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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
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
57 0 years, studies have mechanistically linked obesity and an obese tumor microenvironment with signali
62 ted monocyte genes in childhood obesity with obesity and complexity of coronary atherosclerosis (SYNT
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
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
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
85 However, the associations of post-diagnosis obesity and late outcomes (>/=5 years after diagnosis) h
87 a package of high-quality clinical care for obesity and linkages to community resources resulted in
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
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
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%,
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
109 ue to increased muscular protein catabolism, obesity, and/or increased insulin resistance (IR) or imp
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
119 c enzyme ARG1 opens a therapeutic window for obesity-associated pancreatic cancer.Obesity is an estab
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
131 utrient poor and increase risk of developing obesity, cardiovascular disease, hypertension, obesity-r
135 ated with PCOS only among women with central obesity (chi(2) = 35.0, p < 0.001) and not for the norma
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.
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
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
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.
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
168 total effect model showed those with general obesity in the cohort period presented higher risk of un
175 propose hepatic PTPR-gamma as a link between obesity-induced inflammation and insulin resistance and
177 ce from obesity, but markedly attenuated the obesity-induced lipid accumulation in the kidney and ren
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
183 s that the reduced adipose glucose uptake in obesity is a physiological down-regulation to prevent ex
185 dow for obesity-associated pancreatic cancer.Obesity is an established risk factor for pancreatic duc
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
192 trointestinal and hepatic diseases for which obesity is the direct cause (eg, nonalcoholic fatty live
194 increased effectiveness of MC4R agonists in obesity may be an unexpected outcome of neuronal injury
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
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
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
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
217 g" pattern was associated with overweight or obesity (OR: 1.57; 95% CI: 1.15, 2.13) and central overw
219 984-1.000 per pack-year) and positively with obesity: OR: 1.97 [1.22-3.16], history of atopic disease
221 Under insulin-resistant conditions such as obesity, pancreatic beta-cells proliferate to prevent bl
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
227 s are both associated with increased risk of obesity, potentially attributed to a reduced serotonin t
229 was much lower and hence the ratio of T2D to obesity prevalence was significantly associated with PM2
231 tic review, we expand on previous reviews of obesity prevention interventions by including recent stu
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
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
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
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.
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
260 ing (EOE) has been associated with increased obesity risk, while emotional undereating (EUE) may be p
263 lin signaling cascade, insulin resistance in obesity seems to be largely elicited downstream of these
265 disease, C-reactive protein, HbA1c, height, obesity, smoking status, triglycerides, type 2 diabetes,
267 ular risk factors were measured at baseline (obesity, smoking, diabetes, prehypertension, hypertensio
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
273 In societies characterized by widespread obesity, the sensitivity of reproduction to metabolic im
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.
283 onocyte gene expression profile in childhood obesity using an Illumina microarray platform on sorted
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
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
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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