ライフサイエンスコーパス: lipolysis

1 dy weight while also inducing adipose tissue lipolysis.

2 cerol synthesis, lipid droplet formation and lipolysis.

3 adipocytes that is independent of canonical lipolysis.

4 lin sensitivity, lipid storage capacity, and lipolysis.

5 ty, metabolic energy expenditure, or adipose lipolysis.

6 , the rate-limiting enzyme for intracellular lipolysis.

7 ed suppression of white adipose tissue (WAT) lipolysis.

8 elevated PLIN1 phosphorylation and enhanced lipolysis.

9 naling, resulting in enhanced adipose tissue lipolysis.

10 ase (ATGL), the key enzyme for intracellular lipolysis.

11 on of hormone-sensitive lipase and increased lipolysis.

12 the GTPase ARF1, which is a key activator of lipolysis.

13 I, contributing to VLDL/HDL distribution and lipolysis.

14 ing in WAT through impacting lipogenesis and lipolysis.

15 before digestion but did not affect gastric lipolysis.

16 en transiently adapt to increased peripheral lipolysis.

17 ed hGP but failed to suppress adipose tissue lipolysis.

18 ed SNS signalling and possibly cause reduced lipolysis.

19 tegration and tended to limit the intestinal lipolysis.

20 n of desnutrin/ATGL and HSL and thus adipose lipolysis.

21 d VAT and decrease in insulin suppression of lipolysis.

22 exhibits impaired lipogenesis and increased lipolysis.

23 in oxygen consumption, Ucp1 expression, and lipolysis.

24 rementioned features, in turn, can influence lipolysis.

25 n-trivial interplays between proteolysis and lipolysis.

26 re via sympathetic control of adipose tissue lipolysis.

27 dipocytes in vitro directly stimulated basal lipolysis.

28 hibited similar suppression rates of EGP and lipolysis.

29 ADM dose dependently increased ex vivo lipolysis.

30 metabolite reservoir linked to ATGL-mediated lipolysis.

31 acid, activation of hepatic FXR, and hepatic lipolysis.

32 and increases in metabolites associated with lipolysis (1-methylnicotinamide, +33%; P=6.1x10(-67)), n

33 sity(1), and defects in thermogenesis(2) and lipolysis(3), both of which are adipose tissue functions

34 all adipose cells; increase in VAT, IHL, and lipolysis; 45% worsening of IMGU; and decreased expressi

35 issue inflammation and insulin regulation of lipolysis.A double-blind, placebo-controlled study compa

36 y resulting from unrestrained adipose tissue lipolysis, accompanies the lack of rapid changes in insu

37 Moreover, FAs from higher lipolysis activate peroxisome proliferator-activated rec

38 We found that lipolysis activates the JNK/NFkappaB signaling pathway a

39 The structural determinants of ABHD5 lipolysis activation, however, are unknown.

40 years ago, to identify determinants of ABHD5 lipolysis activation.

41 ts in dysfunctional elevated lipogenesis and lipolysis activities in mouse WAT as well as in stromal

42 Macrophage-induced WAT lipolysis also stimulates hepatic gluconeogenesis, promo

43 duces FGF21, which suppresses adipose tissue lipolysis, ameliorating hepatic steatosis.

44 hepatocytes is mediated by a combination of lipolysis and a selective autophagic mechanism called li

45 urs) induction of gene networks that promote lipolysis and adipogenesis in mammalian adipocytes.

46 anced basal and impaired insulin-inhibitable lipolysis and altered adipokine secretion, and in human

47 expression of genes related to proteolysis, lipolysis and amino acid/lipid catabolism and significan

48 th fatty acids generated from adipose tissue lipolysis and beta-adrenergic activation of brown adipos

49 emic insulin resistance by stimulating basal lipolysis and by activating macrophages in adipose tissu

50 rointestinal (GI) conditions on proteolysis, lipolysis and calcium and vitamins A and D3 bioaccessibi

51 , a direct relationship was observed between lipolysis and carotenoid micellarisation for all emulsio

52 , such as changes in rates of adipose tissue lipolysis and de novo lipogenesis, impaired mitochondria

53 However, the role of AMPK in lipolysis and FA metabolism in adipose tissue has been c

54 itines, fatty acids, and other byproducts of lipolysis and fatty acid oxidation.

55 atic steatosis include reductions in adipose lipolysis and food intake.

56 in sensitivity (inhibition of adipose tissue lipolysis and glucose production and stimulation of musc

57 ngements increase white adipose tissue (WAT) lipolysis and hepatic acetyl-CoA content, rates of hepat

58 tivated macrophages markedly increased basal lipolysis and impaired insulin-mediated lipolysis suppre

59 xpression of FGF21 suppressed adipose tissue lipolysis and improved hepatic steatosis in these mice.

60 ice showed reduced adipocyte respiration and lipolysis and increased de novo lipogenesis, culminating

61 e size of lipid droplets (LDs) and inhibited lipolysis and insulin signaling.

62 cytokines and stress hormones that stimulate lipolysis and ketogenesis.

63 uding impaired insulin action in suppressing lipolysis and lipid oxidation, accompanied by beta-cell

64 or of plasma TG levels through regulation of lipolysis and lipid synthesis.

65 ermogenic gene expression, and downregulated lipolysis and lipogenesis genes in epididymal WAT.

66 nerve fibres in response to perturbations in lipolysis and lipogenesis.

67 ight, but correlated with down-regulation of lipolysis and lipogenic indices.

68 LIP and PNLIPRP2 were equipotent in inducing lipolysis and lipotoxic injury, CEL required bile acid c

69 issue insulin action results in unrestrained lipolysis and lipotoxicity, which are hallmarks of the m

70 associated with greater suppression rates of lipolysis and lower intrahepatic lipid and plasma triacy

71 Orlistat significantly reduced lipolysis and MDA formation.

72 ase during tricaprylin digestion (intestinal lipolysis and micellar solubilization).

73 he decreased LD formation is due to enhanced lipolysis and not caused by reduced triglyceride synthes

74 s homeostatic functions such as proteolysis, lipolysis and nutrient transport.

75 ronment and the type of protein can modulate lipolysis and oxidation during in vitro digestion.

76 ence of ovalbumin and soy protein isolate on lipolysis and oxidation taking place during in vitro gas

77 (orlistat) and tocopherols to cod liver oil, lipolysis and oxidation was also studied.

78 hospholipids (PL) are the main substrates of lipolysis and oxidation.

79 ling in POMC neurons controls adipose tissue lipolysis and prevents high-fat diet-induced hepatic ste

80 oreover, adipose OGT overexpression inhibits lipolysis and promotes diet-induced obesity.

81 improved insulin-mediated suppression of WAT lipolysis and reduced ectopic lipid content in liver and

82 imulated suppression of white adipose tissue lipolysis and reduced inflammation.

83 I, a critical inhibitor of triglyceride (TG) lipolysis and remnant TRL clearance.

84 ncy reduces the basal rate of adipose tissue lipolysis and results in adipocyte hypertrophy upon agin

85 ne) infusion profoundly stimulated adipocyte lipolysis and simultaneously triggered insulin resistanc

86 This led to an increase in lipolysis and specific amelioration of hepatic insulin r

87 riglyceride (TG) turnover (representing both lipolysis and synthesis at steady state), without signif

88 ce in the gastric environment, which reduced lipolysis and the formation of advanced oxidation specie

89 Br2 mediates ER stress-induced inhibition of lipolysis and thermogenesis in BAT.

90 ns adrenergic signaling, thereby attenuating lipolysis and thermogenic respiration.

91 le in the regulation of ACTH-induced adipose lipolysis and whole-body energy balance.

92 which is necessary and sufficient to induce lipolysis and, as a result, increase body temperature af

93 ults suggest that increased turnover of TGs (lipolysis) and of mature adipocytes in both abdominal an

94 nt, chemical stability (pH, lipid oxidation, lipolysis), and optical properties.

95 ater circulating TG disposal, lower systemic lipolysis, and better fatty acid handling by lean tissue

96 ory cytokines and stress hormones, increased lipolysis, and decreased G0S2 and increased CGI-58 mRNA

97 compartments, with effects on adipogenesis, lipolysis, and ectopic fat accumulation.

98 Insulin is a key regulator of adipose tissue lipolysis, and impaired adipose tissue insulin action re

99 cells showed visible LDs, glucose-responsive lipolysis, and impairment of GSIS after ATGL silencing.

100 cells showed visible LDs, glucose responsive lipolysis, and impairment of GSIS after ATGL silencing.

101 doplasmic reticulum (ER) stress, potentiated lipolysis, and insulin resistance.

102 T) thermogenesis, white adipose tissue (WAT) lipolysis, and insulin sensitivity.METHODSWe treated 14

103 al metabolism by controlling insulin action, lipolysis, and mitochondrial respiration to control the

104 nuclear retention, enhances lipid uptake and lipolysis, and potentiates UCP1 expression.

105 lish is required to restrain fasting-induced lipolysis, and thus conserve cellular triglyceride level

106 ulators involved in fatty acid oxidation and lipolysis, and thus promoted hepatic steatosis.

107 file, mitochondrial capacity, fat oxidation, lipolysis, and tissue-specific insulin sensitivity.

108 unction, absent browning of WAT, and reduced lipolysis, and were therefore cold-intolerant.

109 ntial for regulating adaptive thermogenesis, lipolysis, and whole-body energy metabolism.

110 ine molecular mechanisms by which GH induces lipolysis are described.

111 te the structural basis for LPL-mediated TRL lipolysis as well as LPL stabilization and transport by

112 We investigated whole-body lipolysis, ATIS, and beta-cell function relative to ATIS

113 ize and the initial rate and final extent of lipolysis based on the digested triolein.

114 hawing and pasteurization increased the milk lipolysis before digestion but did not affect gastric li

115 With higher overall adipose lipolysis, both models of AMPK-ASKO mice are lean, havin

116 d this medium stimulated UCP1 expression and lipolysis by 3T3-L1 adipocytes.

117 hat genetic or pharmacological activation of lipolysis by ABHD5 potently inhibits mTORC1 signaling, l

118 Mechanistically, we show that intravascular lipolysis by adipocyte lipoprotein lipase and hepatic up

119 inflammasome-activated macrophages improved lipolysis by decreasing levels of MAOA and caspase-1.

120 RP3 in ageing restored catecholamine-induced lipolysis by downregulating growth differentiation facto

121 Stimulation of adipocyte lipolysis by fasting (24 h) or beta3-adrenergic receptor

122 lipolysis is tightly regulated and excessive lipolysis causes hepatic steatosis, as NEFA released fro

123 gy demands under stress, whereas superfluous lipolysis causes metabolic disorders, including dyslipid

124 Progenitor recruitment and adipogenic lipolysis contribute to the anabolic actions of parathyr

125 Chronically enhancing WAT lipolysis could produce ectopic steatosis because of an

126 cell proliferation, in which ABHD5-mediated lipolysis creates an energy-consuming futile cycle betwe

127 affected by oleogel structure: the extent of lipolysis decreased as oleogel strength increased (PS <

128 teolysis was not affected by processing, but lipolysis decreased in marinated (46%) and raw salmon (5

129 In altered conditions, proteolysis and lipolysis decreased to different extents depending on th

130 A lipolysis degree similar to that reported in vivo was re

131 lating levels of the adipokine resistin in a lipolysis-dependent manner.

132 The kinetics of proteolysis and lipolysis differed according to the physiological stage

133 PAHSAs inhibited lipolysis directly in WAT explants and enhanced the acti

134 , 2) that postprandial inhibition of adipose lipolysis does not suppress EGP, and 3) that physiologic

135 ed by impaired suppression of adipose tissue lipolysis due to decreased insulin secretion and to a re

136 hypertriglyceridemia and excessive systemic lipolysis during intravenous lipid overload.

137 d enhanced the action of insulin to suppress lipolysis during the clamp in vivo.

138 to follow this order, mostly due to partial lipolysis during the gastric phase.

139 he evolution of dehydration, proteolysis and lipolysis during the maturation period that precedes the

140 , low-cost technique, termed electrochemical lipolysis (ECLL).

141 This results in enhanced lipolysis, elevated concentrations of free fatty acids,

142 Inhibition of the lipolysis enzyme adipose triglyceride lipase (ATGL) resu

143 tty acid metabolism (lipogenesis, oxidation, lipolysis, esterification) and fatty acid uptake in >900

144 que provides a complete molecular picture of lipolysis, evidencing for the first time, whether prefer

145 Tween80 emulsions led to a higher lipolysis extent (53-57%) and carotenoid bioaccessibilit

146 After in vitro digestion, lipolysis extent was 13% lower in pasteurised human milk

147 al conditions were the major determinants of lipolysis (f-ratio = 58.01).

148 ameliorates ER stress-induced inhibition on lipolysis, fatty acid oxidation, oxidative metabolism, a

149 disposal and insulin-mediated suppression of lipolysis, FFA, and EGP.

150 its role in insulin-mediated suppression of lipolysis, free fatty acids (FFA), and endogenous glucos

151 ant lipoprotein particles (RLPs), derived by lipolysis from VLDL and chylomicrons, contribute to this

152 eported patients with T2D, we also estimated lipolysis (from [(2)H5]glycerol turnover rate and circul

153 GAT lipolysis fuels fatty acid oxidation in LSCs, especially

154 However, the specific roles of lipolysis-generated mediators in adipose inflammation re

155 Excessive adipocyte lipolysis generates lipid mediators and triggers inflamm

156 In agreement with reduced WAT lipolysis, glucocorticoid- initiated hepatic steatosis a

157 Whole-body lipolysis (glycerol appearance rate [GlyRa], [(2)H5]glyc

158 Lipolysis (glycerol turnover), hepatic glucose productio

159 Endogenous glucose production, lipolysis (glycerol, nonesterified fatty acid), and glyc

160 sion and metabolic signatures with activated lipolysis, glycolysis, and metabolic pathways regulated

161 growth hormone (GH) to induce adipose tissue lipolysis has been known for over five decades; however,

162 ic adipose triglyceride lipase, intrahepatic lipolysis, hepatic acetyl-CoA content and pyruvate carbo

163 Leptin infusion reduced rates of lipolysis, hepatic glucose production (HGP), and hepatic

164 Leptin-induced decreases in lipolysis, HGP, and ketogenesis in DKA were also nullifi

165 etic (T1D) rats exhibited decreased rates of lipolysis, HGP, and ketogenesis; these effects were reve

166 It has been known that MEHP has an impact on lipolysis; however, its mechanism on the cellular lipid

167 d identify four potential sources: adipocyte lipolysis, hydrolysis of inorganic pyrophosphate generat

168 Induction of lipolysis (i.e., triacylglycerol hydrolysis) in adipocyt

169 ORLA promotes insulin-induced suppression of lipolysis in adipocytes.

170 sion toward remodeling and inhibited ex vivo lipolysis in adipose tissue, suggesting that PGs favor l

171 rol (TAG) hydrolase activity, lowering basal lipolysis in adipose tissue.

172 P/PKA pathways, contributing to the enhanced lipolysis in Cav-1 KO cells.

173 The impaired lipolysis in global adipose triglyceride lipase (ATGL) k

174 ulate the age-related reduction in adipocyte lipolysis in mice by lowering the bioavailability of nor

175 ed FLD of Angptl4 is sufficient to stimulate lipolysis in mouse primary adipocytes and that increasin

176 an unanticipated role of Cav-1 in regulating lipolysis in non-adipose tissue, indicating that Cav-1 i

177 We found that glucose increases lipolysis in non-diabetic human islets, but not in type

178 We found that glucose increases lipolysis in nondiabetic human islets but not in islets

179 n, energy expenditure and PYY, and decreased lipolysis in overweight/obese men.

180 m in EC and that it regulates cAMP-dependent lipolysis in part via the autocrine production of PGI2.

181 ating an essential requirement for adipocyte lipolysis in promoting stress-induced insulin resistance

182 we identify an essential role for adipocyte lipolysis in regulating inflammation and repair after in

183 like adipocytes, also undergo cAMP-mediated lipolysis in response to beta-AR stimulation.

184 n impact of FA synthesis and mobilization by lipolysis in somatic tissues on oocyte fate in Caenorhab

185 diabetes (T2D), indicating dysregulation of lipolysis in T2D islets.

186 ic (T2D) islets, indicating dysregulation of lipolysis in T2D islets.

187 More globally, we explain lipolysis in terms of GH-induced intracellular signallin

188 atitis-associated adipose tissue had ongoing lipolysis in the absence of adipocyte triglyceride lipas

189 onstrate the central importance of adipocyte lipolysis in the metabolic response to injury.

190 visceral fat loss by specifically promoting lipolysis in visceral fat.

191 overexpression (Ad-FLD) not only induces WAT lipolysis in vivo but also reduces diet-induced obesity

192 and its deficiency enhanced agonist-induced lipolysis in vivo CTRP2-deficient mice also had altered

193 hermogenesis, and white adipose tissue (WAT) lipolysis in vivo.

194 Glucocorticoids promote lipolysis in white adipose tissue (WAT) to adapt to ener

195 however, the regulation of LD mobilization (lipolysis) in human beta cells remains unclear.

196 However, the regulation of LD mobilization (lipolysis) in human beta-cells remains unclear.

197 acid oxidation, derived from adipose tissue lipolysis, in order to preserve glucose for the brain.

198 mmatory process that results in dysregulated lipolysis, increased circulating lipids, ectopic lipid d

199 on, promotes adipose tissue inflammation and lipolysis, increases lipid accumulation in peripheral ti

200 Here we sought to investigate a lipolysis-independent role of G0S2 in hepatic triglyceri

201 can cause excessive visceral adipose tissue lipolysis independently of adipocyte-autonomous ATGL, an

202 In acinar cells, cooling decreased the lipolysis induced by GTL, increased the micellar form of

203 Despite high lipolysis, INSR subjects had low hepatic triglycerides (

204 leagues provide evidence that suppression of lipolysis is a key facet of leptin-mediated restoration

205 Intracellular lipolysis is an enzymatic pathway responsible for the ca

206 in adipocytes is normal in the elderly, how lipolysis is impaired in ageing remains unknown.

207 Lipolysis is increased due to mTORC2 repression, increas

208 Adipose tissue lipolysis is tightly regulated and excessive lipolysis c

209 domain responsible for stimulating adipocyte lipolysis is unknown.

210 zyme that mediates the rate-limiting step in lipolysis, is a key point of this regulation.

211 on reduced the droplet surface area, overall lipolysis kinetics and consequently decreased the extent

212 e aim of this work was to study the in vitro lipolysis kinetics as well as the relationship between t

213 owever, HPO-containing SLNs presented slower lipolysis kinetics during the intestinal phase at increa

214 tric phase were directly associated with the lipolysis kinetics during the intestinal phase.

215 ng gastrointestinal conditions in modulating lipolysis kinetics.

216 intralipids or by inhibiting adipose tissue lipolysis led to failure in EGP suppression, thus suppor

217 We find that inhibition of lipolysis, lipophagy, or both resulted in similar overal

218 tion raised EGP, lowered TGD, and stimulated lipolysis, LOx, and ketogenesis.

219 s TG-lowering alleles involved in peripheral lipolysis (LPL and ANGPTL4) had no effect on liver fat b

220 he RCs to the LDs and interact with the host lipolysis machinery to enable transfer of fatty acids fr

221 he high bile acid requirements for effective lipolysis make CEL an unlikely mediator of lipotoxic inj

222 The results show that IL-6 cytokine-induced lipolysis may be restricted to mesenteric white adipose

223 The dysregulated lipolysis may contribute to LD accumulation and beta cel

224 The dysregulated lipolysis may contribute to LD accumulation and beta-cel

225 rapeutic approach for enhanced PPARalpha and lipolysis may reduce HCV genotype-associated lipid metab

226 the overall lipolysis profile and molecular lipolysis mechanisms under in vitro gastric conditions.

227 ofound insight in in vitro gastric molecular lipolysis mechanisms.

228 The kinetics of lipolysis, micelle formation and carotenoid bioaccessibi

229 knockouts, had lower visceral adipose tissue lipolysis, milder inflammation, less severe organ failur

230 Furthermore, a mechanistic gastric lipolysis model was established based on a reaction sche

231 Lipolysis occurred in milk before digestion and was high

232 Altogether, pasteurisation decreased the pre-lipolysis of human milk.

233 mice by both altering cell fate and inducing lipolysis of marrow adipocytes.

234 allocation toward osteogenesis and inducing lipolysis of mature marrow adipocytes.

235 iggers ER autophagy and subsequent lysosomal lipolysis of TG, followed by mitochondrial oxidation of

236 duced microbial growth, lipid oxidation, and lipolysis of the lamb meat during storage, which led to

237 ein lipase (LPL) activity and stimulates the lipolysis of triacylglycerol stored by adipocytes in the

238 Acute lipolysis of visceral fat or circulating triglycerides m

239 transformed" extract could be used to induce lipolysis on fat tissue.

240 fied fatty acid levels did not increase with lipolysis or correlate with insulin resistance during ac

241 lin-stimulated lipogenesis but did not alter lipolysis or glucose uptake in 3T3-L1 adipocytes.

242 had no beneficial effects on adipose tissue lipolysis or inflammation in insulin-resistant adults.

243 nditure) without any effects on lipogenesis, lipolysis or lipid uptake and transport.

244 s of metabolism, including glucose disposal, lipolysis, oxidative metabolism, and energy expenditure.

245 ected carotenoid bioaccessibility (p<0.001), lipolysis, particle size and zeta potential.

246 Additionally, lipolysis, particle size, and zeta potential of the mice

247 tes between LDs and RCs or inhibition of the lipolysis pathway disrupts RC biogenesis and enterovirus

248 To test whether this beta-AR-dependent lipolysis pathway was altered in a model of alcoholic fa

249 f oat materials varying in complexity on the lipolysis process.

250 Results also suggest that lipolysis products are very rapidly solubilized in the b

251 For the first time, multiple lipolysis products including diolein and monoolein regio

252 fect of droplet size behavior on the overall lipolysis profile and molecular lipolysis mechanisms und

253 Lipolysis promotes mitochondrial biogenesis and oxidativ

254 man milk on its gastrointestinal kinetics of lipolysis, proteolysis and structural disintegration.

255 Together, we show that autophagy-mediated lipolysis provides free fatty acids to support a mitocho

256 eoxy-D-glucose/positron emission tomography, lipolysis (RaGly) with [U-(2) H5 ]-glycerol, oral glucos

257 The estimated lipolysis rate constants of the studied FA (C8:0, C10:0>

258 uction (EGP) that was 2.6-fold greater and a lipolysis rate that was 2.3-fold greater than the formul

259 In SC WAT, mirabegron treatment stimulated lipolysis, reduced fibrotic gene expression, and increas

260 ificant increase in UCP1 mRNA (p = 0.03) and lipolysis-related ATGL mRNA (p = 0.04).

261 Lipidomic analyses indicate that TAG lipolysis releases free fatty acids at a time that corre

262 Glucocorticoid-induced lipolysis requires the phosphorylation of cytosolic horm

263 adipocytes reduced or increased ACTH-induced lipolysis, respectively.

264 spanning neural communication and olfaction, lipolysis, rest-activity cycles, and kinase pathways cri

265 droxybutyrate concentrations and the rate of lipolysis rose markedly.

266 is (PRIM) or secondarily from adipose tissue lipolysis (SEC).

267 Lipolysis showed an early decrease in glycerol release i

268 rves for energy, in such a way that blocking lipolysis starves them to death.

269 ition of the JNK/NFkappaB axis abrogated the lipolysis-stimulated COX-2 expression.

270 involved in binding the host-cell receptor, lipolysis-stimulated lipoprotein receptor.

271 appears to cause exacerbated adipose tissue lipolysis, suggesting that strategies to reduce muscle l

272 asal lipolysis and impaired insulin-mediated lipolysis suppression.

273 se of pro-inflammatory cytokines that impair lipolysis suppression.

274 ndicating a synergistic relationship whereby lipolysis targets larger-sized LDs to produce both size-

275 d LAL resulted in large LDs, suggesting that lipolysis targets these LDs upstream of lipophagy.

276 es of glycolysis, uncoupled respiration, and lipolysis that are responsive to changes in cyclic AMP (

277 adipose triglyceride lipase (ATGL)-mediated lipolysis that plays important roles in metabolism, tumo

278 Catecholamine-induced lipolysis, the first step in the generation of energy su

279 gh ACTH was known to stimulate PKA-dependent lipolysis, the functional involvement of MRAP in adipocy

280 The extent of lipolysis, the molar proportions of acyl groups/fatty ac

281 investigated the contributions of adipocyte lipolysis to the metabolic response to acute stress.

282 , de novo synthesised FA, or FA derived from lipolysis, to generate TAG, as well as being involved in

283 ered lipid metabolism, in particular induced lipolysis upon starvation.

284 Conversely, lipolysis was decreased and lipogenesis was increased in

285 Robustly enhanced lipolysis was found in gonadal fat of Adipoq(-/-) dams.

286 Lipolysis was higher in males than females in C and HG c

287 Insulin-mediated suppression of adipose lipolysis was improved by 40% in Ad-GcR(-/-) mice.

288 VAT ex-vivo lipolysis was increased (p < 0.05) in P-HFHS compared to

289 When lipolysis was inhibited, the stress-induced insulin resi

290 Despite inactivating BSSL, instantaneous lipolysis was not affected by pasteurization (mean +/- S

291 Lipolysis was not stimulated by HG or high hydrocortison

292 Lipolysis was suppressed, mitochondrial carnitine shuttl

293 uced, but the ability of insulin to suppress lipolysis was unaltered.

294 atriuretic peptide, and thus, induce adipose lipolysis, we studied peripheral and systemic metabolism

295 characterising dehydration, proteolysis and lipolysis were individuated and studied by exploiting a

296 olism (particularly fatty acid synthesis and lipolysis), which were disrupted by the FFD, were found

297 s and profound suppression of adipose tissue lipolysis, which decreases delivery of FAs to the liver.

298 e-sensitive lipase and consequently activate lipolysis, which then enables the transfer of fatty acid

299 oncentration in adipose tissue, and restored lipolysis with increased levels of the key lipolytic enz

300 R299N and ABHD5 G328S) selectively disrupted lipolysis without affecting ATGL lipid droplet transloca