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1                                     Systemic obesity-related abnormalities in the peripheral blood T-
2 GC-1alpha protein levels did not correct the obesity-related absolute reduction in FAO or mtDNA conte
3 l fibroblast cross-talk, was enhanced by the obesity-related adipokine leptin.
4 es have addressed causes and consequences of obesity-related adipose tissue hypertrophy and hyperplas
5 o association was observed for either of the obesity-related anthropometric measures after adjustment
6 is compound shows potential in counteracting obesity-related anxiety.
7            Despite this, the role of FFAs in obesity-related aortic stiffness remains unclear.
8                                    Pediatric obesity-related asthma is more severe and less responsiv
9 inical evidence supports the existence of an obesity-related asthma phenotype.
10 ; P = .003) and appear to mediate overweight/obesity-related asthma symptoms.
11 duce their sedentary time to prevent central obesity-related asthma.
12 on deficits found in patients with pediatric obesity-related asthma.
13 ary function deficits found in patients with obesity-related asthma.
14 T) hypoxia has been proposed as the cause of obesity-related AT dysfunction, moving the tissue toward
15 fat cell lipid accumulation; it demonstrates obesity-related attenuated autophagy in adipocytes, and
16 omes in the elderly, the biological bases of obesity-related behaviors during aging are poorly unders
17 eighborhood factors on childhood obesity and obesity-related behaviors, much work remains to be done
18  women from these households adopt different obesity-related behaviors.
19 nd to reduce metabolic endotoxemia and other obesity-related biochemical abnormalities.
20 tudes of correlations of BMI and WC with the obesity-related biologic factors were similar to those o
21 n the whole body and trunk, BMI, and WC with obesity-related biologic factors, including blood pressu
22 ent, as evaluated by their associations with obesity-related biomarkers and prevalence of metabolic s
23 r repletion supports weight loss and changes obesity-related biomarkers is unknown.
24 owever, there are little data on the role of obesity-related biomarkers on liver cancer risk.
25                                Corresponding obesity-related biomarkers were measured in 10 overweigh
26 tions of 95 a priori and recently identified obesity-related (body mass index (weight (kg)/height (m)
27                                        Thus, obesity-related brain adaptations to glucose and fructos
28 9a signaling regulates CSC plasticity during obesity-related breast cancer progression, suggesting a
29  be critical for prevention and treatment of obesity-related cancer.
30 icantly associated with the incidence of all obesity-related cancers (hazard ratio [HR] per 10-y incr
31 esity, cardiovascular disease, hypertension, obesity-related cancers, and dental caries.
32 ty on the prognosis of the three most common obesity-related cancers: prostate, colorectal, and breas
33 namic role between adiponectin and leptin in obesity-related carcinogenesis.
34 herapeutic potential of physical activity in obesity-related cardiac disorders.
35           These findings may shed light onto obesity-related cardiac remodeling and heart failure.
36 sulin resistance may be primary mediators of obesity-related cardiac remodeling independent of body m
37 se tissue dysfunction play a central role in obesity-related cardiometabolic complications.
38      Insulin resistance is a key mediator of obesity-related cardiometabolic disease, yet the mechani
39                                 By contrast, obesity-related cardiometabolic diseases are increasingl
40 abdominal) adipose tissue is associated with obesity-related cardiometabolic diseases, whereas lower-
41                                              Obesity-related cardiovascular disease in children is be
42 t has been implicated in the pathogenesis of obesity-related cardiovascular disease.
43 , we could not separate the contributions of obesity-related cardiovascular risk factors, such as dia
44           Estimates for all-cause mortality, obesity-related causes of death, and other causes of dea
45 e, these results provide first evidence that obesity-related changes in adipose tissue macrophage phe
46  2008, we documented 8,755 incident cases of obesity-related chronic diseases (type 2 diabetes mellit
47              Weight loss improves almost all obesity-related co-morbidities and metabolic markers, re
48 iatric surgery, weight, body mass index, and obesity-related co-morbidities.
49 formin can decrease adiposity and ameliorate obesity-related comorbid conditions, including abnormali
50 ric bypass resulted in large improvements in obesity-related comorbid disease and sustained weight lo
51 mportantly, a highly significant decrease in obesity-related comorbid disease persisted at 10 years o
52 n for long-term weight loss and treatment of obesity-related comorbid disease.
53 ty and increases time taken to conceive, and obesity-related comorbidities (such as type 2 diabetes a
54 s, all of which can result in a reduction in obesity-related comorbidities and improvements in qualit
55 reasing, but data on its long-term effect on obesity-related comorbidities are scarce.
56  disease, has nearly doubled since 1980, and obesity-related comorbidities have become a major threat
57 in treatment causes weight loss and improves obesity-related comorbidities in obese children, who are
58 weight loss and accompanying improvements in obesity-related comorbidities produced by intensive life
59                                         Many obesity-related comorbidities such as diabetes and hyper
60 excess adiposity, often independent of other obesity-related comorbidities such as dyslipidemia and i
61 ve contribution of cardiometabolic and other obesity-related comorbidities to such effects remains un
62 ect higher rates of diabetes mellitus, other obesity-related comorbidities, and mortality.
63                          Excess weight loss, obesity-related comorbidities, and partial and complete
64 cient weight loss and a major improvement in obesity-related comorbidities, with mostly no correlatio
65 ically relevant benefits for the majority of obesity-related comorbidities.
66 ions are currently used to treat obesity and obesity-related comorbidities.
67 o RYGB than LAGB with regard to remission of obesity-related comorbidities.
68  body mass index (BMI) of 35 or greater with obesity-related comorbidities.
69 nd whole milk is associated with obesity and obesity-related comorbidities.
70 ly quantify the indirect effects mediated by obesity-related comorbidities.
71 /m2 or greater in the presence of at least 1 obesity-related comorbidity.
72 ay of multiple organs in the pathogenesis of obesity-related complications such as NAFLD and provides
73 ays a significant role in the development of obesity-related complications, but the molecular events
74 portant role for gastric tissue in promoting obesity-related complications.
75 esent biomarkers and therapeutic targets for obesity-related complications.
76 nalcoholic fatty liver disease (NAFLD) is an obesity-related condition affecting over 50% of individu
77 nonalcoholic fatty liver disease (NAFLD), an obesity-related condition that recently has become the m
78  index of 40 to 45 or 35 to 40 and 1 or more obesity-related condition was conducted at 10 sites in t
79 he use of MBS as a treatment for obesity and obesity-related conditions and, based on recent evidence
80                                              Obesity-related conditions including heart disease, stro
81 r disease (NAFLD) and heart failure (HF) are obesity-related conditions with high cardiovascular mort
82                 The incidence of obesity and obesity-related conditions, such as metabolic syndrome a
83 ffects mediated by cardiometabolic and other obesity-related conditions, suggesting the possible role
84 with diet but contributes to improvements in obesity-related conditions.
85         Given the improvement of established obesity-related CVD risk factors after weight loss, it i
86  Growing evidence indicates that resistin-an obesity-related cytokine-is upregulated in breast cancer
87 ted traits in Mexican American (MA) children.Obesity-related data were obtained from 670 nondiabetic
88                                              Obesity-related diabetes is caused by insulin resistance
89                            The prevalence of obesity-related diabetes is increasing worldwide.
90 sulin to control glucose homeostasis, but in obesity-related diabetes, there is a presumed deficit in
91 nts are less likely to show dMMR, suggesting obesity-related differences in the pathogenesis of colon
92 ing surgical procedures to treat obesity and obesity-related disease are increasing.
93 h lipid overloading, thereby contributing to obesity-related disease.
94 o increase our understanding of skeletal and obesity-related diseases and aid in the development of s
95 el is used to project the extent of obesity, obesity-related diseases and associated healthcare costs
96  why bariatric surgery can be beneficial for obesity-related diseases and why operated individuals su
97                                              Obesity-related diseases are placing a substantial healt
98 udied sirtuin, SIRT1, counteracts aging- and obesity-related diseases by deacetylating many proteins,
99 nt-sensitive candidate genes for obesity and obesity-related diseases for main and dietary interactio
100 dex (BMI) from adolescence to adulthood with obesity-related diseases in young adults has not been co
101 ic cellular and molecular mechanisms in most obesity-related diseases remains an important challenge.
102 ) is commonly recommended for improvement of obesity-related diseases such as NAFLD.
103 h plays a key role in the pathophysiology of obesity-related diseases such as type 2 diabetes and non
104 obesity as physicians caring for people with obesity-related diseases, in addition to their expertise
105 c potential of BAT to counteract obesity and obesity-related diseases, including insulin resistance.
106 (SIRT1) deacetylase delays and improves many obesity-related diseases, including nonalcoholic fatty l
107 WATi) has been linked to the pathogenesis of obesity-related diseases, including type 2 diabetes, car
108  are an important contributor to obesity and obesity-related diseases, including type 2 diabetes.
109 ttractive therapeutic target for obesity and obesity-related diseases, including type 2 diabetes.
110 g new therapeutic approaches for obesity and obesity-related diseases, including type 2 diabetes.
111 tion of AdipoR agonists for the treatment of obesity-related diseases, such as type 2 diabetes.
112 ed molecular features that may contribute to obesity-related diseases.
113 n, providing a potential target for treating obesity-related diseases.
114 l basis for the development of therapies for obesity-related diseases.
115 ic approach for treatment of NAFLD and other obesity-related diseases.
116 e Australian population, taking into account obesity-related diseases.
117 hich may be implicated in the progression of obesity-related diseases.
118                       There is evidence that obesity-related disorders are increased among people wit
119 l--constitutes a substantial risk factor for obesity-related disorders in midlife.
120 ncidence was not associated with obesity and obesity-related disorders including liver steatosis, glu
121 ed increase in the prevalence of obesity and obesity-related disorders is causally linked to a chroni
122 d a significant economic investment to treat obesity-related disorders such as type 2 diabetes, cardi
123 lammation plays a critical role in promoting obesity-related disorders, such as fatty liver disease.
124 ases, such as inflammatory bowel disease and obesity-related disorders.
125 olism and the dysregulation that occurs with obesity-related disorders.
126 hospholipid metabolism in the progression of obesity-related disorders.
127                                              Obesity-related dysregulation of leptin signaling (e.g.,
128 im was to evaluate dietary, reproductive and obesity-related factors and GBD in multiethnic populatio
129           Overall, dietary, reproductive and obesity-related factors are strong risk factors for GBD
130  review will be the impact of these systemic obesity-related factors on cancer biology, incidence, an
131 B homologues are known: ABH1 to ABH8 and the obesity-related FTO.
132 ilities for preventing and controlling human obesity-related gastrointestinal cancers that often exhi
133 T expression of CNV12, which overlap with an obesity related gene Netrin-1 (Ntn1), were consistent wi
134 creased BMI we saw the upregulation of known obesity related genes (the insulin receptor (INSR) and t
135     Discovering the mechanisms through which obesity-related genes influence weight would help pinpoi
136 raits mediate the associations between known obesity-related genetic variants and adiposity.
137 lymorphisms identified in a meta-analysis of obesity-related genome-wide association studies.
138 lated by high glucose and/or fatty acids, in obesity-related glomerulopathy (ORG) and diabetic nephro
139 ry focal segmental glomerulosclerosis coined obesity-related glomerulopathy (ORG).
140 keletal muscle may be effective in reversing obesity-related glucose intolerance and insulin resistan
141 iet providing 42% of energy as fat developed obesity-related glucose intolerance by 6 months.
142 icals that may contribute to diabetes and to obesity-related health outcomes by summarizing relevant
143 o better understand the influence of diet on obesity-related health outcomes, efforts to reduce dieta
144 ass index [BMI] z score, >/=3.0 or >2.3 with obesity-related health problems).
145 cies in the liver, which plays a key role in obesity-related hepatic insulin resistance.
146                                              Obesity-related HFpEF is a genuine form of cardiac failu
147 oints included short-term weight loss, serum obesity-related hormone levels, hunger and satiety asses
148  hepatic gluconeogenesis that contributes to obesity-related hyperglycemia and progression of type 2
149 link may represent an avenue for controlling obesity-related hypertension and CVD without requiring o
150  (PVAT) and has been implicated in resultant obesity-related hypertension and impaired glucose intole
151 chanisms underlying both Liddle syndrome and obesity-related hypertension are different (i.e. genetic
152                                              Obesity-related hypertension has become an epidemic heal
153  in the mediobasal hypothalamus counteracted obesity-related hypertension in a manner that was dissoc
154 lamic IKK-beta and NF-kappaB, which underlie obesity-related hypertension.
155 cap") may play a role in the pathogenesis of obesity-related hypertension.
156 nt (Mc4rKO) mice are severely obese but lack obesity-related hypertension; they also show a reduced p
157 idemic proportions in the United States, and obesity-related illnesses have become a leading preventa
158 ce of obesity on cognition in the absence of obesity-related illnesses.
159  contribute to mitochondrial dysfunction and obesity-related impairments in glucose tolerance.
160 he impact of 12 weeks of aerobic exercise on obesity-related impairments in insulin sensitivity and m
161 33, and gammadelta T cell deficiency reduced obesity-related increases in the response to ozone, incl
162 vestigate the role of Th2/M2 polarization in obesity-related inflammation and insulin resistance, we
163 forging collaboration with groups working on obesity-related initiatives both within and outside of t
164  to failed insulin secretory compensation to obesity-related insulin resistance and dysmetabolism.
165 pies for their potential in the treatment of obesity-related insulin resistance and glucose intoleran
166 y have potential therapeutic implications in obesity-related insulin resistance and other metabolic c
167 y missing links and potential mechanisms for obesity-related insulin resistance and type 2 diabetes t
168                           BACKGROUND & AIMS: Obesity-related insulin resistance contributes to cardio
169  apelin on fatty acid oxidation (FAO) during obesity-related insulin resistance have not yet been add
170                                              Obesity-related insulin resistance is associated with an
171 rcise that produces the greatest reversal of obesity-related insulin resistance is unknown.
172 ose tissue contributes to the development of obesity-related insulin resistance through increased rel
173 duced FoxO1 expression protects mice against obesity-related insulin resistance with marked improveme
174 ofile is highlighted in its association with obesity-related insulin resistance, type 2 diabetes mell
175 AT) as a key contributor to inflammation and obesity-related insulin resistance.
176  thought to contribute to the development of obesity-related insulin resistance.
177 P-Br2-null mice are resistant to obesity and obesity-related insulin resistance.
178 ipogenesis contributes to the development of obesity-related insulin resistance.
179 ue is only one of the important mediators of obesity-related insulin resistance.
180 eptibility to type 1 diabetes results in non-obesity-related, insulin-dependent diabetes, which prese
181 5 have renoprotective roles in diabetes- and obesity-related kidney disease.
182 kers to predict progression and prognosis of obesity related liver diseases.
183 esent a therapeutic target for patients with obesity-related liver disease.
184 es; however, the role of B7 costimulation in obesity-related liver inflammation is unknown.
185 netic inactivation of B7.1/B7.2 deteriorates obesity-related liver steatosis and metabolic dysregulat
186 at the effects of a polygenic risk score (90 obesity-related loci) on measured body mass index and wa
187 mmatory functions of each monocyte subset in obesity-related low-grade inflammation.
188 D2R function better than other commonly used obesity-related measures such as BMI.
189             Metabolic syndrome is a group of obesity-related metabolic abnormalities that increase an
190 ey disease (CKD) among obese persons without obesity-related metabolic abnormalities, called metaboli
191 ts with atypical depression characterized by obesity-related metabolic alterations.
192 Adipose inflammation plays a central role in obesity-related metabolic and cardiovascular complicatio
193 al recognition, intestinal inflammation, and obesity-related metabolic changes.
194 n producing modest weight loss and improving obesity-related metabolic complications in humans, adver
195 ose tissue (AT) and liver, thereby mediating obesity-related metabolic deterioration.
196 e to impaired adipogenic differentiation and obesity-related metabolic disease.
197 p a potentially novel therapeutic avenue for obesity-related metabolic disease.
198 9 may be an effective strategy for combating obesity-related metabolic disease.
199 at depots exhibit opposing associations with obesity-related metabolic disease.
200 and insulin resistance in the development of obesity-related metabolic diseases.
201 tion of adipose is a critical determinant of obesity-related metabolic diseases.
202 ial therapeutic target to combat obesity and obesity-related metabolic diseases.
203 t extensively as a treatment for obesity and obesity-related metabolic diseases.
204 may be a new therapeutic target for treating obesity-related metabolic diseases.
205 s endocrine-disrupting chemicals (EDCs) with obesity-related metabolic diseases.
206                                              Obesity-related metabolic disorders are characterized by
207 rebiotic agents to prevent gut dysbiosis and obesity-related metabolic disorders in obese individuals
208 n sensitivity and has the potential to treat obesity-related metabolic disorders.
209 ntial therapeutic and diagnostic targets for obesity-related metabolic disorders.
210 ty acids have not been fully investigated in obesity-related metabolic disorders.
211  Nonalcoholic fatty liver is associated with obesity-related metabolic disturbances, but little is kn
212 lyphenols, cumulative effects in attenuating obesity-related metabolic dysfunction may require increa
213 gy, prevention, and treatment of obesity and obesity-related metabolic dysfunction, including type 2
214 erventions aimed at ameliorating obesity and obesity-related metabolic dysfunction.
215 ontributor in the development of obesity and obesity-related metabolic dysfunctions, amongst others.
216 may provide a novel therapeutic approach for obesity-related metabolic dysregulation and, especially,
217 tory state present in obesity contributes to obesity-related metabolic dysregulation, including nonal
218 2 (double knockout; DKO) revealed aggravated obesity-related metabolic dysregulation, reduced insulin
219 a lineage associated with protection against obesity-related metabolic events.
220 istory of major depressive disorder (MDD) on obesity-related metabolic responses to high-fat meals.
221 eas CCR5 expression was positively linked to obesity-related metabolic traits.
222 bolomic profiles associated with obesity and obesity-related metabolic traits.
223                   Exercise training reversed obesity-related mitochondrial derangements as evidenced
224  in studies on the role of gut microbiota in obesity-related mood disorders.
225 reported role of FABP4 in the development of obesity-related morbidities, including insulin resistanc
226  loss control groups and in individuals with obesity-related morbidities.
227  to adverse cardiovascular outcomes or other obesity-related morbidity, such as type 2 diabetes.
228 dominantly younger women with a low inherent obesity-related mortality risk.
229 at adiponectin may play an important role in obesity-related myelomagenesis.
230 ure, we identified, reviewed, and classified obesity-related myths and presumptions.
231                          We identified seven obesity-related myths concerning the effects of small su
232 d to improve liver function in patients with obesity-related NAFLD.
233 sted that ITCH deficiency protects mice from obesity-related nonalcoholic fatty liver disease.
234 igher odds of overweight, obesity, and other obesity-related outcomes [body mass index (BMI), BMI z s
235    However, there is marked heterogeneity in obesity-related outcomes among individuals.
236 : does early-life exposure to BPA affect the obesity-related outcomes body weight, fat (pad) weight,
237 or underserved children where disparities in obesity-related outcomes exist.
238 icals of potential interest for diabetes- or obesity-related outcomes using high-throughput screening
239 studies of urinary biomarkers and obesity or obesity-related outcomes, alternative metrics such as ur
240 n studies of urinary analytes and obesity or obesity-related outcomes, controlling for creatinine cou
241 nery consumption and overweight, obesity, or obesity-related outcomes.
242 d to the beneficial action of fruits against obesity-related oxidative stress.
243 postulated to be a major contributor to many obesity-related pathologies.
244 s that may be involved in the development of obesity-related pathologies.
245   Thus, adipose-resident ILC1s contribute to obesity-related pathology in response to dysregulated lo
246 in WAT and a potential target for mitigating obesity-related pathology.
247 rs and liver gene expression traits on mouse obesity related phenotypes, including weight, cholestero
248                We hypothesized that specific obesity-related phenotypes are associated with distinct
249 eutic target for influencing health span and obesity-related phenotypes as well as tumor growth.
250 nic chemicals results in the transmission of obesity-related phenotypes through at least three genera
251 METHODS AND We evaluated the associations of obesity-related phenotypes, including central adiposity,
252 ble genetic influence and is associated with obesity-related phenotypes.
253 od epilepsy and examine associations between obesity-related pregnancy and neonatal complications and
254         The diagnosis of epilepsy as well as obesity-related pregnancy and neonatal complications wer
255 weight or obese mothers was not explained by obesity-related pregnancy or neonatal complications.
256                                              Obesity-related reduction in pulmonary function is a pos
257 cumulation in the kidney (fatty kidney) with obesity-related renal disease.
258 der animals appear to be more susceptible to obesity-related resistance than young animals.
259                        Our results show that obesity-related risk allele carriers of FTO gene show do
260                                Moreover, the obesity-related risk allele is associated with reduced m
261   Women self-reported body weight along with obesity-related risk factors on baseline and annual foll
262    These GPCs may be sensitive indicators of obesity-related risk for CVD outcomes in adults, and may
263 es increased with BMI and the overweight and obesity-related risks were highest for extremely preterm
264 al role of B7 costimulation in the course of obesity-related sequelae, particularly NASH.
265     The authors evaluated the association of obesity-related single nucleotide polymorphisms (SNPs) w
266 ygenic risk score (PRS) comprising 28 common obesity-related single-nucleotide polymorphisms identifi
267 rations in MAIT cells may be contributing to obesity-related sterile inflammation and insulin resista
268                                              Obesity-related structural and functional changes in the
269                                              Obesity-related sub-acute chronic inflammation has been
270 2 antagonism in the treatment of obesity and obesity-related syndromes.
271 black tea (Camellia sinensis) theaflavins on obesity-related targets.
272 ory response is a key etiologic component of obesity-related tissue inflammation and insulin resistan
273 whether SNPs in WNT4 and WNT5A contribute to obesity related traits in Han Chinese population.
274  in studies linking blood gene expression to obesity related traits, whether the fasted or fed state
275 y 69 new genes significantly associated with obesity-related traits (BMI, lipids and height).
276 d a different degree of genetic overlap with obesity-related traits (body mass index [BMI] and levels
277  and examined their genetic relation with 10 obesity-related traits [body mass index (BMI), waist cir
278 d advice provides extra benefits in reducing obesity-related traits compared with the benefits of con
279                                     However, obesity-related traits have not been incorporated in pri
280 is was performed between genetic markers and obesity-related traits i.e., anthropometry, body composi
281 d colleagues show that regional variation of obesity-related traits in a Scottish population is influ
282 ied 16 loci incontrovertibly associated with obesity-related traits in adults.
283 ences on serum carotenoid concentrations and obesity-related traits in Mexican American (MA) children
284  risk had a greater effect on a reduction of obesity-related traits in risk carriers than in nonrisk
285 ons between atypical depressive symptoms and obesity-related traits may arise from shared pathophysio
286                                Using data on obesity-related traits of 11,000 Scottish individuals w
287                               Interestingly, obesity-related traits were associated with distinct asp
288 ide polymorphisms (SNPs) possibly acting via obesity-related traits, hsCRP, based on 16 SNPs from gen
289 dence of gene-smoking interaction (GxSMK) on obesity-related traits.
290 effects in non-candidate genes, at least for obesity-related traits.
291  likely functional polymorphisms influencing obesity-related traits.
292 en investigating the genetic contribution to obesity-related traits.
293 d persist more than other complications, and obesity-related type 2 diabetes could have increasing ef
294 vent about 274,000-309,000 incident cases of obesity-related type 2 diabetes over the two decades aft
295                                 In contrast, obesity-related variables (BMI, weight, leptin) exerted
296                        Baseline insulin- and obesity-related variables exert different patterns of pr
297                                              Obesity-related variables included weight, body mass ind
298 tudies of age at menarche identified several obesity-related variants.
299           We conclude that ceramide mediates obesity-related vascular dysfunction by a mechanism that
300 that represents a novel target for reversing obesity-related vascular dysfunction.

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