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1 tly accentuated the synthesis and storage of hepatic lipid.
2 mals, likely because of slower liberation of hepatic lipid.
3 MTP(-/-)) mice that have low plasma and high hepatic lipids.
4 ed lipidomics were used to examine serum and hepatic lipids.
5 dicate that Torc1 activation is required for hepatic lipid accumulation across models of NAFLD, and i
6                                          The hepatic lipid accumulation and Cd36 induction were also
7 -mediated regulation of chronic EtOH-induced hepatic lipid accumulation and hepatotoxicity.
8 w a novel mechanism by which miR-24 promotes hepatic lipid accumulation and hyperlipidemia by repress
9 the underlying mechanisms linking obesity to hepatic lipid accumulation and insulin resistance are in
10 his transcription factor as a contributor to hepatic lipid accumulation and insulin resistance.
11 augmented eIF2alpha signaling, together with hepatic lipid accumulation and insulin resistance.
12 itochondrial respiratory complexes promoting hepatic lipid accumulation and insulin resistance.
13 nder ER stress conditions through repressing hepatic lipid accumulation and maintaining lipoprotein s
14 onectin potently protect against HFD-induced hepatic lipid accumulation and preserve insulin sensitiv
15 down of miR-24 in those mice caused impaired hepatic lipid accumulation and reduced plasma triglyceri
16    Furthermore, GRbeta-Ad mice had increased hepatic lipid accumulation and serum triglyceride levels
17 ficient for GSK3alpha had significantly less hepatic lipid accumulation and smaller atherosclerotic l
18                 Prenatal TBT exposure led to hepatic lipid accumulation and up-regulated hepatic expr
19 nce of glucose metabolism and the control of hepatic lipid accumulation by skeletal muscle.
20              Earlier studies have shown that hepatic lipid accumulation can occur after 4 d of a high
21 c steatohepatitis (NASH) is characterized by hepatic lipid accumulation combined with inflammation, w
22 posed to ENDS exhibited a marked increase in hepatic lipid accumulation compared with ApoE-/- on a si
23                       Insulin resistance and hepatic lipid accumulation constitute the metabolic unde
24 ipose glucocorticoid action appears to drive hepatic lipid accumulation during stressors such as fast
25              Acute disruption of Vhl induced hepatic lipid accumulation in an HIF-2alpha-dependent ma
26  Simvastatin exposure decreased TCDD-induced hepatic lipid accumulation in both sexes, but was most p
27 ty by promoting adipose tissue expansion and hepatic lipid accumulation in cell-nonautonomous manners
28 lation between miR-27b expression levels and hepatic lipid accumulation in HCV-infected SCID-beige/Al
29                              The decrease in hepatic lipid accumulation in HF-fed itga1(-/-) mice was
30 ondrial function in the liver and to prevent hepatic lipid accumulation in high-fat diet (HFD)-fed ro
31 related factor 2 (Nrf2) being a modulator of hepatic lipid accumulation in models of NAFLD.
32 d levels, and long-term treatments decreased hepatic lipid accumulation in the NAFLD mice.
33 t, hyperglycemic MPCCs displayed significant hepatic lipid accumulation in the presence of insulin, w
34 navir and lopinavir) significantly increased hepatic lipid accumulation in WT mice.
35 er regeneration is impaired in mice in which hepatic lipid accumulation is suppressed by either pharm
36 ciated with obesity and type 2 diabetes, and hepatic lipid accumulation may contribute to insulin res
37  and markedly limited insulin resistance and hepatic lipid accumulation that were induced by prolonge
38  hepatic autophagic activities and increased hepatic lipid accumulation upon starvation.
39                                              Hepatic lipid accumulation was associated with increased
40                                              Hepatic lipid accumulation was significantly reduced in
41 y diminished CGI-58 expression causes severe hepatic lipid accumulation yet paradoxically improves he
42 yte number, adipocyte size, MSC programming, hepatic lipid accumulation, and hepatic gene expression
43 mproved liver dysfunction markers, decreased hepatic lipid accumulation, and inhibited proinflammator
44                                Liver injury, hepatic lipid accumulation, and proinflammatory cytokine
45 of free and mTORC1-associated Raptor governs hepatic lipid accumulation, and uncover the potentially
46   Fish were stained with oil red O to assess hepatic lipid accumulation, and we also performed quanti
47 ion in Pld1(-/-) liver significantly reduced hepatic lipid accumulation, compared with Pld1(-/-) live
48                 These demonstrated increased hepatic lipid accumulation, higher levels of transcripti
49 for the beneficial effects of polyphenols on hepatic lipid accumulation, hyperlipidemia, and atherosc
50 ent of impaired glucose homeostasis, reduces hepatic lipid accumulation, increases white adipose oxid
51 indicated comparable increases in markers of hepatic lipid accumulation, inflammation and collagen de
52 uctose treatment of larval zebrafish induces hepatic lipid accumulation, inflammation, and oxidative
53 a deficiency had no influence on HFD-induced hepatic lipid accumulation, interestingly, it significan
54              Treatment with fructose induced hepatic lipid accumulation, mitochondrial abnormalities,
55 ury correlated positively with the degree of hepatic lipid accumulation.
56 vity and glucose tolerance without affecting hepatic lipid accumulation.
57 curtail glucose production without promoting hepatic lipid accumulation.
58 lation of Insig1, and subsequently decreased hepatic lipid accumulation.
59 with tunicamycin or valinomycin also induced hepatic lipid accumulation.
60 WAT mass and body weight in association with hepatic lipid accumulation.
61 e investigated HIF-1alpha in alcohol-induced hepatic lipid accumulation.
62 nd fatty acid synthase, as well as increased hepatic lipid accumulation.
63 Tgr5 gene in mice alleviated fasting-induced hepatic lipid accumulation.
64 y of weight gain and adiposity and prevented hepatic lipid accumulation.
65 the actions of GCs in the liver, or enhances hepatic lipid accumulation.
66 Rbeta increases inflammation, which leads to hepatic lipid accumulation.
67 (GH) and its mediator, IGF-1, associate with hepatic lipid accumulation.
68      Liver sympathetic innervation modulated hepatic lipid acquisition pathways during obesity.
69 ucose is accompanied by different effects on hepatic lipid anabolism and blood TG profiles.
70 t the FA pathway has sex-specific impacts on hepatic lipid and bile acid metabolism, findings that ex
71 itro and in vivo, correlating with decreased hepatic lipid and cholesterol levels and attenuated live
72  Sirt1LKO mice accumulated larger amounts of hepatic lipid and expressed higher levels of inflammator
73   To examine the role of Them2 in regulating hepatic lipid and glucose homeostasis, we generated Them
74        Bile acids are critical regulators of hepatic lipid and glucose metabolism and signal through
75  evidence for the differential regulation of hepatic lipid and glucose metabolism.
76 ism by which CAR down-regulates key genes in hepatic lipid and glucose metabolism.
77 s may be mediated by the fructose effects on hepatic lipids and ATP levels.
78 ake, energy expenditure, and circulating and hepatic lipids) and glucose metabolism (insulin toleranc
79 sulin sensitivity, tracer incorporation into hepatic lipids, and liver triglyceride export.
80 fed G5G8 KO mice had increased liver weight, hepatic lipids, and plasma alanine aminotransferase comp
81 ritional pathway an important contributor to hepatic lipid balance.
82 atory fatty acids and concomitant control of hepatic lipid biosynthesis, secretion, and deposition.
83 reased liver neutral lipids and induction of hepatic lipid biosynthetic genes when fasted.
84 tablish that Sar1B promotes the secretion of hepatic lipids but also adds regulation of cholesterol s
85 iver significantly increases accumulation of hepatic lipids, but reduces plasma TG levels in mice.
86  of the liver, which leads to alterations in hepatic lipid, carbohydrate, protein, lactate, and uric
87                                              Hepatic lipid catabolism begins with the transport of li
88  Our findings demonstrate that p16 represses hepatic lipid catabolism during fasting and may thus par
89                                  In mammals, hepatic lipid catabolism is essential for the newborns t
90 ob/ob mice, suggesting that rFGF1 stimulates hepatic lipid catabolism.
91 nd PPARalpha mRNA levels as well as impaired hepatic lipid clearance.
92                                              Hepatic lipid composition and histopathology revealed th
93 G production, VLDL particle composition, and hepatic lipid composition but selectively enhanced clear
94                      Specific alterations in hepatic lipid composition characterize the spectrum of n
95                     beta-Catenin ASO altered hepatic lipid composition in high-fat-fed mice.
96  multiecho and spectroscopic measurements of hepatic lipid concentration (r(2) = 0.99, P < .001).
97       Liver-specific deletion of RALY alters hepatic lipid content and serum cholesterol level.
98 s likely to have been on the basis increased hepatic lipid content and/or inflammation.
99 to the CNS via osmotic minipumps reduced the hepatic lipid content as assessed by noninvasive (1)H-MR
100                                BPA increased hepatic lipid content concomitant with increased Nrf2 an
101                                    Increased hepatic lipid content is an early correlate of insulin r
102 he individual contributions of ER stress and hepatic lipid content to the pathogenesis of hepatic ins
103 s used to examine relations between choline, hepatic lipid content, body mass index, glycogen content
104                          BLKO mice had lower hepatic lipid content, increased insulin signaling, and
105 er, both corepressors collaborate to control hepatic lipid content, which likely reflects their coope
106 y and may therefore be predicted to increase hepatic lipid content.
107  mice, which may contribute to the decreased hepatic lipid content.
108 H knockout mice display a modest decrease in hepatic lipid contents, but an increase in plasma trigly
109 odel of high-fat feeding was restored by the hepatic lipid control of CNS glycine sensing.
110 get genes and beta-oxidation, which regulate hepatic lipid degradation, were also suppressed in hepat
111 ibition of hepatic mTOR in Am mice increased hepatic lipid deposition and HIRI.
112 py, which additionally led to a reduction in hepatic lipid deposition and improved phosphorylation of
113 urs under chronic HF diet feeding, increased hepatic lipid deposition and produced a greatly augmente
114 ng FADS1 and its polymorphisms in modulating hepatic lipid deposition by altering gene transcription
115 yperglycemia and HF feeding results in rapid hepatic lipid deposition, fibrosis, and ultimately HCC.
116 in action on glucose metabolism but limiting hepatic lipid deposition.
117 erstanding of the mechanisms by which excess hepatic lipid develops and causes hepatic insulin resist
118 FLD and molecular mechanisms by which excess hepatic lipid develops remain largely unknown.
119 ly Dgat2 ASO treatment significantly reduced hepatic lipids (diacylglycerol and triglyceride but not
120      These data suggest early alterations in hepatic lipid distribution and metabolism during liver i
121                                         This hepatic lipid droplet accumulation coincides with miR-27
122 pposing effects on the secretion of TRLs and hepatic lipid droplet content.
123 t PNPLA3(148M) accumulates to high levels on hepatic lipid droplets (LDs).
124 auses accumulation of both PNPLA3 and TGs on hepatic lipid droplets (LDs).
125 umulation of triglyceride (TG) and PNPLA3 in hepatic lipid droplets (LDs).
126 fibrosis, accompanied by increased levels of hepatic lipid droplets and oxidative stress.
127 tment significantly reduced the formation of hepatic lipid droplets, body weight gain, blood glucose,
128 companied by a 40-fold increase in PNPLA3 on hepatic lipid droplets, with no increase in hepatic PNPL
129 ion of the small GTPase Rac1, which controls hepatic lipid dynamics through ROS-mediated regulation o
130 ring new opportunities to study postprandial hepatic lipid dynamics.
131 r leptin deficiency mediates alcohol-induced hepatic lipid dyshomeostasis, mice were fed alcohol for
132 alongside an insulin-resistant state is that hepatic lipid enzymatic pathways are modulated and overw
133 y acid production and a 2.5-fold increase in hepatic lipid export, both of which explain the reduced
134 the development of fatty liver by modulating hepatic lipid export, uptake, and synthesis, and that th
135                                              Hepatic lipids extracted from mouse liver, epididymal wh
136                     Despite the reduction in hepatic lipids, fasting glucose and insulin concentratio
137 ere examine in rats whether leptin regulates hepatic lipid flux via the brain in a series of stereota
138 bsequently to provide a corrected measure of hepatic lipid fraction.
139 d mediators (BLM), as well as a dysregulated hepatic lipid gene expression profile.
140                          A role of leptin in hepatic lipid handling is highlighted by the observation
141 rs to shared cis-regulatory regions dictates hepatic lipid handling.
142 ect functional role for both HSL and ATGL in hepatic lipid homeostasis and identifies these enzymes a
143 DE) family members (A, B and FSP27) regulate hepatic lipid homeostasis by controlling lipid droplet g
144 bolic signals required for the regulation of hepatic lipid homeostasis is complex.
145 se/endoribonuclease, is required to maintain hepatic lipid homeostasis under ER stress conditions thr
146 al biogenesis for the purpose of maintaining hepatic lipid homeostasis under nutritional stress or ci
147 ggested that CD36 plays an important role in hepatic lipid homeostasis, but the results have been con
148                                      Altered hepatic lipid homeostasis, hepatocellular injury, and in
149 and Npas2 crosstalk is essential to maintain hepatic lipid homeostasis.
150 CREBH transcriptional activity in regulating hepatic lipid homeostasis.
151  ER protein-folding environment and maintain hepatic lipid homeostasis.
152 tabolic regulator of autophagy that controls hepatic lipid homeostasis.
153 tion and gene expression required for normal hepatic lipid homeostasis.
154 n important role in MAPK-mediated control of hepatic lipid homeostasis.
155 ors known to be involved in VLDL assembly or hepatic lipid homeostasis.
156 derlying these beneficial effects of zinc on hepatic lipid homeostasis.
157 VLDL, respectively, act together to maintain hepatic lipid homeostasis.
158 alpha)-regulated genes, and dysregulation of hepatic lipid homeostasis.
159 -oxidant conditions that result in increased hepatic lipid hydroperoxide content.
160 d by VO, and there was a trend for increased hepatic lipid in LO and SO diets.
161 e findings suggest that the sequestration of hepatic lipids in perilipin 2-coated droplets ameliorate
162                                              Hepatic lipids including triglyceride, DAGs, and ceramid
163  fed control bacteria and had alterations in hepatic lipids, including oxylipins.
164 leading to its breakdown, and thus promoting hepatic lipid infiltration through reduced fatty acid ox
165                                              Hepatic lipids, insulin sensitivity, and hepatic insulin
166 ressing Acc1, Acc2, or both Acc1 and Acc2 on hepatic lipid levels and insulin sensitivity.
167 ed late fed-state gut hormones that decrease hepatic lipid levels by unclear mechanisms.
168  in mediating the acute effects of leptin on hepatic lipid levels in lean and DIO animals.
169                            In spite of this, hepatic lipid levels were not affected by the nonsheddin
170 ce hepatic malonyl-CoA levels in vivo, lower hepatic lipids (long-chain acyl-CoAs, diacylglycerol, an
171                                          The hepatic lipid-lowering effect observed in animals cotrea
172 excessive ER stress in response to increased hepatic lipids may decrease the ability of the liver to
173                    In the 25 human subjects, hepatic lipid measured by using HISTO differed significa
174 out mouse model and characterized changes in hepatic lipid metabolism (this report) and bile metaboli
175  homeostasis contributes to dysregulation of hepatic lipid metabolism and contributes to liver-associ
176 ylated FoxO1 in mice (Foxo1(KR/KR)) improves hepatic lipid metabolism and decreases macrophage inflam
177 npoint the key regulatory role of the UPR in hepatic lipid metabolism and demonstrate the potential c
178 with metabolic consequences such as impaired hepatic lipid metabolism and development of nonalcoholic
179 HIF-2 functions as an important regulator of hepatic lipid metabolism and identify HIF-2 as a potenti
180 ion was associated with pathways involved in hepatic lipid metabolism and immunological processes.
181                             Abnormalities in hepatic lipid metabolism and insulin action are believed
182 r macrophages in diet-induced alterations in hepatic lipid metabolism and insulin sensitivity, and su
183 l metabolism.HDAC3 is a critical mediator of hepatic lipid metabolism and its loss leads to fatty liv
184 patocytes and contribute to dysregulation of hepatic lipid metabolism and liver disease.
185 l BVRA-GSKbeta-PPARalpha axis that regulates hepatic lipid metabolism and may provide unique targets
186  Thus, we tested the contribution of ATGL to hepatic lipid metabolism and signaling.
187             We examined the role of PLIN5 on hepatic lipid metabolism and systemic glycemic control u
188  growth hormone secretion are known to alter hepatic lipid metabolism and to underlie sexually dimorp
189      These data indicate that TAK1 regulates hepatic lipid metabolism and tumorigenesis via the AMPK/
190 andidate gene/miRNA interactions involved in hepatic lipid metabolism and validated their function in
191 dependent protein deacetylase that regulates hepatic lipid metabolism by modifying histones and trans
192  show that retinol saturase is implicated in hepatic lipid metabolism by regulating the activity of t
193 provides new insights into the regulation of hepatic lipid metabolism by the ubiquitin-proteasome sys
194                                   Defects in hepatic lipid metabolism cause nonalcoholic fatty liver
195  of cholestasis, Abcb11 KO mice have altered hepatic lipid metabolism coupled with reduced expression
196 chondrial sirtuin SIRT4 in the regulation of hepatic lipid metabolism during changes in nutrient avai
197          We determined the effect of ATF4 on hepatic lipid metabolism in Atf4(-/-) mice fed regular c
198 LOCK) mutant (ClkDelta19/Delta19) protein on hepatic lipid metabolism in C57BL/6 Clkwt/wt and apolipo
199  We sought to determine the role of ACOT1 in hepatic lipid metabolism in C57Bl/6J male mice 1 week af
200 yses to identify alterations in systemic and hepatic lipid metabolism in mice with disruption of the
201 he importance of cell-specific modulation of hepatic lipid metabolism in promoting fibrogenesis in no
202 hat ATF4 plays a critical role in regulating hepatic lipid metabolism in response to nutritional cues
203                      This expression affects hepatic lipid metabolism in these animals and thus provi
204                           Optimal control of hepatic lipid metabolism is critical for organismal meta
205 AFLD, but whether this is causally linked to hepatic lipid metabolism is unclear.
206 itual dietary intake of foods that can alter hepatic lipid metabolism may influence circulating ceram
207 etabolic reprogramming, suggesting increased hepatic lipid metabolism prior to overt tumor developmen
208        Moreover, COP1-mediated regulation of hepatic lipid metabolism requires optimum ATGL expressio
209 22-treated mice revealed novel regulators of hepatic lipid metabolism that are responsive to miR-122
210 anscriptional regulatory cascade controlling hepatic lipid metabolism that identifies retinoic acid s
211 PPARs) play major roles in the regulation of hepatic lipid metabolism through the control of numerous
212 ow that in the LHA kappaOR directly controls hepatic lipid metabolism through the parasympathetic ner
213 s of reduced beta-cell function and abnormal hepatic lipid metabolism were associated with GDM; these
214           The group reports major defects in hepatic lipid metabolism when the torsin system is compr
215                                     Study of hepatic lipid metabolism with respect to the contributio
216 nt may have beneficial effects in regulating hepatic lipid metabolism, adipose tissue function, and i
217  the regulation of appetite and body weight, hepatic lipid metabolism, and fibrosis.
218 sential physiological role in the control of hepatic lipid metabolism, and KOR activation is a permis
219  deacetylase HDAC3 is a critical mediator of hepatic lipid metabolism, and liver-specific deletion of
220 ulin resistance, dysfunction of key steps in hepatic lipid metabolism, atherosclerosis, and hepatic s
221  HNF6 and Rev-erbalpha coordinately regulate hepatic lipid metabolism, each factor also affects addit
222 istology, and gene expression for markers of hepatic lipid metabolism, ER stress, and inflammation we
223  In this review, we will discuss the role of hepatic lipid metabolism, genetic background, diet, and
224                                     Study of hepatic lipid metabolism, insulin resistance, mitochondr
225 xpression and its functional implications in hepatic lipid metabolism, particularly in the context of
226 tabolism, but since many genes contribute to hepatic lipid metabolism, we hypothesized that other suc
227            To elucidate the role of ACSL1 in hepatic lipid metabolism, we overexpressed an Acsl1 aden
228 y in the lateral hypothalamic area modulated hepatic lipid metabolism, whereas the specific activatio
229 o define the function of Notch1 signaling in hepatic lipid metabolism, wild type mice and Notch1 defi
230 uggests several new miRNAs are regulators of hepatic lipid metabolism.
231 lucidate the role of tribbles-1 in mammalian hepatic lipid metabolism.
232 ifferent enzymatic hydrolyzation methods, on hepatic lipid metabolism.
233 ts functional involvement in fasting-induced hepatic lipid metabolism.
234  action of GH is due to direct regulation of hepatic lipid metabolism.
235 ulin action is required for FGF21 to control hepatic lipid metabolism.
236 sis, it is unknown whether p16 also controls hepatic lipid metabolism.
237 rget gene and demonstrate its involvement in hepatic lipid metabolism.
238 cyte Shp1 in the regulation of PPARgamma and hepatic lipid metabolism.
239 cal role in HIV PI-induced dys-regulation of hepatic lipid metabolism.
240 ry, and this gene plays an important role in hepatic lipid metabolism.
241 k and proposed to be a dominant regulator of hepatic lipid metabolism.
242 ects on the cell-autonomous clock as well as hepatic lipid metabolism.
243 S), particularly the hypothalamus, regulates hepatic lipid metabolism.
244 nt, two pathologies associated with impaired hepatic lipid metabolism.
245  fatty acid oxidation, linking chemokines to hepatic lipid metabolism.
246  report a novel role for HIF-2 in regulating hepatic lipid metabolism.
247 nges in the expression of genes required for hepatic lipid metabolism.
248 nship using several murine models of altered hepatic lipid metabolism.
249 r (LXR), a nuclear receptor that coordinates hepatic lipid metabolism.
250  several genes involved in the regulation of hepatic lipid metabolism.
251 te transporter involved in nutrient flux and hepatic lipid metabolism.
252 as srebp-1 and lxralpha, major regulators of hepatic lipid metabolism.
253 ck and functions as a circadian regulator of hepatic lipid metabolism.
254 between protein catabolism, ureagenesis, and hepatic lipid metabolism.
255 high-fat (AHF) diet, massive accumulation of hepatic lipid metabolites and significant increase in pl
256  a role for OSA in inducing abnormalities in hepatic lipid-metabolizing enzymes, endothelial dysfunct
257 le MR spectroscopic sequence for quantifying hepatic lipid noninvasively.
258 nged fasting but cannot overcome the ensuing hepatic lipid overload, resulting in fatty liver.
259                     By concurrently lowering hepatic lipid overloading as well as susceptibility of h
260                                              Hepatic lipid overloading mainly in the form of triglyce
261                   The ketogenic diet induced hepatic lipid oxidation and ketogenesis, and produced mu
262                                High rates of hepatic lipid oxidation and lipogenesis are also central
263   However, the effect of Notch1 signaling on hepatic lipid oxidation has not yet been directly invest
264                                  To increase hepatic lipid oxidation in the presence of glucose, we p
265 hanol exposure caused a >20-fold increase in hepatic lipids, peaking 12 hours after administration.
266                                Elevations in hepatic lipid peroxidation and CYP2E1 expression that ar
267 vs. 22.0 +/- 3.5%, P = 0.006), and increased hepatic lipid peroxidation compared to the HCR.
268        After liver radiation or cholic acid, hepatic lipid peroxidation levels increased, indicating
269                                              Hepatic lipid peroxidation was also elevated in the nose
270                                The amount of hepatic lipid peroxidation was also significantly decrea
271 acetyl coA oxidase messenger RNA involved in hepatic lipid peroxidation were also markedly increased
272 mature HDL particles by direct lipidation of hepatic lipid-poor apoA-I, slowing its catabolism by the
273 age, or transcription of genes that regulate hepatic lipid processing.
274 gs are that FoxO1 protects against excessive hepatic lipid production during hyperglycemia and that i
275             We sought to further analyze the hepatic lipid profile of these mice by electrospray ioni
276 and show enhanced ethanol clearance, altered hepatic lipid profiles in favor of increased levels of p
277                                              Hepatic lipid profiles of L lactis subsp cremoris-supple
278 ed peroxynitrite drove TLR4 recruitment into hepatic lipid rafts and inflammation, whereas the in viv
279  Toll-like receptor (TLR)-4 recruitment into hepatic lipid rafts in nonalcoholic steatohepatitis (NAS
280  liver identifying the role of iPLA2gamma in hepatic lipid second messenger production.
281 on of CAV1 in mice is required for efficient hepatic lipid storage during fasting, liver regeneration
282             MCD feeding triggered steatosis, hepatic lipid storage, and accumulation of free fatty ac
283    Saturated fat ingestion rapidly increases hepatic lipid storage, energy metabolism, and insulin re
284 ing secretion of triglyceride, liver weight, hepatic lipid storage, or transcription of genes that re
285 sduction pathways by which insulin regulates hepatic lipid synthesis and degradation remain largely u
286 ut its contribution to insulin AKT-regulated hepatic lipid synthesis is unclear.
287 t miR-30c mimic significantly down-regulated hepatic lipid synthesis pathways.
288 ipoprotein levels, in addition to decreasing hepatic lipid synthesis through direct targeting of lyso
289 ulin resistance, because the major source of hepatic lipid synthesis, esterification of preformed fat
290 mbination of increased peripheral lipolysis, hepatic lipid synthesis, loss of hepatoprotective mediat
291 ed capacity to burn fat and suppress de novo hepatic lipid synthesis.
292  fatty liver and dyslipidemia with increased hepatic lipid synthesis/flux associated with elevated he
293 nuclear hormone receptor with known roles in hepatic lipid transport.
294                In addition, the pathways for hepatic lipid uptake and lipogenic program are also down
295 ulation of hepatic TH signaling or decreased hepatic lipid utilization.
296                   Elevated futile cycling of hepatic lipids was also observed.
297  tomography-based method for measurements of hepatic lipids, we resolved the temporal events taking p
298                      Postprandial changes in hepatic lipids were measured [Deltahepatocellular lipid
299                                              Hepatic lipids were quantified by capillary gas chromato
300 MET properties and decreased circulating and hepatic lipids when orally administered to dyslipidemic

 
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