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1 on of hormone-sensitive lipase and increased lipolysis.
2 tegration and tended to limit the intestinal lipolysis.
3 n of desnutrin/ATGL and HSL and thus adipose lipolysis.
4 d VAT and decrease in insulin suppression of lipolysis.
5 exhibits impaired lipogenesis and increased lipolysis.
6 in oxygen consumption, Ucp1 expression, and lipolysis.
7 the GTPase ARF1, which is a key activator of lipolysis.
8 ression of endogenous glucose production, or lipolysis.
9 ial targets for treating obesity, as well as lipolysis.
10 hances macrolipophagy, an initiating step in lipolysis.
11 e activity and stimulated glucose uptake and lipolysis.
12 rolase activity and isoproterenol-stimulated lipolysis.
13 olism in response to increased ATGL-mediated lipolysis.
14 size led to an increased rate and extent of lipolysis.
15 inity determines protein localization during lipolysis.
16 restored the ability of insulin to suppress lipolysis.
17 lipase (ATGL), in the regulation of cardiac lipolysis.
18 and anchors LPL to the capillary wall during lipolysis.
19 xpression does not constantly impair cardiac lipolysis.
20 fully rescued the action of insulin against lipolysis.
21 s a key role in the suppression of adipocyte lipolysis.
22 sulin versus niacin-medicated suppression of lipolysis.
23 substrate utilization by regulating cardiac lipolysis.
24 PDE3B were examined for their regulation of lipolysis.
25 I, contributing to VLDL/HDL distribution and lipolysis.
26 t required for insulin to suppress adipocyte lipolysis.
27 d the loss of insulin-mediated inhibition of lipolysis.
28 the surface of lipid droplets and suppressed lipolysis.
29 g a critical role for PKA in Plin5-regulated lipolysis.
30 it inhibits basal and facilitates stimulated lipolysis.
31 le of perilipins 2 and 3 in regulating basal lipolysis.
32 he severe metabolic consequences of impaired lipolysis.
33 diated inhibition of glucose uptake requires lipolysis.
34 and forced expression of miR-145 attenuates lipolysis.
35 n adipocytes, plays a key role in regulating lipolysis.
36 they exhibited altered glucose disposal and lipolysis.
37 lipase (ATGL), a key enzyme in intracellular lipolysis.
38 d in de novo lipogenesis, beta-oxidation, or lipolysis.
39 before digestion but did not affect gastric lipolysis.
40 en transiently adapt to increased peripheral lipolysis.
41 ed hGP but failed to suppress adipose tissue lipolysis.
42 ase (ATGL), the key enzyme for intracellular lipolysis.
43 ed SNS signalling and possibly cause reduced lipolysis.
44 e stimulated both glucose uptake (17.4%) and lipolysis (17.7%); the mRNA expression of glucose transp
45 all adipose cells; increase in VAT, IHL, and lipolysis; 45% worsening of IMGU; and decreased expressi
46 issue inflammation and insulin regulation of lipolysis.A double-blind, placebo-controlled study compa
47 amus (MBH), display impaired fasting-induced lipolysis accompanied by a decreased norepinephrine cont
50 , our data indicate that excessive adipocyte lipolysis activates the JNK/NFkappaB pathway leading to
55 ts in dysfunctional elevated lipogenesis and lipolysis activities in mouse WAT as well as in stromal
59 expression of genes related to proteolysis, lipolysis and amino acid/lipid catabolism and significan
60 anistic insights into the cross talk between lipolysis and autophagy, two key metabolic responses to
62 , a direct relationship was observed between lipolysis and carotenoid micellarisation for all emulsio
65 valuable information about the extent of the lipolysis and enables a rapid discrimination among sampl
67 pocyte-specific gp130 deletion reduced basal lipolysis and enhanced insulin's ability to suppress lip
68 ltransferase-2 (DGAT2), and (b) decreases in lipolysis and FA beta-oxidation that paralleled a prolon
70 c AMP (cAMP)/protein kinase A (PKA)-mediated lipolysis and fatty acid and glucose oxidation, as well
71 al framework for understanding intravascular lipolysis and GPIHBP1 and LPL mutations causing familial
72 xpression of FGF21 suppressed adipose tissue lipolysis and improved hepatic steatosis in these mice.
73 ther metformin has any additional effects on lipolysis and inflammation that will enhance burn recove
74 ction of a beta3-adrenergic agonist, in vivo lipolysis and ketogenesis were decreased in G0S2 transge
76 unted beta-adrenoreceptor (beta-AR)-mediated lipolysis and lipid oxidation in adipose tissue, but the
77 uding impaired insulin action in suppressing lipolysis and lipid oxidation, accompanied by beta-cell
84 issue insulin action results in unrestrained lipolysis and lipotoxicity, which are hallmarks of the m
85 possibly secondary to the effects of reduced lipolysis and lower circulating fatty acid binding prote
86 he decreased LD formation is due to enhanced lipolysis and not caused by reduced triglyceride synthes
87 se cell size, VAT, or insulin suppression of lipolysis and only 8% worsening of insulin-mediated gluc
88 ence of ovalbumin and soy protein isolate on lipolysis and oxidation taking place during in vitro gas
89 leurotus sajor-caju mushroom on lipogenesis, lipolysis and oxidative stress in 3T3-L1 cells were inve
90 ling in POMC neurons controls adipose tissue lipolysis and prevents high-fat diet-induced hepatic ste
91 used by PHD2 inhibition in adipocytes blunts lipolysis and promotes benign adipose tissue expansion a
95 ncy reduces the basal rate of adipose tissue lipolysis and results in adipocyte hypertrophy upon agin
96 These data demonstrate a critical role for lipolysis and substrate delivery to the liver, secondary
97 were treated with isoproterenol to activate lipolysis and the fatty acyl lipidome of released lipids
100 beta3-adrenergic receptors (ADRB3) triggers lipolysis and up-regulates production of IL-6 in adipocy
102 ater circulating TG disposal, lower systemic lipolysis, and better fatty acid handling by lean tissue
103 increased basal and isoproterenol-stimulated lipolysis, and decreased adipocyte differentiation, whil
104 ory cytokines and stress hormones, increased lipolysis, and decreased G0S2 and increased CGI-58 mRNA
105 Insulin is a key regulator of adipose tissue lipolysis, and impaired adipose tissue insulin action re
106 promote hepatic lipogenesis, adipose tissue lipolysis, and impaired beta-oxidation), these factors c
107 us adipose cell size, insulin suppression of lipolysis, and regional fat responses to short-term over
108 y enhancing VLDL-TG uptake, intracellular TG lipolysis, and subsequent mitochondrial fatty acid oxida
110 file, mitochondrial capacity, fat oxidation, lipolysis, and tissue-specific insulin sensitivity.
113 ins that regulate energy homeostasis through lipolysis are thus likely to play an important role in d
115 increasing expression of CPT1A, and inducing lipolysis as indicated by elevation of the lipase ATGL,
116 n of hormone-sensitive lipase and consequent lipolysis, as do knockouts of dopamine beta-hydroxylase,
118 the development of LVH, adipose tissue (AT) lipolysis becomes elevated upon endurance training to co
119 hawing and pasteurization increased the milk lipolysis before digestion but did not affect gastric li
121 eficiency is associated with increased basal lipolysis, 'browning' of white fat and a healthy metabol
122 rom P. sajor-caju stimulated lipogenesis and lipolysis but attenuated protein carbonyl and lipid hydr
124 Mechanistically, we show that intravascular lipolysis by adipocyte lipoprotein lipase and hepatic up
125 inflammasome-activated macrophages improved lipolysis by decreasing levels of MAOA and caspase-1.
126 ific overexpression of G0S2 inhibits cardiac lipolysis by direct protein-protein interaction with ATG
127 RP3 in ageing restored catecholamine-induced lipolysis by downregulating growth differentiation facto
130 pocytes, regulates both basal and stimulated lipolysis by interacting with adipose triglyceride lipas
131 scavenger receptor CD36 and their subsequent lipolysis by lysosomal acid lipase (LAL) was important f
132 lipolysis is tightly regulated and excessive lipolysis causes hepatic steatosis, as NEFA released fro
133 gy demands under stress, whereas superfluous lipolysis causes metabolic disorders, including dyslipid
137 eleased from succinate-induced inhibition of lipolysis, demonstrating a function of Sucnr1 in adipose
139 ovide the first evidence that adipose tissue lipolysis directly promotes the development of exercise-
140 accumulation of sn-1,3 DAG originating from lipolysis does not inhibit insulin-stimulated glucose up
141 ed by impaired suppression of adipose tissue lipolysis due to decreased insulin secretion and to a re
144 y of IKKbeta also leads to increased adipose lipolysis, elevated plasma free fatty acid (FFA) levels,
145 tty acid metabolism (lipogenesis, oxidation, lipolysis, esterification) and fatty acid uptake in >900
146 que provides a complete molecular picture of lipolysis, evidencing for the first time, whether prefer
148 ameliorates ER stress-induced inhibition on lipolysis, fatty acid oxidation, oxidative metabolism, a
149 s and enhanced insulin's ability to suppress lipolysis from mesenteric but not epididymal adipocytes.
150 eported patients with T2D, we also estimated lipolysis (from [(2)H5]glycerol turnover rate and circul
158 liver fat induces mitochondrial metabolism, lipolysis, glyceroneogenesis and a switch from lactate t
159 abetes (T1D) and measure rates of whole-body lipolysis, hepatic acetyl CoA content, pyruvate carboxyl
162 etic (T1D) rats exhibited decreased rates of lipolysis, HGP, and ketogenesis; these effects were reve
163 l size, VAT, IHL, and insulin suppression of lipolysis highlight these factors as potential mediators
165 was found that cranberries directly induced lipolysis in adipocytes and down-regulated the expressio
166 These findings suggest that unsuppressed lipolysis in adipocytes elicited by HFD feeding is linke
168 hereas perilipin 1 potently suppresses basal lipolysis in adipocytes, perilipins 2 and 3 facilitate h
172 We aimed to measure the rate and extent of lipolysis in an in vitro duodenum digestion model, using
175 gene expression at multiple levels, enhances lipolysis in epididymal WAT (eWAT) because of the upregu
177 ulate the age-related reduction in adipocyte lipolysis in mice by lowering the bioavailability of nor
179 ed FLD of Angptl4 is sufficient to stimulate lipolysis in mouse primary adipocytes and that increasin
181 an unanticipated role of Cav-1 in regulating lipolysis in non-adipose tissue, indicating that Cav-1 i
182 ne-depleted adipocytes exhibited lower basal lipolysis in normoxia and reduced beta-adrenergic-stimul
183 ins 2 and 3 facilitate higher rates of basal lipolysis in other tissues where constitutive traffic of
185 m in EC and that it regulates cAMP-dependent lipolysis in part via the autocrine production of PGI2.
186 inhibit beta-adrenoreceptor agonist-promoted lipolysis in primary mouse adipocytes and to promote che
188 n impact of FA synthesis and mobilization by lipolysis in somatic tissues on oocyte fate in Caenorhab
190 overexpression (Ad-FLD) not only induces WAT lipolysis in vivo but also reduces diet-induced obesity
191 he role of AMPK in the regulation of adipose lipolysis in vivo, we generated mice with adipose-tissue
192 ions in hepatic acetyl CoA by suppression of lipolysis in white adipose tissue (WAT) leading to reduc
194 ecessary and sufficient for the induction of lipolysis in white adipose tissue and are an efferent ef
196 Lipolysis in white adipose tissues (WAT) and lipolysis-induced blood glucose rise were increased in I
200 leagues provide evidence that suppression of lipolysis is a key facet of leptin-mediated restoration
206 (FA) of o/w emulsions on both the pancreatic lipolysis kinetics and the bioaccessibility of released
208 ets was the key parameter to control gastric lipolysis kinetics, the pattern of released fatty acids
210 intralipids or by inhibiting adipose tissue lipolysis led to failure in EGP suppression, thus suppor
211 erent in vitro digestion experiments and the lipolysis levels reached were evaluated using (1)H NMR s
213 s TG-lowering alleles involved in peripheral lipolysis (LPL and ANGPTL4) had no effect on liver fat b
214 dicated by elevation of the lipase ATGL, the lipolysis marker glycerol and release of fatty acids.
215 The results show that IL-6 cytokine-induced lipolysis may be restricted to mesenteric white adipose
217 lly, we found that hypothalamic induction of lipolysis mediated the brain's action in promoting this
219 ns 2 or 3 stabilize ABHD5 and suppress basal lipolysis more effectively than WT perilipins 2 or 3.
220 hat, in addition to its ability to stimulate lipolysis, NE induces energy expenditure in BA by promot
224 iggers ER autophagy and subsequent lysosomal lipolysis of TG, followed by mitochondrial oxidation of
225 ein lipase (LPL) activity and stimulates the lipolysis of triacylglycerol stored by adipocytes in the
228 we investigated the impact of adipose tissue lipolysis on the development of exercise-induced cardiac
229 had no beneficial effects on adipose tissue lipolysis or inflammation in insulin-resistant adults.
230 y, catecholamine-induced lipid mobilization (lipolysis), or insulin-stimulated lipid synthesis in adi
234 m cells through necrosis, by attenuating the lipolysis pathway, but spared differentiated cells.
235 report that during catecholamine-stimulated lipolysis, Perilipin 5 is phosphorylated by protein kina
236 n recent work suggesting that pancreatic fat lipolysis plays an important role in SAP, we evaluated t
239 evidence that gp130-mediated adipose tissue lipolysis promotes hepatic steatosis and insulin resista
240 man milk on its gastrointestinal kinetics of lipolysis, proteolysis and structural disintegration.
241 Together, we show that autophagy-mediated lipolysis provides free fatty acids to support a mitocho
242 eoxy-D-glucose/positron emission tomography, lipolysis (RaGly) with [U-(2) H5 ]-glycerol, oral glucos
247 revent lipotoxicity, whereas TAG hydrolysis (lipolysis) remobilizes fatty acids from endogenous stora
257 appears to cause exacerbated adipose tissue lipolysis, suggesting that strategies to reduce muscle l
260 2-deficient hepatocytes exhibit increased TG lipolysis, TG turnover, and fatty acid oxidation as comp
262 adipose triglyceride lipase (ATGL)-mediated lipolysis that plays important roles in metabolism, tumo
264 gh ACTH was known to stimulate PKA-dependent lipolysis, the functional involvement of MRAP in adipocy
266 nd considers CLA's linkage with lipogenesis, lipolysis, thermogenesis, and browning of white and brow
267 ode that links beta-adrenergic signaling and lipolysis to changes in the transcriptional regulation o
268 a highly regulated metabolic process called lipolysis to free fatty acids that serve as energy subst
269 enhance the ability of Atgl/Cgi-58-mediated lipolysis to induce the activity of peroxisome prolifera
270 tochondrial biogenesis, lipid oxidation, and lipolysis under a high fat diet, leading to elevated ene
279 uppress hepatic acetyl CoA, PC activity, and lipolysis was lost in high-fat-fed rats, a phenomenon re
281 Despite inactivating BSSL, instantaneous lipolysis was not affected by pasteurization (mean +/- S
283 In general, results indicated that enzymatic lipolysis was the driving factor influencing the quality
285 atriuretic peptide, and thus, induce adipose lipolysis, we studied peripheral and systemic metabolism
287 ile concentration, on the extent of in vitro lipolysis when using a static model that simulates human
288 ic steatosis due to increased adipose tissue lipolysis, when fasted or fed a high-fat low-carbohydrat
290 s and profound suppression of adipose tissue lipolysis, which decreases delivery of FAs to the liver.
291 hite adipose tissue (WAT) leads to increased lipolysis, which further increases hepatic triglyceride
292 n, hepatic acetyl CoA content and whole-body lipolysis, which results from decreases in plasma ACTH a
294 e-sensitive lipase and consequently activate lipolysis, which then enables the transfer of fatty acid
295 storage and diminish macrophage-induced WAT lipolysis will reverse the root causes of type 2 diabete
296 oncentration in adipose tissue, and restored lipolysis with increased levels of the key lipolytic enz
298 tion of the PKA pathway and of lipid droplet lipolysis with transcriptional regulation to promote eff
300 R299N and ABHD5 G328S) selectively disrupted lipolysis without affecting ATGL lipid droplet transloca
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