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1  increased hepatic FA uptake, and influences hepatic metabolism.
2 are evaluated, including a close look at YC1 hepatic metabolism.
3 isplayed more pronounced improvements in the hepatic metabolism.
4 r (LXR) alpha and beta play crucial roles in hepatic metabolism.
5 e, hepatokine profile, and key components of hepatic metabolism.
6 ited significant improvement in stability to hepatic metabolism.
7 ion of key transcription factors controlling hepatic metabolism.
8 m that plays an important role in regulating hepatic metabolism.
9 ic corticosteroid activity due to first-pass hepatic metabolism.
10 undance and interfere with glucose-regulated hepatic metabolism.
11 mental role in the rhythmic orchestration of hepatic metabolism.
12 duced CRP elevation is related to first-pass hepatic metabolism.
13 hose involving cytochrome P450 isoenzymes in hepatic metabolism.
14  study is focused on the action of leptin on hepatic metabolism.
15  availability as a result of high first-pass hepatic metabolism.
16 ibed as a potent mechanism for orchestrating hepatic metabolism.
17  of excessive weight gain but also impact on hepatic metabolism.
18 ggest TCDD disrupted circadian regulation of hepatic metabolism, altering metabolic efficiency and en
19                                              Hepatic metabolism and biliary transport had an importan
20 -capacity runner (HCR or LCR)] on indices of hepatic metabolism and brain health following a chronic
21 define the mechanisms by which leptin alters hepatic metabolism and corrects steatosis.
22 sing in vitro model for long-term studies of hepatic metabolism and cytotoxicity.
23 as examined, compounds with both significant hepatic metabolism and daily dose >50 mg (n = 50) were s
24 en hepatic adverse events and combination of hepatic metabolism and daily dose was examined, compound
25 ombined with AE are associated with improved hepatic metabolism and decreased hepatic lipid accumulat
26  a study to examine the relationship between hepatic metabolism and DILI of prescription medications.
27                    These risk factors modify hepatic metabolism and excretion of the DILI-causative a
28 nd conserved liver-specific miRNA, regulates hepatic metabolism and functions as a tumor suppressor,
29            Bile acid (BA) receptors regulate hepatic metabolism and gut integrity as central players
30 insulin resistance, contributing to improved hepatic metabolism and increased energy expenditure in m
31 ficiency of these two bile acid receptors on hepatic metabolism and injury in mice.
32   miR-26a targeted several key regulators of hepatic metabolism and insulin signaling.
33 e essential microenvironmental regulation of hepatic metabolism and its human-specific aspects.
34 parts clinically relevant sex differences to hepatic metabolism and liver disease susceptibility.
35 f Phd gene knockouts did not further improve hepatic metabolism and only added toxicity.
36               The loss of HNF4alpha disrupts hepatic metabolism and promotes systemic inflammation, r
37 ion (IVIVE) model using the results of human hepatic metabolism and serum protein binding experiments
38 or potential treatments for inborn errors of hepatic metabolism and suggest that cardiac glycosides c
39 ndings establish IFN-I-induced modulation of hepatic metabolism and the urea cycle as an endogenous m
40   This probably results from the zonation of hepatic metabolism and, in some cases, from differences
41 n of oestradiol (tE2) circumvents first-pass hepatic metabolism and, therefore, should avoid the card
42 -anhydro-D-mannitol (2,5-AM; an inhibitor of hepatic metabolism) and methyl palmoxirate (MP; an inhib
43 r results illustrate how GR and E47 regulate hepatic metabolism, and might provide an entry point for
44 tabolic and genetic abnormalities, defective hepatic metabolism, and problems with diffusion and tran
45  corticosteroid with an extensive first-pass hepatic metabolism appeared promising for the treatment
46 emains unclear whether protective effects on hepatic metabolism are already seen in the offspring ear
47 ant dose-dependency and drugs with extensive hepatic metabolism are associated with higher frequency
48            Reactive metabolites generated by hepatic metabolism are thought to play an important role
49 udies suggest that GPRC6A directly regulates hepatic metabolism as well as regulates the production a
50 pport that PPP1R3B is a crucial regulator of hepatic metabolism beyond glycogen synthesis and that ge
51  a common weight-loss approach that modifies hepatic metabolism by increasing gluconeogenesis (GNG) a
52                         CMPF notably affects hepatic metabolism by increasing mitochondrial fatty aci
53                 Furthermore, TCDD reprograms hepatic metabolism by redirecting glycolytic intermediat
54                          Later, steady-state hepatic metabolism can be assessed using only the arteri
55          Compared with compounds with lesser hepatic metabolism, compounds belonging to the significa
56       These methods were used to analyze the hepatic metabolism considering available data sets obtai
57       However, the role of RR on T2DM-driven hepatic metabolism disorder remains unclear.
58                            The impairment of hepatic metabolism due to liver injury has high systemic
59 have also emerged as players in dysregulated hepatic metabolism due to nutritional overload.
60 metabolites (HO-PCBs) in mice with defective hepatic metabolism due to the liver-specific deletion of
61 r 1alpha (PGC-1alpha), a global regulator of hepatic metabolism during fasting.
62 unction, and inhibition of Foxo1 can improve hepatic metabolism during insulin resistance and the met
63 tient samples at both timepoints showed that hepatic metabolism, especially in peroxisomes, is persis
64 hese studies also indicate distinct roles in hepatic metabolism for Hif-1alpha, which promotes glycol
65 ed for the development of rigorous models of hepatic metabolism for preclinical screening of drug cle
66 lism, compounds belonging to the significant hepatic metabolism group had significantly higher freque
67                     Twelve compounds with no hepatic metabolism had no reports of liver failure, live
68 FXR in regulation of bile acid synthesis and hepatic metabolism has been studied extensively.
69                 However, the role of TGR5 in hepatic metabolism has not been explored.
70  of a comprehensive kinetic model of central hepatic metabolism (Hepatokin1).
71 fect associated with mitochondrial and other hepatic metabolism implications.
72 d progression to liver fibrosis by improving hepatic metabolism in a relatively short period of time.
73 are inconsistent with the canonical model of hepatic metabolism in which Akt is an obligate intermedi
74  the effect of FGF15 on circadian rhythm and hepatic metabolism in wild-type (WT), Fgf15 knockout (KO
75                            Instead, enhanced hepatic metabolism, independent of GLP-1 receptor activa
76 tion, prompting further investigation of how hepatic metabolism influences brain health.
77 ion, hypoxia induced cancer, decreased extra hepatic metabolism, intestinal infarction and lactic aci
78                  During hyperammonemia, when hepatic metabolism is impaired, nonureagenic ammonia dis
79                      These data confirm that hepatic metabolism is the major route of CPA elimination
80 etabolomic profile, characterized by altered hepatic metabolism, lowered NAD flux, increased nucleosi
81       Because tipifarnib undergoes extensive hepatic metabolism, MTD is doubled in patients on EIAEDs
82 were characterized as those with significant hepatic metabolism (n = 149).
83                                              Hepatic metabolism of 22:6,n-3, however, generates 20:5,
84  device was proven to be able to reflect the hepatic metabolism of a drug, drug distribution in the t
85 -position trideuteration (12-D(3)NVP) on the hepatic metabolism of and response to NVP.
86                                              Hepatic metabolism of ethanol by cytochrome P450 2E1 (CY
87        However, the patients showed impaired hepatic metabolism of FMZ.
88 est that these effects result from the rapid hepatic metabolism of fructose catalyzed by fructokinase
89                                              Hepatic metabolism of fructose favors de novo lipogenesi
90 ies, adverse glycemic effects, and increased hepatic metabolism of fructose leading to de novo lipoge
91                                              Hepatic metabolism of glucose, fatty acids, and lipoprot
92 levels, and alterations in the regulation of hepatic metabolism of lipids and cholesterol.
93 clinical samples led us to reinvestigate the hepatic metabolism of mesna and dimesna.
94            This clearance is probably due to hepatic metabolism of the immune complexes.
95 ctivated transcription factor, regulates the hepatic metabolism of therapeutics as well as endobiotic
96     This is used in studies of regulation of hepatic metabolism of, for example, (18)F-FDG and (11)C-
97  provide a means for assessing the impact of hepatic metabolism on amino acid availability to periphe
98 rtnership that mediates endocrine control of hepatic metabolism plays a role in cellular homeostasis
99  modular platform to emulate and investigate hepatic metabolism processes, with particular potential
100 clic groups designed to decrease the rate of hepatic metabolism provided analogues with improved phar
101 ability in murine and human blood plasma and hepatic metabolism, providing a basis for future develop
102 nd were classified as signs of adaptation of hepatic metabolism rather than hepatotoxicity.
103 asing evidence for HSCs in the regulation of hepatic metabolism, regeneration, immunity, and carcinog
104                However, the effects of CR on hepatic metabolism remain unknown.
105                                              Hepatic metabolism requires mitochondria to adapt their
106 anges of biological cascades associated with hepatic metabolism, response to hormone stimuli, glucone
107 his is true, then compounds with significant hepatic metabolism should cause more DILI than those wit
108 BCB11 deficiency may cause unique changes in hepatic metabolism that are predictive of liver injury.
109 uses a primary defect in gene expression and hepatic metabolism that leads to the eventual developmen
110 le disorders are a group of inborn errors of hepatic metabolism that result in often life-threatening
111                       In addition to reduced hepatic metabolism, there was reduced long chain fatty a
112 fect on the core clock but rather reprograms hepatic metabolism through altered pro-inflammatory resp
113 aintenance of hepatic homeostasis by linking hepatic metabolism to circadian rhythm.
114                                  PQ requires hepatic metabolism to exert activity against gametocyte
115 pressor p53 is involved in the adaptation of hepatic metabolism to nutrient availability.
116 iabetes, yet its contribution to deregulated hepatic metabolism under diseased states is not well und
117 s nitric oxide synthase inhibitor, undergoes hepatic metabolism via dimethylarginine-dimethylamino-hy
118                                              Hepatic metabolism was analyzed using in vivo 13C/31P/1H
119                                 To this end, hepatic metabolism was assessed in wild-type (WT) and PG
120 enotyping, subjects fasted for 24 hours, and hepatic metabolism was interrogated using a combination
121                                 Dysregulated hepatic metabolism was linked to sustained disruption of
122     By contrast, in the B-D model, the whole hepatic metabolism was severely altered with a significa
123                                        Local hepatic metabolism was studied in vivo in male Sprague-D
124 ted in vitro in a cellular environment where hepatic metabolism was well maintained.
125 he effect of reduced mitochondrial fusion on hepatic metabolism, we generated mice with a liver-speci
126                          Compounds with >50% hepatic metabolism were characterized as those with sign
127 eal key roles for Them2 in the regulation of hepatic metabolism, which are potentially mediated by PC
128 ncentrations, which are determined mainly by hepatic metabolism, which may be increased or decreased
129 f the autonomic control in the regulation of hepatic metabolism, which plays a major role in the deve
130                     Mass-balance analysis of hepatic metabolism will be useful in characterizing chan
131 2 have complementary roles in the control of hepatic metabolism, with IRS-1 more closely linked to gl
132  receptor (PXR) is an important regulator of hepatic metabolism, yet mechanistic insights into the ef
133  The seminal event in halothane hepatitis is hepatic metabolism, yet the enzyme responsible for oxida

 
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