hepatosplenomegaly, hypertriglyceridemia, hypofibrinogenemia, thrombocytopen
199 tional CREB-H protein in humans with extreme hypertriglyceridemia, implying a crucial role for CREB-H
201 acid substitution (apoE4[Phe265Ala]) induced hypertriglyceridemia in apoE-/- or apoA-I-/- mice, promo
202 xpression of apolipoprotein E (apoE) induces hypertriglyceridemia in apoE-deficient mice, which is ab
203 l study population, occurrence of high-grade hypertriglyceridemia in bexarotene-treated patients stro
204 Conversely, overexpression of Atg14 improves hypertriglyceridemia in both high fat diet-treated wild-
209 einemia in young adulthood, hypertension and hypertriglyceridemia in middle age, and diabetes later;
211 rtriglyceridemic pancreatitis; or diagnosing hypertriglyceridemia in patients who require therapy for
213 ted against the development of steatosis and hypertriglyceridemia in response to high fructose feedin
216 nal obesity, hypo-alpha-lipoproteinemia, and hypertriglyceridemia in young adulthood, hypertension in
217 What are the roles of n-3 fatty acids in hypertriglyceridemia, in the metabolic syndrome and type
219 wn of TRAP80 ameliorated liver steatosis and hypertriglyceridemia induced by LXR activation and maint
221 f adipose tissue often accompanied by severe hypertriglyceridemia, insulin resistance, diabetes, and
231 complex," the main features of which include hypertriglyceridemia, low HDL cholesterol levels, qualit
232 by a constellation of fasting hyperglycemia, hypertriglyceridemia, low HDL cholesterol, hypertension,
233 iver fat with hypertension, type 2 diabetes, hypertriglyceridemia, low HDL-cholesterol concentration,
234 and each component, including hypertension, hypertriglyceridemia, low high-density lipoprotein chole
235 ted the TD lipid phenotype with postprandial hypertriglyceridemia, markedly decreased LDL, and near a
236 obtained in the fasting state, postprandial hypertriglyceridemia may play an important role in ather
238 -release mitochondrial protonophore reverses hypertriglyceridemia, nonalcoholic steatohepatitis, and
239 lin resistance, dyslipidaemia, hypertension, hypertriglyceridemia, obesity and cardiovascular disease
240 a role for phospholipid transfer protein in hypertriglyceridemia, obesity, diabetes, inflammation an
241 eline triglycerides (P=5.5x10(-5)) and lower hypertriglyceridemia (odds ratio, 0.73; 95% confidence i
242 with insulin receptor mutations develop the hypertriglyceridemia or hepatic steatosis associated wit
243 riants predisposing to familial and sporadic hypertriglyceridemias or to hypertriglyceridemias and hy
244 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
246 d pressure (OR, 1.18; 95% CI, 0.96 to 1.44), hypertriglyceridemia (OR, 1.25; 95% CI, 1.04 to 1.51), a
247 ratio [OR]: 1.21 for SAT; OR: 1.30 for VAT), hypertriglyceridemia (OR: 1.15 for SAT; OR: 1.56 for VAT
248 lipase deficiency (cld) mutation show severe hypertriglyceridemia owing to a decrease in the activity
249 sed age (P < 0.0001), male sex (P < 0.0001), hypertriglyceridemia (P < 0.04), low high-density lipopr
250 nding of truncated apoA-V contributes to the hypertriglyceridemia phenotype associated with truncatio
252 knockdown animals developed hypoglycemia and hypertriglyceridemia, phenotypes observed in Ppara-/- mi
253 cholesterol concentration, hypertension, and hypertriglyceridemia-predict cardiovascular disease, but
255 hypertension, hypercholesterolemia, profound hypertriglyceridemia, proteinuria, and renal failure.
256 best with hypertension (r = 0.2, P < 0.05), hypertriglyceridemia (r = 0.37, P < 0.001), and insulin
258 s the leading cause of death in the USA, and hypertriglyceridemia represents an independent risk fact
259 thrombocytopenia, neutropenia, anorexia, and hypertriglyceridemia, resulting in a MTD of vorinostat 1
260 (APOC3) that are known to be associated with hypertriglyceridemia (rs2854116 [T-455C] and rs2854117 [
261 oprotein C3 (APOC3) that have been linked to hypertriglyceridemia (rs2854117 C > T and rs2854116 T >
264 n glycemic control itself, and prevention of hypertriglyceridemia should be a major focus of clinical
265 tely blocks the fasting-induced hypoglycemia/hypertriglyceridemia, suggesting that these abnormalitie
266 g triacylglycerol and a higher prevalence of hypertriglyceridemia than did subjects in the protective
267 he265 play an important role in apoE-induced hypertriglyceridemia, the accumulation of free cholester
268 gion of residues 261-265 on the induction of hypertriglyceridemia, the esterification of cholesterol
269 ants in human subjects correlate with severe hypertriglyceridemia, the lipid binding properties of ap
271 ed from light and medium LDL to dense LDL in hypertriglyceridemia through a quartet of kinetic pertur
272 etin-like 4 (Angptl4) links proteinuria with hypertriglyceridemia through two negative feedback loops
275 riglycerides (100-149 mg/dL); (3) borderline hypertriglyceridemia triglycerides (150-199 mg/dL); (4)
276 triglycerides (150-199 mg/dL); (4) moderate hypertriglyceridemia triglycerides (200-499 mg/dL); (5)
277 n apolipoprotein E (apoE) that contribute to hypertriglyceridemia, two sets of conserved, hydrophobic
278 FAs include treatment of severe and moderate hypertriglyceridemia, use in statin-treated patients wit
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
288 ce with rosiglitazone ameliorated the IR and hypertriglyceridemia, we hypothesized that the hypertrig
289 To better understand the pathophysiology of hypertriglyceridemia, we studied hepatic regulation of t
290 In addition, high education and avoidance of hypertriglyceridemia were associated with exceptional su
292 iants more frequently identified in isolated hypertriglyceridemias were rs7412 in APOE and rs1800795
293 Here, we show that T0901317 produces massive hypertriglyceridemia when given to mice lacking low dens
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
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