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1 or metolazone increased the concentration of serum triglyceride.
2 correlated with a postprandial elevation of serum triglycerides.
3 correlated with a postprandial elevation in serum triglycerides.
4 tabolizing enzymes and resultant decrease of serum triglycerides.
5 rance, which resulted in decreased levels of serum triglycerides.
6 atitis even in the absence of a reduction in serum triglycerides.
7 hanged by adjustment for body mass index and serum triglycerides.
8 inefficiency, and improved fetal weights and serum triglycerides.
9 g from rheumatologic conditions and reducing serum triglycerides.
10 Os) have anti-inflammatory effects and lower serum triglycerides.
11 tein, fasting glucose-insulin metabolism, or serum triglycerides.
12 f glucokinase regulatory protein (GCKR) with serum triglycerides.
13 gh blood pressure (1.24; 1.04-1.48) and high serum triglycerides (1.18; 1.00-1.39), with a trend of i
14 into 5 groups according to strata of fasting serum triglycerides: (1) low-normal triglycerides (<100
15 Significant reductions were seen in mean serum triglycerides (1206-->226 mg/dL, P = .002), glucos
16 ed by dyslipidemic (>30% elevated, P < 0.05) serum triglycerides (139 mg/dl), very-LDLs (27.8 mg/dl),
18 elihood ratio test suggested interactions on serum triglycerides (4 SNP - SNP pairs), LDL cholesterol
19 detected by magnetic resonance imaging), and serum triglycerides (-51%), improved glucose tolerance,
20 r small VLDL), which produced an increase in serum triglycerides; a decrease in LDL size as a result
21 MA-IR, body mass index, waist circumference, serum triglycerides, aminotransferase level, and histolo
22 nuated triglyceride secretion, and decreased serum triglyceride and alanine aminotransaminase levels.
25 ding induced hepatic steatosis and increased serum triglyceride and cholesterol levels in the KO mice
26 abolic parameters, UDCA-LPE reduced elevated serum triglyceride and cholesterol values in HFD mice.
27 causes insulin-resistant diabetes, elevated serum triglyceride and fatty acid levels, and massive tr
34 as associated with a dramatic improvement in serum triglyceride and VLDL concentrations, a significan
37 diabetes and FCHL, both predisposing to high serum triglycerides and glucose intolerance, we tested t
38 rol in type 2 diabetics results in increased serum triglycerides and has a negative influence on all
40 n-3 (omega-3) fatty acid supplementation on serum triglycerides and markers of insulin sensitivity w
43 erences in the concentrations of hemoglobin, serum triglyceride, and serum cholesterol were found bet
45 ificant after adjustment for exercise level, serum triglycerides, and BMI (P = 0.02) but was no longe
48 are frequently used strategies for reducing serum triglycerides, and, yet, there is no information r
49 ive correlation of antibody levels and total serum triglycerides, apolipoprotein B, and apolipoprotei
50 serum HDL-cholesterol and a 71% reduction in serum triglycerides at the highest dose administered (10
52 2.03]; I(2)=78%), and when the difference in serum triglycerides between the two interventions at fol
53 e to Wy-14,643 effects on beta-oxidation and serum triglycerides but resistant to hepatocellular prol
54 iation between serum PCSK9 concentration and serum triglyceride, but care has to be taken in interpre
57 l/liter (0.258, 0.355) [mean (95% C.I.)] and serum triglyceride by 0.164 mmol/liter (0.12, 0.209) alt
59 ion of hepatic apolipoprotein C-III mRNA and serum triglycerides compared with untreated controls.
60 tudies have reported on associations between serum triglyceride concentrations and the risk of corona
61 sterol concentrations increased slightly and serum triglyceride concentrations decreased slightly in
62 eated men had significantly higher follow-up serum triglyceride concentrations over baseline than did
65 ty acid supplementation dramatically reduced serum triglycerides, decreased arachidonic acid in the p
66 entrations (four patients), and increases in serum triglycerides (eight patients) and aspartate amino
67 in clozapine-treated patients; screening for serum triglyceride elevations may be warranted before tr
69 dominal adiposity; hepatosteatosis; elevated serum triglycerides, FFAs, and LDL-cholesterol; and dimi
70 n dosed chronically in DIO mice and depleted serum triglycerides following a lipid challenge in a dos
72 en); fasting blood glucose > or = 100 mg/dL; serum triglycerides > or = 150 mg/dL; blood pressure > o
73 7; 95% confidence interval [CI]: 1.15-9.89), serum triglycerides >/=150 mg/day (OR 4.35; 95% CI: 1.70
74 glucose level) and insulin resistance (e.g., serum triglycerides, high density lipoprotein cholestero
75 ncarriers had lower fasting and postprandial serum triglycerides, higher levels of HDL-cholesterol an
77 that regulate lipid metabolism, and reduced serum triglycerides in a PPARalpha-dependent mechanism.
78 APOC3/APOA5 constitutes a major locus for serum triglycerides in Amerindians, especially the Pimas
80 ound a statistically significant decrease in serum triglycerides in germ-free rats fed a high sugar d
81 ar role for PPARbeta in regulating levels of serum triglycerides in mice on a high fat Western diet b
82 CK sensitivity best correlated with elevated serum triglycerides in normal-weight participants and wi
83 proportion to the increase in liver fat and serum triglycerides in subjects with PNPLA3-148IIbut not
88 those of a pharmaceutical dose (3.4 g/d) on serum triglycerides, inflammatory markers, and endotheli
89 are positively correlated with FEV1, whereas serum triglycerides, LDL cholesterol, and apoB are assoc
90 21, P = .048), IMCL (r = 0.27, P = .02), and serum triglyceride level (r = 0.33, P = .001), independe
93 ssue in preventive cardiology is whether the serum triglyceride level is an independent risk factor f
94 analysis in nonobese patients, only elevated serum triglyceride level was independently associated wi
95 antipsychotic dose, total cholesterol level, serum triglyceride level, and concurrent medications wer
96 patic lipids (IHL), serum cholesterol level, serum triglyceride level, and measures of insulin resist
99 w-carbohydrate diet had greater decreases in serum triglyceride levels (change, -0.84 mmol/L vs. -0.3
100 I (OR: 0.62 per 1 SD; 95% CI: 0.40 to 0.94), serum triglyceride levels (OR: 0.66 per 1 SD; 95% CI: 0.
101 at feeding resulted in a greater increase in serum triglyceride levels and an accelerated appearance
103 that carry this T-87C polymorphism had lower serum triglyceride levels and significantly reduced risk
106 eing glucose intolerant, and having elevated serum triglyceride levels compared to any other genotype
109 roved adipose tissue lipid storage and lower serum triglyceride levels in the fed state, but do not c
110 h the intestinal epithelium and elevation of serum triglyceride levels in the IAP-deficient mice comp
115 had increased hepatic lipid accumulation and serum triglyceride levels possibly due to the activation
116 ded otherwise healthy patients with elevated serum triglyceride levels to patients presenting with ac
117 n Old Order Amish participants whose fasting serum triglyceride levels were at the extremes of the di
120 sis model assessment values were highest and serum triglyceride levels were lowest among African-Amer
124 creased body-mass index, waist-to-hip ratio, serum triglyceride levels, and systolic blood pressure a
125 cardial blood volume changed with increasing serum triglyceride levels, indicating lack of vasomotion
134 ficant association with GFR (P = 0.0006) and serum triglycerides levels (P = 0.003), after accounting
135 and body fat and increased hepatic, but not serum, triglyceride levels compared to control rats that
136 hepatic apolipoprotein A-I, C-III mRNA, and serum triglycerides observed in wild-type mice is mediat
138 l did not statistically significantly change serum triglycerides or very-low-density lipoprotein conc
140 emic cardiovascular benefits of exercise, as serum triglyceride, oxidized low density lipoprotein-cho
144 y mass index (p = 0.01) and higher levels of serum triglycerides (p = 0.05), and they were inversely
145 and obesity in mice, have elevated levels of serum triglycerides primarily associated with very low d
146 ations between small LDL particle number and serum triglycerides (r=0.61, P<0.0001) and HDL-C (r=-0.5
147 of 1-3 grams of nicotinic acid per day lower serum triglycerides, raise high density lipoprotein chol
148 P=0.03), cell volume (rho(G)=-0.73, P=0.04), serum triglycerides (rho(G)=-0.67, P=0.03), and between
149 dex, resting heart rate, C-reactive protein, serum triglycerides, serum creatinine, and measures of d
150 t exhibited significantly lower postprandial serum triglycerides, suggestive of a role for TM6SF2 in
151 low-density lipoprotein (LDL) cholesterols, serum triglycerides, systolic and diastolic blood pressu
152 h fasting insulin, insulin sensitivity (Si), serum triglyceride (TG) concentration, or serum HDL chol
154 t to assess the association, if any, between serum triglyceride (TG) levels and gemfibrozil consumpti
155 Biochemical parameters measured included serum triglyceride (TG), total cholesterol (TC), low-den
156 57; 95%CI 1.45-1.69, P = 3.84 x 10(-31)) and serum triglycerides (TG) (beta = 0.067, P = 4.5 x 10(-21
160 l (TC), low-density lipoproteins (LDLs), and serum triglycerides (TGs) were significantly higher in p
161 o the identification and characterization of serum triglycerides (TGs), was assessed using extracted
162 stasis model assessment-insulin resistance), serum-triglyceride-to-serum-high-density lipoprotein-cho
164 nsplant patients were found to have elevated serum triglycerides, total cholesterol/ high-density lip
166 e in HDL-cholesterol and an 84% reduction in serum triglycerides under the same treatment conditions.
167 gpat2 deficiency reports marked reduction in serum triglyceride upon feeding a fat-free diet, which s
170 and high density lipoprotein cholesterol and serum triglyceride were measured after a 14-hour fast.
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