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1 ddition, LDP enhances the effect of high-fat diet induced obesity.
2 n resistance, particularly in the context of diet-induced obesity.
3 f alternative splicing to the development of diet-induced obesity.
4 adipose remodeling and adipocyte survival in diet-induced obesity.
5 tained glucose tolerance and did not develop diet-induced obesity.
6 stance and as a novel therapeutic target for diet-induced obesity.
7 iR-155 (-5p and -3p) in female mice prevents diet-induced obesity.
8 7 also prevented kidney disease in mice with diet-induced obesity.
9 a central mechanism for beta cell failure in diet-induced obesity.
10 ate during and after development of high-fat diet-induced obesity.
11 oc in mice (Noc KO) results in resistance to diet-induced obesity.
12 itochondrial oxidation and susceptibility to diet-induced obesity.
13 rature and energy expenditure and preventing diet-induced obesity.
14 ivation precipitates vascular dysfunction in diet-induced obesity.
15 repression increased with aging and high-fat diet-induced obesity.
16 and, as adults, were protected from high fat diet-induced obesity.
17  display reduced adiposity and resistance to diet-induced obesity.
18 bitor decreased adipogenesis and ameliorated diet-induced obesity.
19 cient mice were also evaluated in a model of diet-induced obesity.
20 oding MGAT2 (Mogat2(-/-)) are protected from diet-induced obesity.
21 iture, decreased fat mass, and resistance to diet-induced obesity.
22 ficient to prevent both genetic and high-fat diet-induced obesity.
23 abolic derangements associated with high fat diet-induced obesity.
24 nsitivity and are more resistant to high fat diet-induced obesity.
25 PR-B signaling is important for the onset of diet-induced obesity.
26  oxidation and ketone body production during diet-induced obesity.
27 on and decreased BAT activity under high fat diet-induced obesity.
28 es fatty acid oxidation and protects against diet-induced obesity.
29 2 on effects of fibrates in a mouse model of diet-induced obesity.
30  Foxo1KO(Nkx2.1) mice are not protected from diet-induced obesity.
31 in resistance, but KO mice were resistant to diet-induced obesity.
32  the liver-related consequences of long-term diet-induced obesity.
33 e: ob/ob, GLUT4(+/-), and mice with high-fat diet-induced obesity.
34 hat mediate the resistance of female mice to diet-induced obesity.
35 pression in heart tissue in a mouse model of diet-induced obesity.
36 t and glucose homeostasis in mouse models of diet-induced obesity.
37  show that Dexras1 mediates adipogenesis and diet-induced obesity.
38 CHR1 are lean, hyperactive, and resistant to diet-induced obesity.
39 ed exercise tolerance and protection against diet-induced obesity.
40  inflammation in adipose tissue and prevents diet-induced obesity.
41 ntimal hyperplasia, which was exacerbated by diet-induced obesity.
42 ding a high-fat/high-sucrose diet, mimicking diet-induced obesity.
43 al temperature homeostasis and resistance to diet-induced obesity.
44  from pH1N1 infection using a mouse model of diet-induced obesity.
45 rvention protects offspring against high-fat diet-induced obesity.
46 high lipid content, and did not protect from diet-induced obesity.
47 rogenesis despite similar fat accretion with diet-induced obesity.
48 liver disease (NAFLD) and in mouse models of diet-induced obesity.
49 that lack functional SFRP5 were resistant to diet-induced obesity.
50 ro, in fasted mice, and in mice subjected to diet-induced obesity.
51 al white adipose tissue (WAT) in response to diet-induced obesity.
52 a marked increase in their susceptibility to diet-induced obesity.
53  2 diabetes, and C57BL/6J mice with high-fat diet-induced obesity.
54 d insulin resistance despite protection from diet-induced obesity.
55 lin and leptin receptors in animal models of diet-induced obesity.
56 ic reticulum contacts in POMC neurons during diet-induced obesity.
57 ylcholinesterase (BChE), in a mouse model of diet-induced obesity.
58 s control pancreatic dysfunction in high-fat-diet-induced obesity.
59 f Bmal1 also worsens chronic inflammation in diet-induced obesity.
60  deletion exerts a protective effect against diet-induced obesity.
61 increased oxygen consumption during high-fat-diet-induced obesity.
62 ation of hepatic Dpp4 in young mice prone to diet-induced obesity.
63 nd appetitive motivation under conditions of diet-induced obesity.
64 tervention in dealing with the prevalence of diet-induced obesity.
65 is in the beta-cell compensatory response to diet-induced obesity.
66 tion prior to high calorie feeding prevented diet-induced obesity.
67  electrophysiological properties observed in diet-induced obesity.
68 des in adipocytes and protected animals from diet-induced obesity.
69 5(-/-) (double knock-out (DKO)) mice show HF diet-induced obesity, adipocyte hypertrophy, and present
70                                              Diet-induced obesity also affected the morphological pro
71               Thus, both food withdrawal and diet-induced obesity alter the sensitivity of vagal affe
72                                              Diet-induced obesity alters the biophysical, pharmacolog
73 he comorbidities of Pb exposure and high-fat diet-induced obesity amplify skeletal deficits independe
74  define whether activated calpains influence diet-induced obesity and adipose tissue macrophage accum
75 O) was sufficient to protect adult mice from diet-induced obesity and associated metabolic alteration
76 ctoside-binding lectin, accelerates high-fat diet-induced obesity and diabetes.
77 ve therapeutic potential in the treatment of diet-induced obesity and dyslipidemia.
78 R-378 and miR-378* are resistant to high-fat diet-induced obesity and exhibit enhanced mitochondrial
79 n this tissue are strongly protected against diet-induced obesity and exhibit increased energy expend
80                      We engaged the model of diet-induced obesity and found that expression of C5aR w
81 t KLF3-null mice are lean and protected from diet-induced obesity and glucose intolerance.
82         The knock-out mice were resistant to diet-induced obesity and had abnormal lipid metabolism i
83 issues were resistant to developing high-fat diet-induced obesity and had significantly reduced white
84 ally reducing dietary BCAAs rapidly reverses diet-induced obesity and improves glucoregulatory contro
85                Importantly, loading relieves diet-induced obesity and improves glucose tolerance.
86 tivation of Hh signaling suppresses high-fat-diet-induced obesity and improves whole-body glucose tol
87     However, in wild-type mice with high-fat-diet-induced obesity and in ob/ob mice, the marked downr
88                                 In addition, diet-induced obesity and insulin resistance are exacerba
89 nd adipose tissue mass and were resistant to diet-induced obesity and insulin resistance due to a com
90      NSG mice were completely protected from diet-induced obesity and insulin resistance with signifi
91 homeostasis in a preclinical murine model of diet-induced obesity and insulin resistance, making the
92 ound, lymphocytes, and cytokine signaling in diet-induced obesity and insulin resistance.
93 roved metabolic profiles and protection from diet-induced obesity and insulin resistance.
94 for 15 weeks, after which the mice exhibited diet-induced obesity and insulin resistance.
95      Mice lacking PEMT are protected against diet-induced obesity and insulin resistance.
96 e tissue browning, and protects mice against diet-induced obesity and insulin resistance.
97                     ACF was found to prevent diet-induced obesity and insulin resistance.
98 ncreased in the skeletal muscle of mice with diet-induced obesity and insulin resistance.
99 ial fatty acid oxidation, thereby preventing diet-induced obesity and insulin resistance.
100 ion of Tst in adipocytes protected mice from diet-induced obesity and insulin-resistant diabetes.
101 teries is an early event that coincides with diet-induced obesity and IR in primates.
102 e deficient for Akt1 exhibit protection from diet-induced obesity and its associated insulin resistan
103 epresents a promising approach to ameliorate diet-induced obesity and leptin resistance.
104 y regulated in white and brown fat depots of diet-induced obesity and leptin-deficient ob/ob mouse mo
105 geted activation of Hh signaling ameliorates diet-induced obesity and may be explored for pharmaceuti
106 endothelial dysfunction, occurs early during diet-induced obesity and may serve as a mediator of athe
107 crobial community structure can protect from diet-induced obesity and metabolic disease.
108  potential therapeutic targets for combating diet-induced obesity and metabolic disease.
109 dy suggests that blocking of CB1 ameliorates Diet-Induced Obesity and metabolic disorder by modulatin
110 KKbeta-deficient mice were also resistant to diet-induced obesity and metabolic disorders.
111 egulated microbiota protect BALB/c mice from diet-induced obesity and metabolic dysfunction.
112 Finally, moderate alcohol prevented high-fat diet-induced obesity and metabolic dysfunction.
113 the discovery of new molecular therapies for diet-induced obesity and metabolic syndrome.
114 ockout of Maf1 in mice confers resistance to diet-induced obesity and nonalcoholic fatty liver diseas
115          Egr-1 null mice were protected from diet-induced obesity and obesity-associated pathologies
116 ing a foothold in the pathways that regulate diet-induced obesity and offering the potential for ther
117  lacking hepatic ZFP36L1 were protected from diet-induced obesity and steatosis.
118            HFD-fed TG mice rapidly developed diet-induced obesity and systemic insulin resistance, bu
119 DZ-RhoGEF-deficient mice were protected from diet-induced obesity and T2D.
120  results of VSG surgery applied to mice with diet-induced obesity and targeted genetic disruption of
121 ver, the transgenic mice were protected from diet-induced obesity and type 2 diabetes.
122 Shp inactivation may be beneficial to combat diet-induced obesity and uncover that hepatic SHP is nec
123 a therapeutic target for insulin resistance, diet-induced obesity, and associated metabolic dysfuncti
124 proves insulin sensitivity, protects against diet-induced obesity, and elicits the browning of white
125 at they were protected from atherosclerosis, diet-induced obesity, and insulin resistance.
126 ic insulin resistance and hepatosteatosis in diet-induced obesity are associated with various metabol
127         Mice lacking LR11 are protected from diet-induced obesity associated with an increased browni
128 ong reduction of adiposity and resistance to diet-induced obesity, associated with overall better met
129  confers long-term metabolic protection from diet-induced obesity at the cost of moderate skin oxidat
130                                        Since diet-induced obesity attenuates the responsiveness of ga
131 effector protein SMAD3 are protected against diet-induced obesity because of browning of their white
132                                    Following diet-induced obesity, biochemical analysis of livers rev
133 ting) and excessive energy storage (high-fat diet-induced obesity) blunt the effect of leptin.
134 lin resistance and insulin resistance due to diet-induced obesity both depend on muscle TRIB3.
135                            The 16 week HF/HS diet induced obesity, but did not significantly affect t
136 ansfer in mice suppressed the development of diet-induced obesity, but did not affect pre-existing ad
137 om brain cells is known to protect mice from diet-induced obesity, but the effects on HCD-induced inf
138 ient mice have been shown to be resistant to diet-induced obesity, but the mechanism behind this rema
139  knockdown in WAT and liver protects against diet-induced obesity by augmenting cellular energy expen
140 mproves insulin sensitivity substantially in diet-induced obesity by both peripheral and central mech
141 sociated with obesity, we induced long-term, diet-induced obesity by challenging mice to high-fat die
142 -PAR2 signaling in adipocytes contributes to diet-induced obesity by decreasing metabolism and energy
143 ight a protective effect of NT-PGC-1alpha on diet-induced obesity by enhancing diet-induced thermogen
144 se tissue LPL improves glucose metabolism in diet-induced obesity by improving the adipose tissue phe
145 in proopiomelanocortin neurons and prevented diet-induced obesity by increasing WAT browning and ener
146 esults implicate a new class of compounds in diet-induced obesity-C18 epoxide and diol oxylipins.
147                                              Diet-induced obesity can induce low-level inflammation a
148 eered mice on different diets, we found that diet-induced obesity caused a loss of guanylin expressio
149                                              Diet-induced obesity causes chronic macrophage-driven in
150                                           In diet-induced obesity, cellular Ca(2+) handling propertie
151                                              Diet-induced obesity compromises the excitability and re
152                         We hypothesized that diet-induced obesity could lead to alterations of the NR
153                  In this study, we show that diet-induced obesity did not impact the maintenance of p
154 s to identify the pathologic consequences of diet induced obesity (DIO) on the lymphatic system.
155                           C57BL/6J mice with diet-induced obesity (DIO mice) displaying a cardiac phe
156       PDE10A-deficient mice are resistant to diet-induced obesity (DIO) and associated metabolic dist
157 ed metabolic abnormalities both in mice with diet-induced obesity (DIO) and in leptin-deficient (ob/o
158  Global deletion of Ip6k1 protects mice from diet-induced obesity (DIO) and insulin resistance, but t
159 dipose tissue (VAT), thereby contributing to diet-induced obesity (DIO) and insulin resistance.
160 genic enzymes and spare lipogenic enzymes in diet-induced obesity (DIO) are obscure.
161                           The development of diet-induced obesity (DIO) can potently alter multiple a
162 d that the increase in leptin levels seen in diet-induced obesity (DIO) drives an increase in BP in r
163                                              Diet-induced obesity (DIO) has been shown to alter the b
164 th regular chow, increased susceptibility to diet-induced obesity (DIO) in males but not in females,
165 meostasis centers of the hypothalamus during diet-induced obesity (DIO) in rodent models, but the cha
166 ought to establish whether the propensity to diet-induced obesity (DIO) is associated with addictive-
167 ic distribution, 17- to 18-week-old lean and diet-induced obesity (DIO) mice were studied.
168                                  In db/db or diet-induced obesity (DIO) mice, hepatic expression of A
169                                Here we use a diet-induced obesity (DIO) mouse model and compare metab
170 lates development of insulin resistance in a diet-induced obesity (DIO) mouse model by ameliorating l
171  reduces obesity and insulin resistance in a diet-induced obesity (DIO) mouse model.
172 HGA(273-301)) by investigating the effect of diet-induced obesity (DIO) on insulin sensitivity of the
173                               The effects of diet-induced obesity (DIO) on tau pathology remain unkno
174   Impaired adipogenic differentiation during diet-induced obesity (DIO) promotes adipocyte hypertroph
175 t received low perinatal n-6/n-3 ratios were diet-induced obesity (DIO) resistant and had a lower pos
176 und that withaferin-A treatment of mice with diet-induced obesity (DIO) resulted in a 20-25% reductio
177 hat STAT4(-/-)C57Bl6/J mice develop high-fat diet-induced obesity (DIO) similar to wild-type controls
178  laboratory demonstrated earlier that in the diet-induced obesity (DIO) state, the appetite-suppressi
179                                        Here, diet-induced obesity (DIO) studies in mice with genetic
180 oregulatory role of GIP in a murine model of diet-induced obesity (DIO) using the long-acting GIP ana
181 ever, when females were fed a high-fat diet, diet-induced obesity (DIO) wild-type (DIO-WT) mice were
182 essential for weight gain in mouse models of diet-induced obesity (DIO), but the pathways that cause
183 gh behavioural rhythmicity was maintained in diet-induced obesity (DIO), gene expression profiling re
184 othelial explants excised from mice modeling diet-induced obesity (DIO), in which they were fed a "We
185                                      Thus in diet-induced obesity (DIO), lack of GH action on the MPh
186 a cannabinoid receptor 1 (CB1) antagonist on Diet-Induced Obesity (DIO), specifically whether such a
187 in resistance in C57Bl6/J mice with high-fat diet-induced obesity (DIO), using JD5037, a peripherally
188  TNF receptor-associated factors (TRAFs), in diet-induced obesity (DIO).
189 H NPY mRNA expression is observed only after diet-induced obesity (DIO).
190 hyperphagic conditions such as lactation and diet-induced obesity (DIO).
191            We found that rats susceptible to diet-induced obesity displayed heightened conditioned ap
192                                 We show that diet-induced obesity does not impair NRG1 signalling in
193                                              Diet-induced obesity drove early production of interleuk
194 d muscle glucose metabolism and resistant to diet-induced obesity due to increased energy expenditure
195  deterioration of glucose homeostasis during diet-induced obesity, due to enhanced resistance to insu
196 dipose tissue development, but its effect on diet-induced obesity during postnatal life is not known.
197 PQQ, provided prenatally in a mouse model of diet-induced obesity during pregnancy, could protect obe
198  and suggest a novel mechanism through which diet-induced obesity during puberty imposes its long-las
199                             In primates with diet-induced obesity, endothelial inflammatory activatio
200 exercise on type II diabetes risk under a HF diet-induced obesity environment.
201  control region mice on a high fat diet with diet-induced obesity following single oral doses of 3 an
202 ascularization, including leptin deficiency, diet-induced obesity, genetic ablation of the secreted f
203      Whey protein has been indicated to curb diet-induced obesity, glucose intolerance and delay the
204 ke receptor 4 expression was observed in the diet-induced obesity HCC animal model.
205                               We developed a diet-induced obesity HCC mouse model and examined TnC ex
206 lays a protective role in the progression of diet-induced obesity, hepatosteatosis, and atheroscleros
207 wild-type and Itch(-/-) mice in a context of diet-induced obesity (high-fat diet [HFD]).
208 nhanced leptin signaling and protection from diet-induced obesity; however, whether additional signal
209 eficient mice are more resistant to high-fat diet-induced obesity, hyperleptinemia, and glucose intol
210   This study evaluates the role of cafeteria diet-induced obesity/hyperlipidemia (CAF) on alveolar bo
211                              In a context of diet-induced obesity, IL-21 KO mice, compared with WT an
212                                              Diet-induced obesity impaired AT1-ILC killing ability.
213 MH-specific inhibition of TBK-1 in mice with diet-induced obesity impaired glucose metabolism and AKT
214 nfirmed in both serum and liver of mice with diet-induced obesity, implying that such a metabolic alt
215 ggerated the detrimental effects of maternal diet-induced obesity in adipose tissue.
216                We investigated the effect of diet-induced obesity in C57BL6J mice upon rhythmic trans
217                                              Diet-induced obesity in mice demonstrated that IL-6 expr
218                            Here we show that diet-induced obesity in mice is associated with persiste
219        Pharmacological inhibition of CBR1 in diet-induced obesity in mice results in more marked gluc
220         To test the role of JNK, we examined diet-induced obesity in mice with targeted ablation of J
221 rotein produces a phenotype of resistance to diet-induced obesity in mice, we hypothesized that this
222 and deletion of theNrf2gene protects against diet-induced obesity in mice.
223 on of Id1 causes age-associated and high-fat diet-induced obesity in mice.
224 odulates traits of the metabolic syndrome in diet-induced obesity in mice.
225 mide N-methyltransferase (NNMT)-ASO prevents diet-induced obesity in mice.
226 AL) in a skeletal muscle model system and in diet-induced obesity in mice; however, potential functio
227 4 is a negative regulator of inflammation in diet-induced obesity, in part through regulation of macr
228                                     Maternal diet-induced obesity increased miR-126 expression howeve
229                                              Diet-induced obesity increased the expression of MHC II
230               In mice with a GSNOR deletion, diet-induced obesity increases lysosomal nitrosative str
231           According to our previous results, diet-induced obesity induces epigenetic modifications to
232 nvestigated the effects of Lcn2 depletion on diet-induced obesity, inflammation, and PDAC development
233 y, microbial and dietary factors incurred by diet-induced obesity influence underlying innate and ada
234      Here, we demonstrate that resistance to diet-induced obesity inNrf2(-/-)mice is associated with
235 w that intestinal PPARdelta protects against diet-induced obesity, insulin resistance and dyslipidemi
236 he fDsbA-L mice also displayed resistance to diet-induced obesity, insulin resistance, and hepatic st
237 tion, transgenic mice were protected against diet-induced obesity, insulin resistance, and inflammati
238                   Additionally, in mice with diet-induced obesity, INT-767 prevented mitochondrial dy
239                                     High-fat diet-induced obesity is a major risk factor for osteoart
240                                              Diet-induced obesity is associated with strong circadian
241                                              Diet-induced obesity leads to devastating and common chr
242    Previous studies have shown that maternal diet-induced obesity leads to increased risk of type 2 d
243 tion protected homozygous mice from high fat diet-induced obesity, likely by promoting enhanced energ
244    Moreover, there is emerging evidence that diet-induced obesity locks the phenotype of vagal affere
245                              During high fat diet-induced obesity, macrophages are activated by lipid
246 suggest that the memory-impairing effects of diet-induced obesity may potentially be mediated by neur
247                 We studied C57BL/6 mice with diet-induced obesity, MC4R-deficient mice, and mice that
248 our unique gut microbiota with resistance to diet-induced-obesity-mediated alteration of the gut micr
249 ce but increased over time in overweight and diet-induced obesity mice, suggesting CR obviates epigen
250                                    We used a diet-induced obesity model to show that Thy1-null mice g
251 e metabonomics data and microbiome data in a diet-induced obesity model using C57BL/6 mice.
252                                      Using a diet-induced obesity model, we show that TLR3-deficient
253                                              Diet-induced obesity modulates the excitability and resp
254 ose at 30 mg/kg in a streptozotocin-treated, diet-induced obesity mouse pharmacodynamic assay and blu
255 recapitulates the leanness and resistance to diet-induced obesity of RIIbeta KO mice.
256 f increased susceptibility to the effects of diet-induced obesity on amygdala function.
257 nockout (ob/ob) obese mice, and in mice with diet-induced obesity, orexinergic neurons receive predom
258 tatively contributing to protection from the diet-induced obesity phenotype.
259 y robust to alter the effects of fibrates on diet-induced obesity phenotypes.
260 e long-term impact of transient peripubertal diet-induced obesity (ppDIO, induced between 4 and 10 we
261 oreover, betaine administration to mice with diet-induced obesity prevents the development of impaire
262  by increased intestinal permeability during diet-induced obesity promotes insulin resistance in mice
263                    Male Long-Evans rats with diet-induced obesity received AGB implantation or sham s
264 iated downregulation of miR-34a in mice with diet-induced obesity reduced adiposity, improved serum p
265 zed to receive a CR, overweight-inducing, or diet-induced obesity regimen (n = 27/group).
266               Relative to the overweight and diet-induced obesity regimens, CR decreased body weight,
267    TTR-ASO treatment of mice with genetic or diet-induced obesity resulted in an 80-95% decrease in c
268 lantation of subcutaneous fat into mice with diet-induced obesity showed a loss of metabolic benefit
269 ific Fxr-null (Fxr(DeltaIE)) mice show lower diet-induced obesity, similar to tempol-treated wild-typ
270    In a rat model of breast cancer driven by diet-induced obesity, STAT3 blockade suppressed the CSC-
271 ficient (Mfge8(-/-)) mice are protected from diet-induced obesity, steatohepatitis and insulin resist
272          Moreover, this function of SphK1 in diet-induced obesity suggests a potential role for SphK1
273                 Recent studies revealed that diet-induced obesity suppressed guanylin and uroguanylin
274                 Our study indicates that, in diet-induced obesity, these circadian fluctuations in ga
275            We used a mouse model of maternal-diet induced obesity to define predictive correlations b
276 l of individual susceptibility to junk-foods diet-induced obesity to determine whether there are pre-
277  the current study, we used a mouse model of diet-induced obesity to identify putative cellular mecha
278 use models of a regular diet and of high-fat-diet-induced obesity to investigate the role of dietary
279                                     Maternal diet-induced obesity, together with androgen excess, aff
280                                In a model of diet-induced obesity, Tregs from the visceral adipose ti
281 ssels as a basis for vascular dysfunction in diet-induced obesity via a mechanism involving type 2 pr
282                     The effect of adjunctive diet-induced obesity was defined.
283                         Here, a rat model of diet-induced obesity was used to explore changes in brai
284                Here, using a murine model of diet-induced obesity, we determined that obesity causes
285 he consequences of hepatic BIM deficiency in diet-induced obesity, we generated liver-specific BIM-kn
286                          In a mouse model of diet-induced obesity, we show that adipose tissue macrop
287  and the metabolic complications of high fat diet-induced obesity were dependent on C1q.
288 ceptor 4 mutant mice (C3H/HeJ) with high-fat-diet-induced obesity were not protected against insulin
289  mice have increased food intake and greater diet-induced obesity when fed high-fat diet.
290 ptive response is the complete resistance to diet-induced obesity when POLG mice are placed on a high
291                                     In mice, diet-induced obesity, which decreases insulin sensitivit
292 ssions in the mutant pedigrees and mice with diet-induced obesity, which showed that each obesity mou
293 er show that loss of Sln predisposes mice to diet-induced obesity, which suggests that Sln-mediated N
294 pha in the MeA partially prevented mice from diet-induced obesity, while chemogenetic activation of S
295 ator (SRA) (SRAKO) are resistant to high fat diet-induced obesity with a phenotype that includes impr
296 Our findings suggest that the combination of diet-induced obesity with other risk factors may increas
297 ale mice results in protection from high fat diet-induced obesity, with a preferential loss of s.c. f
298      SRA(-/-) mice are resistant to high fat diet-induced obesity, with decreased fat mass and increa
299 duces WAT lipolysis in vivo but also reduces diet-induced obesity without affecting LPL activity.
300 ote tumorigenesis, we examined the effect of diet-induced obesity, without ongoing high fat diet, on

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