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1 d by a high accumulation of body fat (severe obesity).
2  inflammatory conditions including aging and obesity.
3 he lean state and metabolic dysregulation in obesity.
4  adolescent adiposity and risk of overweight/obesity.
5 erebrovascular dysfunction despite prolonged obesity.
6 f too much fat and to protect adults against obesity.
7 ting pandemic of metabolic disease driven by obesity.
8  as rheumatoid arthritis, liver fibrosis, or obesity.
9 ity is reduced in breast epithelial cells in obesity.
10 ck Children (2002-2011), excluding prevalent obesity.
11 reatment of drug addiction, anxiety, pain or obesity.
12 growth restriction (IUGR) leads to offspring obesity.
13 etween inflammation and the comorbidities of obesity.
14 inhibits lipolysis and promotes diet-induced obesity.
15 of meals are also potential risk factors for obesity.
16  increasing energy expenditure to counteract obesity.
17 a novel therapeutic target for patients with obesity.
18 k indirectly through their relationship with obesity.
19 ls display distinct metabolic adaptations to obesity.
20  could be a potential therapeutic target for obesity.
21 een implicated in substance use disorder and obesity.
22 tion for patients with cirrhosis and extreme obesity.
23  is associated with many diseases, including obesity.
24 e system in the inception and progression of obesity.
25 metabolism and is implicated in diet-induced obesity.
26 d protects from inflammation, steatosis, and obesity.
27 ycerides, and female-specific overweight and obesity.
28 ildren might not lower the risk of childhood obesity.
29 in fat intake and development of fat-induced obesity.
30  opportunity for preventing subsequent adult obesity.
31  limits its application for the treatment of obesity.
32 e immunity and metabolic disorders including obesity.
33  later life and is associated with childhood obesity.
34 set metabolic diseases, such as diabetes and obesity.
35 energy metabolism driving toward age-related obesity.
36 a-arrestin family previously linked to human obesity.
37  highly palatable food (HPF), that may drive obesity.
38 r that contributes to hedonic overeating and obesity.
39 een healthy individuals and individuals with obesity.
40 owth and protects against the development of obesity.
41 ltiple species, an effect that is blunted by obesity.
42 ion and timing in relation to overweight and obesity.
43  are selectively reduced in a mouse model of obesity.
44 and metabolic disease including diabetes and obesity.
45 n anabolic hormones, such as insulin, during obesity.
46 ful alcohol use, 1.4 (0.9-2.0, p = 0.10) and obesity, 1.4 (0.9-2.2, p = 0.13) We found no evidence th
47 the adjusted incidence rate among women with obesity (2.29 [95% CI, 2.02-2.56]), high triglycerides (
48 us physical activity) in pregnant women with obesity (294 contol, 263 intervention).
49                      Cumulative incidence of obesity 5-years posttransplant was 24.1%.
50 nequality in the risk for obesity and severe obesity across GPS tenths.
51  were age, hypertension, diagnoses including obesity, alcohol, sleep apnea, diabetes, chronic obstruc
52 oth rodents and non-human primates, maternal obesity also predicts a preference for palatable foods i
53 e, we report on a monogenic form of IR-prone obesity, Alstrom syndrome (ALMS).
54 vascular diseases, type 2 diabetes mellitus, obesity, amnesia among other disorders.
55 quantify the potential benefit of decreasing obesity among at-risk women.
56 determined the incidence and risk factors of obesity among pediatric solid-organ transplant recipient
57 ta from Eurostat show that the prevalence of obesity among those aged 15-19 years remains under 5%, w
58 tients with coronavirus disease 2019 include obesity, an elevated d-dimer value, elevated C-reactive
59              In total, 281 incident cases of obesity and 777 cases of overweight were identified duri
60 elian randomization (MR) to evaluate whether obesity and AD are causally interlinked.
61                               Likewise, both obesity and addictive behaviours have similar correlatio
62 e to exercise, yet chronically elevated with obesity and aging.
63    We also discuss the major contribution of obesity and alcohol to the ten most common cancers as we
64                     With the rising rates of obesity and associated metabolic disorders, there is a g
65 uggest a neurobiological interaction between obesity and brain structure under physiological and path
66 s suggesting FABP4 as a novel player linking obesity and breast cancer risk.
67 mmune cells in human WAT under conditions of obesity and calorie restriction (CR) is not fully unders
68 dv36 seropositivity and its association with obesity and diabetes among adults attending a diabetes c
69 isease and general health conditions such as obesity and diabetes are closely linked by sharing commo
70 etween early-life nutrition and the risks of obesity and diabetes.
71 irubin levels are negatively associated with obesity and diabetes.
72 3 has been implicated in the pathogenesis of obesity and diabetes; however, the mechanisms and tissue
73 iota composition, and 4) prevent and reverse obesity and dysregulated glucose homeostasis in multiple
74 ze the transplant candidacy of patients with obesity and end-stage organ disease and improve perioper
75                                     In PDAC, obesity and excess fatty acids accelerate tumor growth a
76           A genetic predisposition, smoking, obesity and hormonal factors are established aetiologica
77                      The mechanisms by which obesity and hypertension may synergistically induce macr
78 ffects of bariatric surgery on patients with obesity and hypertension remain uncertain.
79 ose tissue and protects mice from developing obesity and insulin resistance.
80  renders BAT as an attractive target against obesity and insulin resistance.
81 ut (Opn3-KO) mice were prone to diet-induced obesity and insulin resistance.
82  myeloid KLF2 protects mice from HFD-induced obesity and insulin resistance.
83 d energy expenditure is crucial to combating obesity and its comorbidities.
84                    The escalating problem of obesity and its multiple metabolic and cardiovascular co
85 th brain-penetrant CB1R blockers, ameliorate obesity and its multiple metabolic complications.
86 factor 2 (KLF2) as an essential regulator of obesity and its sequelae.
87 h2b1/SNS/BAT/thermogenesis axis that combats obesity and metabolic disease.
88 s that have shown effects in mouse models of obesity and metabolic disorders, and how these might be
89 chedule is associated with increased risk of obesity and metabolic dysfunction in humans.(1-9) Howeve
90 ve, we highlight 1) the relationship between obesity and metabolic pathways putatively driving hepati
91 this field of research on innate immunity in obesity and metabolic perturbation, as well as future di
92 and April 2018, we randomized 24 adults with obesity and mild-moderate insulin resistance (homeostati
93  this has contributed to increasing rates of obesity and non-alcoholic fatty liver disease(2-4).
94 l upper airway soft tissues in subjects with obesity and OSA.
95 ity are associated with an increased risk of obesity and related metabolic disorders, but the role of
96 omes, 8 on cardiovascular disease, 3 each on obesity and rheumatoid arthritis, and 2 on chronic kidne
97  reveal a growing inequality in the risk for obesity and severe obesity across GPS tenths.
98 es evaluated the relationship between severe obesity and short-term outcomes and long-term mortality.
99 e impact of costly, chronic diseases such as obesity and substance use disorders.
100 findings shed light on the interplay between obesity and T2D in stroke recovery.
101                                              Obesity and type 2 diabetes mellitus are global emergenc
102 d is a promising target for the treatment of obesity and type 2 diabetes mellitus.
103 estinal microbiome have been associated with obesity and type 2 diabetes, in epidemiological studies
104     Here we seek to empirically test whether obesity and UE overlap behaviourally with addiction and
105 ic islets from obese animals and humans with obesity and/or T2DM.
106 icronutrient deficiencies, or on overweight, obesity, and dietary excess.
107 l to reduce the risk of both undernutrition, obesity, and DR-NCDs.
108                      A subgroup of the Diet, Obesity, and Genes (DiOGenes) study (n = 209) was recrui
109  metabolic syndrome, hypertension, abdominal obesity, and hypertriglyceridemia.
110 the chronic inflammation observed in cancer, obesity, and other conditions.
111                                   Lifestyle, obesity, and the gut microbiome are important risk facto
112 -related, toxic and haemodynamic factors and obesity are also important causes of podocyte injury and
113                      Although overweight and obesity are assumed to arise from an energy imbalance, e
114                               Both aging and obesity are characterized by profound systemic metabolic
115 rrently, type 2 diabetes mellitus (T2DM) and obesity are major global public health issues, and their
116                    Geographic remoteness and obesity are risk factors for specific causes of SCD in t
117 etabolic disorders, has been associated with obesity, arrhythmias, cardiac ischemia, insulin resistan
118 ere used to assess the role of pre-pregnancy obesity as a mediator in the association between materna
119  plays a central role in the pathogenesis of obesity as well as in the associated cardiovascular comp
120 ulin action that manifests with diet-induced obesity, as insulin action is preserved to protect funda
121 deficient (CysC knockout [KO]) mice worsened obesity-associated adipose tissue inflammation and dysfu
122  fatty acid binding protein (FABP4) promotes obesity-associated breast cancer development, thus sugge
123 rainstem, contributes to the pathogenesis of obesity-associated cerebrovascular dysfunction.
124 ipheral insulin-sensitive tissues and, thus, obesity-associated deterioration of glucose metabolism.
125 ntally validate the predicted function of an obesity-associated lncRNA, LINC01018, in regulating the
126 ovel viable approaches to prevent or relieve obesity-associated neuropathies.
127  molecular and cellular mechanism underlying Obesity-associated neuropathy and PNS dysfunction.
128 nificant pancreatic islet cell adaptation in obesity-associated tumors.
129 tion were significantly higher in women with obesity at the begining of pregnancy (mean difference: -
130 n health and disease with a special focus on obesity, bariatric surgery-induced weight loss, and immu
131 well as body mass index (BMI) as a marker of obesity (BMI > 30 kg/m(2)).
132                                              Obesity (BMI > 30 kg/m2) was more prevalent in the class
133                                              Obesity (BMI > 30) was significantly associated with cor
134                 Seventy-one individuals with obesity (BMI: 34.6 +/- 3.4 kg/m2; age: 45.4 +/- 8.2 y; 3
135 nts and Main Results: Subjects with ARDS and obesity (BMI=57+/-12 kg/m(2)), following LRM, required a
136 trolled diabetes (hemoglobin A1c level >8%), obesity (body mass index >30), and depressive symptoms (
137   We assessed their penetrance and effect on obesity (body mass index [BMI] >= 30 kg/m2) in >450,000
138 could play a role in cancer etiology through obesity but also through inflammatory and oxidative mech
139  weight in patients with type 2 diabetes and obesity but have limited weight-lowering efficacy and mi
140 tively associated with adolescent overweight/obesity but not with suicidal ideation with planning.
141      Epidermal thickness did not differ with obesity but the expression of genes encoding proteins as
142  weight loss option for Veterans with severe obesity, but fewer than 0.1% of Veterans with severe obe
143 ed protein S-glutathionylation and developed obesity by an unknown mechanism.
144 to-high penetrance and increased the odds of obesity by more than 2-fold.
145 and epidermal FABP (E-FABP) in the fields of obesity, chronic inflammation, and cancer development.
146     In conclusion, CysC is upregulated under obesity conditions and thereby counteracts inflammation
147 ctal adenocarcinoma (PDAC), yet how and when obesity contributes to PDAC progression is not well unde
148 on, diabetes with chronic complications, and obesity demonstrated age-dependent effects, with the hig
149 t may protect against this drive and prevent obesity development.
150 g pregnancy is rising as older maternal age, obesity, diabetes mellitus and hypertension become more
151              Mid-life metabolic disease (ie, obesity, diabetes, and prediabetes) causes vascular dysf
152 n considered a culprit in the development of obesity/diabetes mellitus-induced cardiomyopathy.
153 as a research tool for diagnostic imaging of obesity/diabetes, bacterial infection, and cancer.
154                                              Obesity/diabetes-associated liver tumors are specificall
155                                  Adults with obesity diagnosis who underwent primary bariatric surger
156           Its reduced levels in diet-induced obesity (DIO) contribute to hyperleptinemia and leptin r
157                                              Obesity disrupts physiological homeostasis and alters bo
158                             Individuals with obesity do not represent a homogeneous group in terms of
159 eworthy because they may in part explain how obesity drives colon cancer progression.
160 al therapeutic target of anticancer and anti-obesity drugs by inhibiting its DNA-binding activities.
161     For HbA1c, however, the association with obesity duration persisted, independent of obesity sever
162 ally adjusted models, male sex, underweight, obesity, education, poor self-rated health, television-v
163 nd how macrophage-driven inflammation due to obesity enhances tumor formation, mice were treated with
164 nts could inform policies for control of the obesity epidemic in India and other urbanising LMICs.
165  results agree with previous reports showing obesity exacerbates AD-related pathology and symptoms in
166 pe 2 diabetes mellitus, ubiquitous abdominal obesity, exposure to the world's highest levels of air p
167 oss BMI groups, except in women with class 3 obesity, for whom low weight gain and weight loss may be
168                  Participants with class III obesity had a greater risk of metabolic syndrome than th
169                                    Childhood obesity has become a global pandemic in developed countr
170                                              Obesity has been firmly established as a major risk fact
171                                              Obesity has tripled worldwide since 1975 as environments
172 lationships between gut microbiome and PN in obesity have yet to be explored.
173 tive association between plasma ANGPTL5, and obesity, high sensitivity C-reactive protein (HsCRP) and
174                     NAFLD is associated with obesity; however, it can occur in normoweight (lean) pat
175  that subsequently inhibit food consumption, obesity, hyperglycemia, and liver steatosis in HFD-treat
176  for established CKD risk factors, including obesity, hypertension, and type 2 diabetes.
177 tal heart disease, various cardiomyopathies, obesity, hypertension, diabetes, and chronic kidney dise
178 he influence of the metabolic syndrome (MS) (obesity, hypertension, elevated triglycerides, reduced l
179                    Patterns of reporting for obesity, hypertension, heart conditions, or hypercholest
180              Emerging evidence suggests that obesity impacts brain physiology at multiple levels.
181 n of P2Y(6)R protects mice from diet-induced obesity, improving glucose tolerance and insulin sensiti
182  PWS are replaced with excessive feeding and obesity in childhood through adulthood.
183                            The prevalence of obesity in children and adolescents worldwide has quadru
184               Using a high-fat diet model of obesity in mice and breast tissue from women, we observe
185 urons during the development of diet-induced obesity in mice.
186 entify the prevalence of hypoalbuminemia and obesity in orthopaedic trauma patients with high-energy
187 ative stress and point to a critical role of obesity in T2DM cardiomyopathy.
188 d explore potential interventions to address obesity in these populations.
189  2015-2018 the US prevalence of youth severe obesity increased in Hispanics and non-Hispanic blacks (
190 2 in macrophage activation in the context of obesity-induced adipose tissue inflammation and insulin
191 lium-dependent vasodilation is a hallmark of obesity-induced hypertension.
192 al women seem to be generally protected from obesity-induced metabolic and cardiovascular complicatio
193          However, the mechanism by which HFD/obesity induces chondrocyte apoptosis is not clearly und
194                  We hypothesized that unique obesity-inflammation HFpEF phenotypes exist and are asso
195                                              Obesity influences asthma severity and may impair respon
196    Oral administration of UAB126 ameliorated obesity, insulin resistance, hepatic steatosis, and hype
197            In addition, a significant age-by-obesity interaction on cortical thickness emerged driven
198    Despite the rising incidence of childhood obesity, international data from Eurostat show that the
199  tissue integrity, and beta-cell mass during obesity is a major challenge.
200                                              Obesity is a major modifiable risk factor for pancreatic
201                                     Although obesity is an established risk factor for morbidity and
202                                              Obesity is an important independent risk factor for seve
203 t increased insulin secretion in people with obesity is associated with excess adiposity itself and i
204                     We hypothesize that this obesity is caused by TH(+) cell loss or altered phenotyp
205                                       Severe obesity is characterized by specific additional cardiova
206 earch should put to rest the contention that obesity is common in severe COVID-19 because it is commo
207 tients with myocardial infarction and severe obesity is increasing and there is a lack of evidence ho
208                                              Obesity is known to increase breast cancer incidence and
209 ed from transplantation until development of obesity, last follow-up, or end of study.
210 drupled since 1975 and is a key predictor of obesity later in life.
211  (primary cause) with multiple sclerosis and obesity listed as secondary causes.
212                     Here we show that during obesity MAIT cells promote inflammation in both adipose
213                                              Obesity may contribute to adverse outcomes in coronaviru
214 gest that interaction between gingivitis and obesity may exhibit disease reciprocity in which activat
215                    Our findings suggest that obesity may indeed be related to an imbalance in behavio
216 en the PRSBMI, eating behavior patterns, and obesity measures.
217 vestigated the extent to which pre-pregnancy obesity mediates the association between maternal place
218 hway of asthma pathogenesis in patients with obesity/metabolic syndrome, in which the GRK2-mediated s
219 Stable metabolically unhealthy overweight or obesity (MUOO) (HR 2.22, 95% confidence interval [CI] 2.
220  moderate (type 2 diabetes, n = 9), or mild (obesity, n = 8).
221 roportions with the increasing prevalence of obesity, nonalcoholic liver disease, and alcohol overuse
222   Analysis indicated a significant impact of obesity on gingivitis.
223                      We review the impact of obesity on kidney, liver, and cardiothoracic transplant
224 transplantation recapitulated the effects of obesity on microglial activation and IL-1beta gene expre
225  preventing the negative effects of maternal obesity on offspring development and adult health.
226 owever, we don't understand the influence of obesity on susceptibility to infection or on non-severe
227 IF1L is not essential for the development of obesity or impaired glucose handling due to HFD, and adv
228 lead to several metabolic diseases including obesity or type 2 diabetes.
229 weeks either a high-fat diet (HFD) to induce obesity, or chow as reference group.
230 tigates how changes in population weight and obesity over time are associated with genetic predisposi
231                                 Finally, the obesity paradox was not observed after including Acute P
232 the prevention of diseases such as diabetes, obesity, Parkinson's, Alzheimer's, and others.
233                                              Obesity plays a profound role in risk for death from COV
234 dle-aged mice, we modeled metabolic disease (obesity/prediabetes) via chronic high-fat (HF) diet and
235 riation in underweight and overweight and/or obesity prevalence in the country, adjusted for cluster
236 rs and consider future priorities for global obesity prevention.
237 fying them as a novel therapeutic target for obesity-related asthma, a disease that is suboptimally r
238 gested a modest association for leucine with obesity-related cancers (1.04 [1.00-1.08]), and no assoc
239 on in obese AT, lending further insight into obesity-related comorbidities in humans.
240 of 40 or higher or 35 or higher with serious obesity-related comorbidities.
241 lular metabolism are unclear but relevant to obesity-related diseases.
242 myeloid leukemia, debilitating fibroses, and obesity-related liver dysfunction.
243 mation (metaflammation) is characteristic of obesity-related metabolic disorders, associated with inc
244 ntial outcome approach was used to determine obesity-related periodontitis risk using the Australian
245           To avoid the confounding effect of obesity-related steatosis, only 70 individuals who had c
246 tion analysis including 21 inversions and 25 obesity-related traits on a total of 408,898 Europeans a
247 relationship between mean adipocyte area and obesity-related traits, and identify genetic factors ass
248                                              Obesity remains a risk factor for CVD independent of maj
249 of genetic regulation of leptin in polygenic obesity remains poorly understood.
250 the activity of these circuits is altered in obesity remains poorly understood.
251                                 We find that obesity-repressed LincIRS2 is controlled by MAFG and obs
252 rate the need for sex-specific approaches in obesity research and potentially treatment.
253 d as a prophylactic therapy for diabetes and obesity, respectively.
254   A prominent hypothesis is that people with obesity respond to rewards similarly to people with addi
255 dministration of FMT capsules in adults with obesity results in gut microbiota engraftment in most re
256                             Its expansion in obesity results in increased mortality and morbidity, wi
257 h obesity duration persisted, independent of obesity severity.
258 ocarcinoma, such as older age, male sex, and obesity, should undergo endoscopy.
259                                              Obesity significantly enhanced the incidence of tumors o
260 x and gestational weight gain predict future obesity status of the offspring.
261 m p62 deficiency is manifest after birth and obesity subsequently develops despite normal food intake
262 4 to 8 times larger projected impact against obesity than would be achieved though reformulation alon
263 es define microenvironmental consequences of obesity that foster tumorigenesis rather than new driver
264 the presence of metabolic stress, such as in obesity, the resulting degradation products may play a d
265 f Medical Officer to combat rising levels of obesity-the highest of any country in the west.
266 ogram and may present as a future target for obesity therapeutics.
267        For middle aged and older adults with obesity there was also a slight increase in susceptibili
268 r microstructure in children with overweight/obesity; those findings indicate that the association of
269      Here, we used a mouse model of maternal obesity to investigate the importance of early life ER s
270                                              Obesity, tobacco smoking, and genetic predisposition inc
271         Models included adjustment for race, obesity, tobacco use, hypertension (HTN), atrial fibrill
272  high-intensity, lifestyle-based program for obesity treatment delivered in primary care clinics in w
273  This review addresses the interplay between obesity, type 2 diabetes mellitus, and cardiovascular di
274  a potential target to decrease the risks of obesity, type 2 diabetes, and cardiovascular disease, an
275 e is now recognized as a key risk factor for obesity, type 2 diabetes, and cardiovascular diseases.
276 ng pancreatic cancer include family history, obesity, type 2 diabetes, and tobacco use.
277 of metabolic diseases (hypertriglyceridemia, obesity, type 2 diabetes, hypertension, metabolic syndro
278  but fewer than 0.1% of Veterans with severe obesity undergo it.
279  cardiovascular and cerebrovascular disease, obesity, undernutrition, or hypercholesterolemia.
280 we highlight variants in candidate genes for obesity warranting further investigation.
281 portion of T2DM incident cases attributed to obesity was 55.6% in 1990, 59.5% in 2020, and 62.6% in 2
282         Among adults with H1N1pdm infection, obesity was associated with increased likelihood of symp
283                                    Recipient obesity was defined as body mass index (BMI) >35 adjuste
284                                     Maternal obesity was established by prepregnant HF (ppHF) feeding
285                                 Donor severe obesity was not associated with adverse post-transplant
286 rts, we investigated whether the duration of obesity was related to heterogeneity in cardiometabolic
287                         However, the risk of obesity was significantly higher in the sub-analysis of
288 ncrease in the average BMI and prevalence of obesity was steeper among the genetically predisposed.
289 on identifying the genetic susceptibility to obesity, we performed a GWAS on metabolically healthy th
290                     Male sex, older age, and obesity were associated with higher concentrations of in
291                             OR of sarcopenic obesity were higher for men 2.17 (1.70-2.76), those repo
292                 The effects of gingivitis on obesity were in the same direction but generally not sta
293 hypertension with chronic complications, and obesity were risk factors in most age-groups, with highe
294 ome, Charlson Comorbidity Index, diabetes or obesity when compared to no-CCY (all P > 0.05), but were
295 ght loss on insulin secretion in people with obesity who did not improve insulin sensitivity despite
296 oV-2 burden, demographic characteristics and obesity with a minor contribution of chronic comorbid co
297                                    To detect obesity with body mass index (BMI), the meta-analyses re
298 trongly associated with the co-occurrence of obesity with other common diseases.
299 ese findings provide one explanation for how obesity worsens cancer outcomes and may point to a new m
300 ings in a cohort of children with overweight/obesity, young adults and middle-age adults.

 
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