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1 lowest rate of isolated T2DM (without HTN or obesity).
2  utility of targeting oxytocin signalling in obesity.
3 e gastrointestinal signals in order to treat obesity.
4 tential pharmacotherapy for the treatment of obesity.
5 the identification of novel targets to treat obesity.
6  cholesterol, blood pressure, and overweight/obesity.
7 function, which may contribute to sarcopenic obesity.
8 eening children with high risk of developing obesity.
9 ity as a cost of longer lifetime exposure to obesity.
10 risk for chronic disease including childhood obesity.
11 ion contributes to the metabolic sequelae of obesity.
12 reatment of obesity, in patients with severe obesity.
13  food reward behavior, ultimately leading to obesity.
14 ry is a promising candidate for treatment of obesity.
15 ions for the pathological metabolic state of obesity.
16 e higher, given the increasing prevalence of obesity.
17 e gut dysbiosis and inflammation produced by obesity.
18 tic Dpp4 in young mice prone to diet-induced obesity.
19 st strongly and reproducibly associated with obesity.
20 of testosterone in men with hypogonadism and obesity.
21 rinary arsenic concentration and measures of obesity.
22 everses mitochondrial elongation and reduces obesity.
23  to therapeutic intervention in diabetes and obesity.
24 o the development of new therapies to combat obesity.
25 licated to play a role in the development of obesity.
26 ermogenesis, and renders mice susceptible to obesity.
27 ological properties observed in diet-induced obesity.
28 ivery and training initiatives for childhood obesity.
29 ence energy balance to prevent or even treat obesity.
30 1 (95% CI, 44.8-78.9) for women with class 3 obesity.
31 icated in joint susceptibility to asthma and obesity.
32 ocyanidins as putative targets to ameliorate obesity.
33  PAM as a promising therapeutic approach for obesity.
34  compatible with the food addiction model of obesity.
35 d improved insulin kinetics in children with obesity.
36 nd biological or behavioural determinants of obesity.
37 the USA, but have a more minor effect on the obesity.
38 evels of which were dramatically elevated in obesity.
39 iological features of insulin resistance and obesity.
40 c fibrosis in patients with severe to morbid obesity.
41 t activities, which is approved for treating obesity.
42 alamus may contribute to the pathogenesis of obesity.
43  in the PVN increases food intake and causes obesity.
44  expression of the latter was upregulated in obesity.
45 ebiotics or other agents to prevent or treat obesity.
46 s modulators of atrial fibrillation risk and obesity.
47 day is associated with poor diet quality and obesity.
48 , ZFR2 and ZNF169) newly implicated in human obesity, 2 variants were in genes (MC4R and KSR2) previo
49 years for high alcohol intake, 0.7 years for obesity, 3.9 years for diabetes, 1.6 years for hypertens
50 erweight (25.0-29.9 kg/m(2)), class I (mild) obesity (30.0-34.9 kg/m(2)), and class II and III (sever
51 9 (95% CI, 15.7-34.6) for women with class 1 obesity, 35.8 (95% CI, 23.1-49.5) for women with class 2
52                                 We show that obesity alters the composition of the HSC compartment an
53 e trends in the prevalence of overweight and obesity among children and adults between 1980 and 2015.
54  global rise in the prevalence of adolescent obesity, an unprecedented phenomenon of type 2 diabetes
55 previously observed to be mutated in extreme obesity and 2 variants were in GIPR.
56                      We now demonstrate that obesity and aging precipitate alterations of TRIM28-depe
57 0 years, studies have mechanistically linked obesity and an obese tumor microenvironment with signali
58 activity may be a potential strategy against obesity and associated comorbidities.
59 iniphila to mice prevents the development of obesity and associated complications.
60                                              Obesity and asthma often coexist.
61                                         Both obesity and atrial fibrillation (AF) are increasing in e
62 ted monocyte genes in childhood obesity with obesity and complexity of coronary atherosclerosis (SYNT
63                                              Obesity and diabetes are associated with increased chron
64 tween these neighborhood characteristics and obesity and diabetes diagnoses (Type 1 and Type 2).
65 ntervention could combat the transmission of obesity and diabetes to subsequent generations.
66                  Comorbidities, specifically obesity and diabetes, are previously unidentified risk f
67  promising target for vascular prevention in obesity and diabetes.
68 nificant increase in the association between obesity and disability from 1988 to 2004, calling attent
69 e trend of an increasing association between obesity and disability has leveled off in more recent ye
70           With continued high rates of adult obesity and DM along with an aging population, NAFLD-rel
71 s to reduce the global epidemic of childhood obesity and encourage mechanistic studies.
72  balance and adiposity, have been related to obesity and glucose metabolism.
73 esistant to developing high-fat diet-induced obesity and had significantly reduced white adipose tiss
74  plasma shows a positive correlation between obesity and hepatic C18 oxylipin metabolites of omega-6
75 abolic consequences, including overweight or obesity and high blood pressure.
76 roved family-centered outcomes for childhood obesity and improvements in child BMI.
77                              Diets promoting obesity and insulin resistance can lead to severe metabo
78 e leaner and resistant to hepatic steatosis, obesity and insulin resistance under a lipogenic diet.
79 g7(h&mKO) mice were better protected against obesity and insulin resistance with increased circulatin
80 of substrate oxidation in the development of obesity and insulin resistance.
81 hly translatable option for the treatment of obesity and insulin resistance.
82 nistic connections between hyperinsulinemia, obesity and insulin resistance.
83 lkB dioxygenase family and is linked to both obesity and intellectual disability.
84                               Traditionally, obesity and its correlate, insulin resistance, have been
85  However, the associations of post-diagnosis obesity and late outcomes (>/=5 years after diagnosis) h
86 romising approach to ameliorate diet-induced obesity and leptin resistance.
87  a package of high-quality clinical care for obesity and linkages to community resources resulted in
88 al effects in protecting against HFD-induced obesity and metabolic disorders.
89  is known to ameliorate menopause-associated obesity and metabolic dysfunction for reasons that are u
90 hnological and methodological limitations in obesity and microbiome research have made it difficult t
91 ponse to a positive energy balance underlies obesity and occurs through both hypertrophy of existing
92 its and harms of screening and treatment for obesity and overweight in children and adolescents to in
93 ly to be relevant to the association between obesity and reflux disease.
94                                              Obesity and type 2 diabetes are significant risk factors
95 portant feature of chronic disorders such as obesity and type 2 diabetes.
96  therapeutic importance for the treatment of obesity and type-2 diabetes.
97                                              Obesity and underweight BMI were associated with increas
98 8 (95% CI, 23.1-49.5) for women with class 2 obesity, and 61.1 (95% CI, 44.8-78.9) for women with cla
99  association of TV watching with the risk of obesity, and an inverse association of either indoor act
100  insulin and HDL cholesterol concentrations, obesity, and coronary atherosclerosis.
101 e performance of HealthLNK for hypertension, obesity, and diabetes mellitus diagnosis by using Intern
102   The prevalence of general obesity, central obesity, and hypertension among the children was 11.1%,
103            Ascites, liver disease, diabetes, obesity, and primary suture repair without mesh are asso
104 ine into ornithine and urea, is induced upon obesity, and silencing or loss of ARG2 markedly suppress
105 that arsenic exposure is not associated with obesity, and that urinary creatinine and osmolality may
106 phageal reflux disease, Barrett's esophagus, obesity, and tobacco smoking.
107            Loss of Cadm1 protected mice from obesity, and tract-tracing analysis revealed Cadm1-posit
108  consequences of excess alcohol consumption, obesity, and viral hepatitis.
109 ue to increased muscular protein catabolism, obesity, and/or increased insulin resistance (IR) or imp
110                      Maternal overweight and obesity are associated with increased risks of preterm d
111               Both anorexia nervosa (AN) and obesity are complicated by affective comorbidities and h
112                                Psoriasis and obesity are strongly linked, and weight loss appears to
113 y liver disease (NAFLD) is closely linked to obesity, around 10%-20% of nonobese Americans and Asians
114  the causal pathway from arsenic exposure to obesity, as common descendants of hydration and body com
115 ed by body mass index, and that of abdominal obesity, as measured by waist-to-hip ratio, have distinc
116 he disclosure of information on fat-mass and obesity-associated (FTO) genotype risk had a greater eff
117 y syndrome may be protective with respect to obesity-associated cardiovascular disease.
118                                 Fat mass and obesity-associated gene (FTO) is a member of the Fe (II)
119 c enzyme ARG1 opens a therapeutic window for obesity-associated pancreatic cancer.Obesity is an estab
120 acterized RNA demethylase, FTO (fat mass and obesity-associated) in memory.
121 8 months and the prevalence of overweight or obesity at 24 months.
122 5% CI: 0.02, 0.15) and risk of overweight or obesity at age 7 y [adjusted RR (aRR) comparing the high
123  a >2-fold increase in the risk of offspring obesity at ages 6-11 y (adjusted RR: 2.39; 95% CI: 1.97,
124 ntial reciprocal links between appraisal and obesity, based on the well-documented evidence that obes
125 nce considered a problem of Western nations, obesity (body mass index >/=30 kg/m(2)) has rapidly incr
126 ing much time sitting have increased risk of obesity but the mechanism for the antiobesity effect of
127 l tubule cells did not protect the mice from obesity, but markedly attenuated the obesity-induced lip
128 on models from evolutionary ecology to human obesity by assessing the role of information.
129 in sensitivity substantially in diet-induced obesity by both peripheral and central mechanisms.
130 , based on the well-documented evidence that obesity can cause cognitive deficits.
131 utrient poor and increase risk of developing obesity, cardiovascular disease, hypertension, obesity-r
132 for the contrasts in mortality rates between obesity categories.
133                                              Obesity causes insulin resistance, and PPARgamma ligands
134                    The prevalence of general obesity, central obesity, and hypertension among the chi
135 ated with PCOS only among women with central obesity (chi(2) = 35.0, p < 0.001) and not for the norma
136           Further studies targeting specific obesity classes within preschool-aged children are warra
137                                        Donor obesity, defined as donor body mass index (D-BMI) of 30
138 larly, children at a higher genetic risk for obesity demonstrated larger NAcc volumes.
139 ly events that contribute to weight gain and obesity development.
140 actors include sedentary lifestyle, smoking, obesity, diabetes mellitus, obstructive sleep apnea, and
141 n be a barrier to greater acceptance of anti-obesity drugs as appropriate options for treatment.
142 try were at 51% increased risk of developing obesity during childhood and adolescence compared with c
143 uctive sleep apnoea, vocal cord dysfunction, obesity, dysfunctional breathing and anxiety/depression.
144  and the intestinal microflora in the rising obesity epidemic.
145 on projections from 2016 to 2030 to forecast obesity estimates and NASH-related LT waitlist additions
146 ilure is higher in patients with diabetes or obesity, even with optimal medical treatment, and the in
147                                           In obesity fasting levels of both glucagon and insulin are
148 ion of population disability attributable to obesity followed a similar trend.
149 iome research as it relates to understanding obesity from the perspective of both communities, outlin
150 f a validated genetic profile risk score for obesity (GPRS-obesity) with body mass index (BMI) and wa
151 34.9 kg/m(2)), and class II and III (severe) obesity (&gt;/=35.0 kg/m(2)).
152                                              Obesity had a strong independent association with RTT (O
153                                              Obesity has adverse effects on cardiovascular hemodynami
154                                              Obesity has been increasing worldwide.
155                                     Although obesity has risen steeply in Australia, some evidence su
156 al and genetic determinants or correlates of obesity have been identified to date.
157 sues to orthodontic force in the presence of obesity have potential short- and long-term clinical imp
158  intake is protective against overweight and obesity; however, results of intervention studies have b
159 ealth burden in the United States, including obesity, hypertension, type 2 diabetes mellitus, and car
160 nhibition of TBK-1 in mice with diet-induced obesity impaired glucose metabolism and AKT activation.
161                                              Obesity impairs the relaxant capacity of adipose tissue
162 plementation in children with overweight and obesity improved subjective appetite ratings.
163 ygous Gsalpha-inactivating mutations lead to obesity in Albright hereditary osteodystrophy (AHO) pati
164 USPSTF recommends that clinicians screen for obesity in children and adolescents 6 years and older an
165 jection paradigm reduced high-fat intake and obesity in diet-induced obese (DIO) mice.
166 eproduces olanzapine-induced hyperphagia and obesity in female C57BL/6 mice.
167 ill help in understanding the development of obesity in females.
168 total effect model showed those with general obesity in the cohort period presented higher risk of un
169                                Prevention of obesity in women of reproductive age is widely recognise
170  endovascular procedure for the treatment of obesity, in patients with severe obesity.
171 o assess associations of asthma history with obesity incidence during follow-up.
172                        Maternal diet-induced obesity increased miR-126 expression however levels of t
173                                              Obesity increases risk for liver toxicity by the anti-le
174                                              Obesity increases the risk of clinical decompensation in
175 propose hepatic PTPR-gamma as a link between obesity-induced inflammation and insulin resistance and
176 enetic ligand for endothelial FcgammaRIIB in obesity-induced insulin resistance.
177 ce from obesity, but markedly attenuated the obesity-induced lipid accumulation in the kidney and ren
178  broad range of health indicators, including obesity, injury, and psychopathology.
179 mmation is a central pathologic component of obesity, insulin resistance, type 2 diabetes and associa
180 hronic low-grade inflammation, a hallmark of obesity, involves immune cell infiltration into expandin
181                                              Obesity is a heritable trait that contributes to substan
182                                              Obesity is a multifactorial condition influenced by gene
183 s that the reduced adipose glucose uptake in obesity is a physiological down-regulation to prevent ex
184                                              Obesity is a serious and growing worldwide health challe
185 dow for obesity-associated pancreatic cancer.Obesity is an established risk factor for pancreatic duc
186                                              Obesity is an important public health priority in the Un
187                                              Obesity is associated with hypothalamic inflammation (HI
188 for the treatment of adolescents with severe obesity is becoming more common, but data on cost-effect
189 ological overeating underlying some forms of obesity is compulsive in nature and therefore contains e
190                                              Obesity is linked to alterations in the functional conne
191                                              Obesity is repeatedly emphasized as a risk factor for at
192 trointestinal and hepatic diseases for which obesity is the direct cause (eg, nonalcoholic fatty live
193 r prevalence of metabolic disorders, such as obesity, is currently of great societal concern.
194  increased effectiveness of MC4R agonists in obesity may be an unexpected outcome of neuronal injury
195       Therefore, brain insulin resistance in obesity may have unfavorable consequences for whole-body
196 that altered myocellular lipid metabolism in obesity may lead to increased insulin resistance (IR) th
197  between major depressive disorder (MDD) and obesity may stem from shared immunometabolic mechanisms
198 ential alternatives, currently approved anti-obesity medications and best practices to individualize
199 ked to severe metabolic disorders, including obesity, metabolic syndrome, lipodystrophy, and cachexia
200 b genes which likely play important roles in obesity metabolism and identified microRNAs that signifi
201 enges, and suggest directions to advance the obesity-microbiome field as a whole, with particular emp
202 tokine secretion and/or Ab production across obesity models.
203 o a variety of diseases, including diabetes, obesity, neurodegenerative disorders, aging, and cancer,
204      Patients with anorexia nervosa (AN) and obesity (OB) were investigated in reference to normal we
205 ted with patient-level factors that included obesity, obstructive sleep apnea, higher comorbidity, an
206 l studies support causal effects of maternal obesity on offspring outcomes, which are mediated at lea
207 ohort study was to investigate the effect of obesity on orthodontic tooth movement.
208 vel approaches for offsetting the effects of obesity on prostate cancer progression.
209 ption) combined with diet-induced overweight/obesity on the risk of periodontitis.
210           In studies of urinary analytes and obesity or obesity-related outcomes, controlling for cre
211 ne and proline significantly associated with obesity (OR = 1.57; 95%CI 1.45-1.69, P = 3.84 x 10(-31))
212 ied (OR = 1.57, 95%CI = 1.04, 2.36), general obesity (OR = 1.77, 95%CI = 1.11, 2.81), central obesity
213               In the adjusted model, central obesity (OR = 1.88, 95%CI = 1.18, 3.01) and consumption
214 ity (OR = 1.77, 95%CI = 1.11, 2.81), central obesity (OR = 2.09, 95%CI = 1.46,3.01) and consumption o
215 idence interval [CI]: 3.69-9.55) and central obesity (OR = 3.45, 95% CI: 2.27-5.23) were strongly ass
216                                      General obesity (OR = 5.94, 95% confidence interval [CI]: 3.69-9
217 g" pattern was associated with overweight or obesity (OR: 1.57; 95% CI: 1.15, 2.13) and central overw
218 5% CI: 1.15, 2.13) and central overweight or obesity (OR: 1.73; 95% CI: 1.19, 2.50).
219 984-1.000 per pack-year) and positively with obesity: OR: 1.97 [1.22-3.16], history of atopic disease
220       The food addiction model proposes that obesity overlaps with addiction in terms of neurobiologi
221   Under insulin-resistant conditions such as obesity, pancreatic beta-cells proliferate to prevent bl
222                           The current global obesity pandemic is clearly linked to both the increasin
223           We sought to determine whether the obesity paradox observed in cardiac surgery is attributa
224 e pulmonary disease, hypertension, diabetes, obesity, percent of population 65 years of age and older
225  FTO gene variants have been associated with obesity phenotypes in sedentary and obese populations, b
226                     T2DM arises largely from obesity, poor diet, and lack of exercise, but it also in
227 s are both associated with increased risk of obesity, potentially attributed to a reduced serotonin t
228                                The effect on obesity prevalence corrected for poverty, race education
229 was much lower and hence the ratio of T2D to obesity prevalence was significantly associated with PM2
230 lopment of microbiome-targeted therapies for obesity prevention and treatment.
231 tic review, we expand on previous reviews of obesity prevention interventions by including recent stu
232 th implications for health-care delivery and obesity prevention strategies.
233 ctive of weight gain to inform the design of obesity-preventive programs in adolescents.
234                                     Maternal obesity programmed increased adiposity and liver triglyc
235                    In this respect, although obesity promotes hyperlipidemia and hypothalamic injury,
236  One hypothesis is that increasing childhood obesity rates may explain part of this increase, but, as
237 cioeconomic status, obstetric complications, obesity, recent interpersonal violence, pre- and early p
238  Relative to the overweight and diet-induced obesity regimens, CR decreased body weight, adiposity, a
239 es have addressed causes and consequences of obesity-related adipose tissue hypertrophy and hyperplas
240 esity, cardiovascular disease, hypertension, obesity-related cancers, and dental caries.
241           These findings may shed light onto obesity-related cardiac remodeling and heart failure.
242      Insulin resistance is a key mediator of obesity-related cardiometabolic disease, yet the mechani
243 ays a significant role in the development of obesity-related complications, but the molecular events
244                                              Obesity-related conditions including heart disease, stro
245 oints included short-term weight loss, serum obesity-related hormone levels, hunger and satiety asses
246  (PVAT) and has been implicated in resultant obesity-related hypertension and impaired glucose intole
247 e to impaired adipogenic differentiation and obesity-related metabolic disease.
248  in studies on the role of gut microbiota in obesity-related mood disorders.
249  loss control groups and in individuals with obesity-related morbidities.
250 n studies of urinary analytes and obesity or obesity-related outcomes, controlling for creatinine cou
251 weight or obese mothers was not explained by obesity-related pregnancy or neonatal complications.
252                                              Obesity-related sub-acute chronic inflammation has been
253 d advice provides extra benefits in reducing obesity-related traits compared with the benefits of con
254  risk had a greater effect on a reduction of obesity-related traits in risk carriers than in nonrisk
255 ide polymorphisms (SNPs) possibly acting via obesity-related traits, hsCRP, based on 16 SNPs from gen
256 ir contribution to metabolic inflammation in obesity remain to be fully elucidated.
257        The tendency to hold the patient with obesity responsible for their condition can be a barrier
258                                              Obesity results from increased energy intake or defects
259 hma rescue medication use appeared to reduce obesity risk independent of physical activity.
260 ing (EOE) has been associated with increased obesity risk, while emotional undereating (EUE) may be p
261 sition in early life, a known contributor to obesity risk.
262  to improve energy self-regulation and lower obesity risk.
263 lin signaling cascade, insulin resistance in obesity seems to be largely elicited downstream of these
264         The incidence of 3 CVD risk factors (obesity, sleep complaints, and depression) was predicted
265  disease, C-reactive protein, HbA1c, height, obesity, smoking status, triglycerides, type 2 diabetes,
266 ors in promoting oxidative stress: diabetes, obesity, smoking, and excessive pollution.
267 ular risk factors were measured at baseline (obesity, smoking, diabetes, prehypertension, hypertensio
268 n-Y gastric bypass, in the Adolescent Morbid Obesity Surgery (AMOS) study.
269 ericans, and are candidates to contribute to obesity susceptibility in humans.
270  Thus, it has been assumed that melanocortin obesity syndrome may be protective with respect to obesi
271 nhibitory mechanism of beige adipogenesis in obesity that required direct adhesive interactions betwe
272         Given the current level of childhood obesity, the models predicted that a majority of today's
273     In societies characterized by widespread obesity, the sensitivity of reproduction to metabolic im
274                        Most satiety-inducing obesity therapeutics, despite modest efficacy, have safe
275 r in question being dismissed as a potential obesity therapy.
276  Although psoriasis has been associated with obesity, there are few prospective studies with objectiv
277 s a novel metabolic/immune regulator linking obesity to adipose tissue inflammation and insulin resis
278  used a mouse model of maternal-diet induced obesity to define predictive correlations between matern
279 to the pesticide DDT and its metabolites and obesity to develop hazard identification conclusions.
280 tabolic disease, spanning conditions such as obesity to type 2 diabetes mellitus with excess cardiova
281 lic disorders and it tightly associates with obesity, type 2 diabetes, and cardiovascular disease.
282                                              Obesity typically is linked to caloric imbalance as a re
283 onocyte gene expression profile in childhood obesity using an Illumina microarray platform on sorted
284                                   Overweight/obesity was associated with earlier FPM emergence, parti
285                                       Severe obesity was defined as a body-mass index (BMI, the weigh
286                                              Obesity was strongly associated with severe malaria, bot
287 and the rising rates of pediatric overweight/obesity, we sought to examine the association of body ma
288 and extramyocellular lipid (EMCL) content in obesity, we utilized a new four-dimensional multi echo e
289 0-F3 patients with mild, moderate, or severe obesity were $48,836/QALY, $24,949/QALY, and $19,222/QAL
290 ant risk for developing metabolic disease in obesity whereas preferential expansion of subcutaneous w
291                The association of overweight/obesity with disease progression in patients with autoso
292 examined associations of general and central obesity with hypertension, and between body mass index (
293 tially regulated monocyte genes in childhood obesity with obesity and complexity of coronary atherosc
294 suggest that the combination of diet-induced obesity with other risk factors may increase the risk of
295               We examined the association of obesity with residential density in a large and diverse
296 genetic profile risk score for obesity (GPRS-obesity) with body mass index (BMI) and waist circumfere
297 ibiotic use in infancy and risk of childhood obesity, with implications for health-care delivery and
298 with increasingly elevated ORs for unhealthy obesity, with individuals in quartile 4 having an OR of
299 ciation of select claudins, modulated by the obesity, with signaling and metabolic pathways of pathol
300 ronment might be amplifying genetic risk for obesity, yet those at highest risk could mitigate this r

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