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1 ice an HFD for 16 wk to initiate HFD-induced metabolic disorder.
2 r, cardiovascular disease, autoimmunity, and metabolic disorder.
3 robiotics to attenuate high-fat diet-related metabolic disorder.
4 nd adoptive transfer of AT1-ILCs exacerbated metabolic disorder.
5 dities, including cardiovascular disease and metabolic disorder.
6 as a consideration in the treatment of liver metabolic disorders.
7 , non-alcoholic steatohepatitis, and related metabolic disorders.
8 4 in managing obesity and obesity-associated metabolic disorders.
9 e (NNMT), an enzyme implicated in cancer and metabolic disorders.
10 ts a therapeutic avenue for the treatment of metabolic disorders.
11 mproved therapeutic strategies for combating metabolic disorders.
12 ssociated with increased risk for immune and metabolic disorders.
13 ntergenerational inheritance of diet-induced metabolic disorders.
14 iabetes may lead to promising treatments for metabolic disorders.
15 d has the potential to treat obesity-related metabolic disorders.
16 contribute to muscle wasting associated with metabolic disorders.
17 and excessive storage is a feature of common metabolic disorders.
18 le similar to dysbiotic states described for metabolic disorders.
19 rone is associated with all "Western" cardio-metabolic disorders.
20 c and diagnostic targets for obesity-related metabolic disorders.
21 who may be at higher risk for cardiovascular/metabolic disorders.
22 Indians are known to be at elevated risk for metabolic disorders.
23 cluster of cardiovascular (hypertension) and metabolic disorders.
24 -MCA may be a candidate for the treatment of metabolic disorders.
25 ives to combat the rising global epidemic of metabolic disorders.
26 be associated with chronic liver disease and metabolic disorders.
27 reat neuroinflammation, obesity, and related metabolic disorders.
28 rnutrition increases the risk of obesity and metabolic disorders.
29 ce their pathogenic role in inflammatory and metabolic disorders.
30 on that contributes to bone dysregulation in metabolic disorders.
31 omic loci contributing to cardiovascular and metabolic disorders.
32 nalog, could be developed as a treatment for metabolic disorders.
33 broader significance to other peripheral and metabolic disorders.
34 mation in the pathophysiology of obesity and metabolic disorders.
35 ed to aging, neurodegenerative diseases, and metabolic disorders.
36 rapeutic route to combat obesity and related metabolic disorders.
37 al approach to reversing obesity and related metabolic disorders.
38 and represents a possible new drug target in metabolic disorders.
39 l treatment for human obesity and associated metabolic disorders.
40 e treatment of stress-related psychiatric or metabolic disorders.
41 rnal desynchrony, which promotes obesity and metabolic disorders.
42 receptor (LepR) leads to severe obesity and metabolic disorders.
43 e also resistant to diet-induced obesity and metabolic disorders.
44 vators in the treatment of insulin-resistant metabolic disorders.
45 tors are required for long-term treatment of metabolic disorders.
46 investigate the connection between IL-22 and metabolic disorders.
47 n, and reduce cardiac derangements caused by metabolic disorders.
48 raphical disparities, such as autoimmune and metabolic disorders.
49 d with high-fat diet are prone to developing metabolic disorders.
50 in energy expenditure and in age-associated metabolic disorders.
51 arning and are implicated in glucose-related metabolic disorders.
52 but these pathways are often dysregulated in metabolic disorders.
53 ortant role in determining susceptibility to metabolic disorders.
54 dults opens attractive perspectives to treat metabolic disorders.
55 y contributes to the pathogenesis of diverse metabolic disorders.
56 utive enzymatic treatment of other inherited metabolic disorders.
57 a inhibitors in the treatment of obesity and metabolic disorders.
58 teria induce a metabolic endotoxemia leading metabolic disorders.
59 LT2B1b as a potential therapeutic target for metabolic disorders.
60 olong sitting has been found associated with metabolic disorders.
61 egy for combating obesity and its associated metabolic disorders.
62 romising drug candidate for the treatment of metabolic disorders.
63 hat has recently been implicated in mood and metabolic disorders.
64 ctive strategy to inhibit the development of metabolic disorders.
65 cidate the effect of KHK inhibition on these metabolic disorders.
66 ces dysbiosis, which is associated with host metabolic disorders.
67 present a potential drug target for treating metabolic disorders.
68 eratrol as a human nutritional supplement in metabolic disorders.
69 ch ratios as a new clinical biomarker for Fe metabolic disorders.
70 besity is a primary risk factor for multiple metabolic disorders.
71 ls as potential risk factors for obesity and metabolic disorders.
72 of photosensitivity to inherited genetic or metabolic disorders.
73 nt and nonmalignant hematologic diseases and metabolic disorders.
74 cRNA roles in complex neurodevelopmental and metabolic disorders.
75 ant for the treatment of obesity and related metabolic disorders.
76 , is a sensitive clinical biomarker for iron metabolic disorders.
77 etabolism that mitigates the consequences of metabolic disorders.
78 and potentially new targets in treatment of metabolic disorders.
79 molecule activators of AMPK for treatment of metabolic disorders.
80 ly possible applications in the treatment of metabolic disorders.
81 es a promising approach for the treatment of metabolic disorders.
82 a risk factor for various cardiovascular and metabolic disorders.
83 ential cofactor in inflammatory diseases and metabolic disorders.
84 as the premature aging disease progeria and metabolic disorders.
85 oordinated treatment of functionally related metabolic disorders.
86 n or treatment of obesity and its associated metabolic disorders.
87 ic target for the intervention of cancer and metabolic disorders.
88 und benefits in the treatment of obesity and metabolic disorders.
89 utic strategy to protect against obesity and metabolic disorders.
90 that central vascular impairments may cause metabolic disorders.
91 sing CRISPR/Cas9, as a new strategy to model metabolic disorders.
92 ating obesity, diabetes and their associated metabolic disorders.
93 e promising agents for treating a variety of metabolic disorders.
94 cally relevant for the prevention of glucose metabolic disorders.
95 munity to pathogens/tumors and in autoimmune/metabolic disorders.
96 safety profiles in the treatment of complex metabolic disorders.
97 ptation to ER stress associated with chronic metabolic disorders.
98 in the aetiology of sleep, mental health and metabolic disorders.
99 t been fully investigated in obesity-related metabolic disorders.
100 n protecting against HFD-induced obesity and metabolic disorders.
101 logical iron reduction on the development of metabolic disorders.
102 as a protective factor in obesity and other metabolic disorders.
103 tential therapeutic target for mTORC1-driven metabolic disorders.
104 esting potential target for the treatment of metabolic disorders.
105 eurodegenerative diseases are accompanied by metabolic disorders.
106 rimary cause of obesity and other eating and metabolic disorders.
107 n and oxidative stress in an animal model of metabolic disorders.
108 Its dysregulation causes diabetes and other metabolic disorders.
109 ight serve as a therapeutic target in common metabolic disorders.
110 ising target for therapeutic intervention in metabolic disorders.
111 ency hematologic disease (15.4%; p = 0.020), metabolic disorder (8.1%; p < 0.001), or solid malignanc
113 Maple syrup urine disease (MSUD) is a rare metabolic disorder, affecting the metabolism of branched
114 obesity (MO) programs offspring obesity and metabolic disorders, although the underlying mechanisms
115 ovide one of the first examples of ERT for a metabolic disorder and suggest that PEGylated CBS should
119 ons have not been described in OTCD or other metabolic disorders and are not an associated finding in
120 ulin resistance are among the most prevalent metabolic disorders and are tightly associated with obes
125 processing of IL1beta, contributing to many metabolic disorders and directing adipocytes to a more i
126 inhibition approaches for treating other PIP metabolic disorders and highlight the importance of modi
127 nding of the function of innate receptors in metabolic disorders and implicate TLR3 as a key control
128 ntially in those who are obese or have other metabolic disorders and in response to ingested nutrient
130 y liver disease is one of the most prevalent metabolic disorders and it tightly associates with obesi
131 this coupling is associated with a number of metabolic disorders and neurodegenerative diseases inclu
132 with a high impact on public health, such as metabolic disorders and neurodegenerative diseases.
135 TX could represent a novel strategy to treat metabolic disorders and overcome current limitations of
136 y, potential functional interactions between metabolic disorders and psychiatric diseases are discuss
137 This knowledge has enabled the treatment of metabolic disorders and the development of antivirals an
138 we were able to show the true prevalence of metabolic disorders and therefore provided a valuable co
143 ion, autoimmune diseases, cardiovascular and metabolic disorders, and cancer reported in shift worker
146 tant information about inherited or acquired metabolic disorders, and for monitoring the biochemical
155 triggered significant inflammation and host metabolic disorders as a result of activation of bacteri
156 ently become a highly interesting target for metabolic disorders as well as for hepatitis C virus (HC
157 l polycystic ovary syndrome (PCOS), a common metabolic disorder associated with excess circulating an
159 ch reduced with this technology, diminishing metabolic disorders associated with cooling and minimizi
160 ide a potential therapeutic means to control metabolic disorders associated with its dysregulated sec
163 This suggests the presence of an underlying metabolic disorder beyond fatty liver that may be causat
164 effects and mechanisms of PM2.5 exposure in metabolic disorders, but also revealed the pleotrophic a
165 ed in neurodegenerative, cardiovascular, and metabolic disorders, but the role of phospholipids, part
166 of CB1 ameliorates Diet-Induced Obesity and metabolic disorder by modulating macrophage inflammatory
167 nd shows that susceptibility of offspring to metabolic disorder can likely be attributed to epigeneti
168 remendous opportunities for the treatment of metabolic disorders, cancer, autoimmune diseases and etc
172 n metabolism that can accumulate in numerous metabolic disorders, causing neurological dysfunction ra
173 irment in patients with diabetes mellitus, a metabolic disorder characterized by chronic hyperglycaem
174 Niemann-Pick Type C disease (NPC) is a rare metabolic disorder characterized by disruption of normal
178 iderable value to the treatment algorithm of metabolic disorders characterized by dysregulated fatty
179 itive association between obesity-associated metabolic disorders (e.g., hyperlipidemia and diabetes)
181 phalopathy (eg, caused by hepatic failure or metabolic disorders), encephalitis (caused by direct vir
182 tion, pneumonia, septicemia, nutritional and metabolic disorders, esophagitis, gastroenteritis, and d
183 gs should raise suspicion for this treatable metabolic disorder, especially when in the context of re
184 in the development of childhood obesity and metabolic disorders, especially when exposure occurs ear
186 at restore physiological feedback control in metabolic disorders foster advanced gene- and cell-based
190 pesticides (OCPs) have been linked to adult metabolic disorders; however, few studies have examined
191 rtant role in the development of obesity and metabolic disorders; however, it has not been fully unde
192 sing, metabolic switch implicated in various metabolic disorders; however, its role in inflammation i
193 ical molecular link between inflammation and metabolic disorders; however, the role of adipocyte IKKb
199 ptibility locus for dyslipidemia and related metabolic disorders in congenic and subcongenic rat stra
207 ful for treating HFD-induced skeletal muscle metabolic disorders in such pathophysiological condition
208 from HFD males into normal zygotes generated metabolic disorders in the F1 offspring and altered gene
213 risk in pregnancies complicated by maternal metabolic disorders, including diabetes and obesity.
214 stress, whereas superfluous lipolysis causes metabolic disorders, including dyslipidemia and hepatic
215 ila treatment reversed high-fat diet-induced metabolic disorders, including fat-mass gain, metabolic
216 omeostasis and its alterations contribute to metabolic disorders, including fatty liver and diabetes.
217 n obese mice and reversed the progression of metabolic disorders, including hepatic steatosis, glucos
219 s largely unknown despite important roles in metabolic disorders, including obesity and nonalcoholic
220 pathogenic factor that characterizes various metabolic disorders, including obesity and type 2 diabet
222 sue compartments is tightly linked to severe metabolic disorders, including obesity, metabolic syndro
226 ents a potential target for the treatment of metabolic disorders, including type 2 diabetes and obesi
227 p duration has been associated with risk for metabolic disorders, including weight gain, diabetes, ob
228 eficiency diseases or obesity and associated metabolic disorders, increased risk of cardiovascular di
229 chanism by which hypercholesterolemia or any metabolic disorder increases cancer risk remains unknown
230 training reduced the severity of most of the metabolic disorders induced by a fructose-rich diet and
231 aerobic, strength, and combined training on metabolic disorders induced by a fructose-rich diet.
232 se tissue endocannabinoid levels and prevent metabolic disorders induced by a later high-fat diet (HF
233 results suggest a novel mechanism by which a metabolic disorder induces epigenetic changes to reduce
234 the treatment of conditions associated with metabolic disorders, inhibit KSHV lytic replication.
236 Impaired AKT activation is a key factor in metabolic disorders involving insulin resistance, wherea
237 ension and related cardiovascular, renal and metabolic disorders is likely to become even more import
239 ormerly obese individuals are susceptible to metabolic disorders later in life, even after lifestyle
241 ncludes the sections: Hypertension, Imaging, Metabolic Disorders & Lipids, Neurovascular & Neurodegen
242 ncludes the sections: Hypertension, Imaging, Metabolic Disorders & Lipids, Neurovascular & Neurodegen
243 Part Two includes the sections: Imaging, Metabolic Disorders & Lipids, Rhythm Disorders, Statisti
244 Part Two includes the sections: Imaging, Metabolic Disorders & Lipids, Rhythm Disorders, Statisti
245 urea cycle disorders (UCDs), rare inherited metabolic disorders manifested by hyperammonemia and neu
248 etroviral therapy frequently develop various metabolic disorders, neurocognitive abnormalities, and c
250 Dyslipidemia is a frequent component of the metabolic disorder of diabetic patients contributing to
251 e intermittent porphyria (AIP), an inherited metabolic disorder of heme biosynthesis in which an accu
254 novel therapeutic targets for patients with metabolic disorder or T2D who suffer from anxiety and de
261 vity leads to debilitating neuroendocrine or metabolic disorders such as Cushing's syndrome (CS).
262 he association between sleep deprivation and metabolic disorders such as diabetes and obesity require
265 zing radiation increases the risk of chronic metabolic disorders such as insulin resistance and type
266 ntributes to the dyslipidemia seen in common metabolic disorders such as insulin-resistant states and
267 Moreover, we also discuss advances on how metabolic disorders such as metabolic syndrome and diabe
268 in epigenetic regulation are associated with metabolic disorders such as obesity and diabetes that ar
272 ne with age and is implicated in age-related metabolic disorders such as obesity and type 2 diabetes
273 between intestinal microbial composition and metabolic disorders such as obesity and type 2 diabetes.
274 ute an appealing target for the treatment of metabolic disorders such as obesity, diabetes and hyperl
275 ection between an altered gut microbiota and metabolic disorders such as obesity, diabetes, and cardi
276 rcadian clock disruption are associated with metabolic disorders such as obesity, insulin resistance,
277 ontribute to neuronal function as well as to metabolic disorders such as type 2 diabetes mellitus, ob
278 tis has been implicated as a risk factor for metabolic disorders such as type 2 diabetes, atheroscler
279 R stress has been implicated in a variety of metabolic disorders, such as obesity and type 2 diabetes
280 cerbate the development and/or prevalence of metabolic disorders, such as obesity, is currently of gr
281 considered promising therapeutics for common metabolic disorders, such as obesity, liver steatosis, a
283 uman adipose tissue (hAT) is a key player in metabolic disorders, such as Type 2 Diabetes Mellitus (T
284 AIT cell abnormalities in patients harboring metabolic disorders, suggesting their potential role in
285 HCS cause holocarboxylase deficiency, a rare metabolic disorder that can be life-threatening if left
286 liver disease (NAFLD), a widespread hepatic metabolic disorder that is believed to be a risk factor
287 r, had preventive and therapeutic effects on metabolic disorders that were dependent on intestine HIF
288 ced gene expression patterns associated with metabolic disorders that were identified in blastocysts
289 sorders, such as cardiovascular diseases and metabolic disorders, that influence significantly (and i
290 in the development of obesity and associated metabolic disorders, the incidence of metabolic syndrome
291 ed lipolysis is linked to the development of metabolic disorders, the inhibition of ATGL by G0S2-deri
292 are linked to diseases spanning genetic and metabolic disorders to cancer and neurodegeneration.
294 een shown to exhibit increased prevalence of metabolic disorders (type-2 diabetes, cardiovascular dis
297 ckout model demonstrates multiple immune and metabolic disorders, we investigated the role of each re
298 sed dysregulated splicing events and hepatic metabolic disorders, which trigger endoplasmic reticulum
299 iencies (MADDs) are a heterogeneous group of metabolic disorders with combined respiratory-chain defi
300 er, the role of adipocytes in linking energy metabolic disorders with insulin regulation is unknown i
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