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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
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
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
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
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
89 nd adipose tissue mass and were resistant to diet-induced obesity and insulin resistance due to a com
91 homeostasis in a preclinical murine model of diet-induced obesity and insulin resistance, making the
100 ion of Tst in adipocytes protected mice from diet-induced obesity and insulin-resistant diabetes.
102 e deficient for Akt1 exhibit protection from diet-induced obesity and its associated insulin resistan
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
109 dy suggests that blocking of CB1 ameliorates Diet-Induced Obesity and metabolic disorder by modulatin
114 ockout of Maf1 in mice confers resistance to diet-induced obesity and nonalcoholic fatty liver diseas
116 ing a foothold in the pathways that regulate diet-induced obesity and offering the potential for ther
120 results of VSG surgery applied to mice with diet-induced obesity and targeted genetic disruption of
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
126 ic insulin resistance and hepatosteatosis in diet-induced obesity are associated with various metabol
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
131 effector protein SMAD3 are protected against diet-induced obesity because of browning of their white
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.
148 eered mice on different diets, we found that diet-induced obesity caused a loss of guanylin expressio
154 s to identify the pathologic consequences of diet induced obesity (DIO) on the lymphatic system.
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
162 d that the increase in leptin levels seen in diet-induced obesity (DIO) drives an increase in BP in r
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-
170 lates development of insulin resistance in a diet-induced obesity (DIO) mouse model by ameliorating l
172 HGA(273-301)) by investigating the effect of diet-induced obesity (DIO) on insulin sensitivity of the
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
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
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
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
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
206 lays a protective role in the progression of diet-induced obesity, hepatosteatosis, and atheroscleros
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
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
221 rotein produces a phenotype of resistance to diet-induced obesity in mice, we hypothesized that this
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
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
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
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
246 suggest that the memory-impairing effects of diet-induced obesity may potentially be mediated by neur
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
254 ose at 30 mg/kg in a streptozotocin-treated, diet-induced obesity mouse pharmacodynamic assay and blu
257 nockout (ob/ob) obese mice, and in mice with diet-induced obesity, orexinergic neurons receive predom
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
264 iated downregulation of miR-34a in mice with diet-induced obesity reduced adiposity, improved serum p
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
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
281 ssels as a basis for vascular dysfunction in diet-induced obesity via a mechanism involving type 2 pr
285 he consequences of hepatic BIM deficiency in diet-induced obesity, we generated liver-specific BIM-kn
288 ceptor 4 mutant mice (C3H/HeJ) with high-fat-diet-induced obesity were not protected against insulin
290 ptive response is the complete resistance to diet-induced obesity when POLG mice are placed on a high
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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