ライフサイエンスコーパス: metabolic disease

1 has also emerged as a strategy to attenuate metabolic disease.

2 n a constant body temperature and counteract metabolic disease.

3 ing hepatic glucose metabolism in health and metabolic disease.

4 ticularly harmful role in the development of metabolic disease.

5 se, stable metabolic disease, or progressive metabolic disease.

6 uggest its therapeutic potential in treating metabolic disease.

7 to novel strategies to uncouple obesity from metabolic disease.

8 elopment of therapeutic approaches to manage metabolic disease.

9 hole-body glucose regulation in diet-induced metabolic disease.

10 rther investigation into the role of oxFA in metabolic disease.

11 ro overnutrition can predispose offspring to metabolic disease.

12 ng a potential approach for the treatment of metabolic disease.

13 ng human adipose tissue function and role in metabolic disease.

14 ial as investigational metabolites to modify metabolic disease.

15 lp to elucidate disease-specific pathways in metabolic disease.

16 isioned drugs targeting this tissue to treat metabolic disease.

17 /thermogenesis axis that combats obesity and metabolic disease.

18 ipogenic differentiation and obesity-related metabolic disease.

19 w their perturbations contribute to systemic metabolic disease.

20 ical regulator of fetal programming of adult metabolic disease.

21 ngenital generalized lipodystrophy (CGL) and metabolic disease.

22 hy and inflammation, thereby contributing to metabolic disease.

23 they are not homologous in the aetiology of metabolic disease.

24 hesis of C17:0 and recognizing its link with metabolic disease.

25 pability could be leveraged as a therapy for metabolic disease.

26 ionships among fatty acids, metabolites, and metabolic disease.

27 erm delivery of low birth weight infants and metabolic disease.

28 lays an important role in the development of metabolic disease.

29 function is relevant in both homeostasis and metabolic disease.

30 nimals against hypothermia and to counteract metabolic disease.

31 y as indicated for management of obesity and metabolic disease.

32 s disease (AD) can, in part, be considered a metabolic disease.

33 could eventually be a strategy for improving metabolic disease.

34 ding new insight into the pathophysiology of metabolic disease.

35 es to alleviate the metaflammation typifying metabolic disease.

36 c genes known to have perturbations in human metabolic disease.

37 of a microbial peptide-based therapeutic for metabolic disease.

38 a prerequisite for gout and associated with metabolic disease.

39 3-fold increased risk of cardiovascular and metabolic disease.

40 ortant role in physiological homeostasis and metabolic disease.

41 can program offspring for increased risk for metabolic disease.

42 rrelate with cardiovascular risk factors and metabolic disease.

43 promote skeletal muscle health and attenuate metabolic disease.

44 apeutics to reduce ceramide levels to combat metabolic disease.

45 g the protective effects of estrogen against metabolic disease.

46 g how changes in creatine metabolism lead to metabolic disease.

47 tress in the nutritional programming of this metabolic disease.

48 capacity and protects against cardiovascular/metabolic disease.

49 eropathogens(2,3,9) and for the treatment of metabolic diseases.

50 ns with chronic infectious, inflammatory, or metabolic diseases.

51 ctions in many cardiovascular, pulmonary and metabolic diseases.

52 rage, but which now confer susceptibility to metabolic diseases.

53 to complications such as catheter sepsis and metabolic diseases.

54 ndidate for the treatment of obesity-related metabolic diseases.

55 ween circadian rhythms and the microbiome in metabolic diseases.

56 ut microbiome, IL-17/IL-22, and the onset of metabolic diseases.

57 stance is associated with the development of metabolic diseases.

58 rage in macrophages, a cell type involved in metabolic diseases.

59 ulated, and its disturbance is implicated in metabolic diseases.

60 t decision in cardiovascular, pulmonary, and metabolic diseases.

61 on the risk of developing cardiovascular and metabolic diseases.

62 ative diseases, certain cancer types, and in metabolic diseases.

63 tance and higher risk of type 2 diabetes and metabolic diseases.

64 and are suggested as candidates for treating metabolic diseases.

65 of complex lipid interactions that regulate metabolic diseases.

66 h, as their dysfunction has been linked with metabolic diseases.

67 issues and a potential therapeutic target in metabolic diseases.

68 development, which predisposes offspring to metabolic diseases.

69 ully explain obesity's propensity to promote metabolic diseases.

70 rovide new ways to treat obesity and related metabolic diseases.

71 are to diagnose kidney and urinary tract and metabolic diseases.

72 pids, which may have implications diagnosing metabolic diseases.

73 new strategy to control obesity and related metabolic diseases.

74 ber of signaling pathways that could lead to metabolic diseases.

75 sign against a repertoire of eFGF-associated metabolic diseases.

76 erapeutic to treat PKU and potentially other metabolic diseases.

77 PA1 activity with potential implications for metabolic diseases.

78 eutic agents for treating these inflammatory metabolic diseases.

79 rtant therapeutic approach to manage various metabolic diseases.

80 lipid droplets (LD) has been linked to many metabolic diseases.

81 for susceptibility to other neurological and metabolic diseases.

82 prevention and treatment of obesity-induced metabolic diseases.

83 ways, which may indicate its significance in metabolic diseases.

84 ral human cancers and has been implicated in metabolic diseases.

85 nteractions contribute to the development of metabolic diseases.

86 in lipid homeostasis, with impact on various metabolic diseases.

87 n and have been implicated in autoimmune and metabolic diseases.

88 ystem, muscle development, and especially to metabolic diseases.

89 oxidation whose plasma levels associate with metabolic diseases.

90 entral role in susceptibility to obesity and metabolic diseases.

91 ted FXR as therapeutic target in hepatic and metabolic diseases.

92 treating obesity-associated inflammatory and metabolic diseases.

93 tential impact in the understanding of human metabolic diseases.

94 ntly contribute to the growing prevalence of metabolic diseases.

95 t for gender dissimilarity in metabolism and metabolic diseases.

96 and novel therapeutic target for OP-related metabolic diseases.

97 upting chemicals (EDCs) with obesity-related metabolic diseases.

98 s, in adipose tissue (AT) are deleterious in metabolic diseases.

99 ulate cg00574958 methylation and the risk of metabolic diseases.

100 rturbations applied to genes associated with metabolic diseases.

101 ool for the identification of drugs to treat metabolic diseases.

102 the major risk factor for cardiovascular and metabolic diseases.

103 ancer and neurodegenerative, autoimmune, and metabolic diseases.

104 nges in the fungal communities can aggravate metabolic diseases.

105 ction are associated with the development of metabolic diseases.

106 ns for the treatment of diabetes and related metabolic diseases.

107 methylation, thereby increasing the risk of metabolic diseases.

108 t members known to play an important role in metabolic diseases.

109 at may allow for therapeutic interference in metabolic diseases.

110 ing cells plays a role in the development of metabolic diseases.

111 ctivation also reduced high-fat diet-induced metabolic diseases.

112 on-haematopoietic cells in neurodegenerative metabolic diseases.

113 rug targets for treating obesity and related metabolic diseases.

114 role of WNT-CTNNB1 signaling in obesity and metabolic diseases.

115 humans causes obesity and is associated with metabolic diseases(1).

116 t with hepatic injury because of a suspected metabolic disease; - 1 incidental finding revealed befor

117 uberous sclerosis complex (9 of 11 [81.8%]), metabolic diseases (11 of 14 [78.6%]), and brain malform

118 categories: (1) endocrine, nutritional, and metabolic diseases; (2) nervous diseases; (3) circulator

119 (1) leukodystrophies; (2) deficiency-related metabolic diseases; (3) genetic and acquired toxic/metab

120 ng the inhibition of ACLY as a treatment for metabolic diseases(8).

121 otyping of individuals at increased risk for metabolic diseases, a reliable automated segmentation of

122 etes(T2D) are the most prevalent and serious metabolic diseases affecting people worldwide.

123 which develop obesity and provide models of metabolic disease alongside early stage T2D.

124 posure to DDTs may contribute to the risk of metabolic disease among Asian Indians by affecting hepat

125 normal Cu levels are associated with anemia, metabolic disease and cancer.

126 nvestigate the contribution of iNKT cells to metabolic disease and found a pathogenic role of these c

127 pulation, is more prevalent in patients with metabolic disease and obesity, progresses to cirrhosis i

128 ythms are a feature of aging associated with metabolic disease and reduced levels of NAD(+), yet whet

129 t LSG may have weight-independent effects on metabolic disease and should be considered in the treatm

130 licate TM6SF2 as a causative gene underlying metabolic disease and trait associations at the 19p13.11

131 birth weight (LBW) have an increased risk of metabolic disease and type 2 diabetes.

132 ion, a dietary regimen that protects against metabolic diseases and aging, represses cancer growth an

133 eir function can protect against age-related metabolic diseases and can extend lifespan.

134 tense interest in targeting SCD1 for various metabolic diseases and cancers.

135 uropsychiatric disease to cardiovascular and metabolic diseases and Crohn's disease.

136 ents a potential target for the treatment of metabolic diseases and has been extensively investigated

137 e microbial components of these interrelated metabolic diseases and identify dietary and medication e

138 Paolo Hospital, Milan, outpatient clinic for metabolic diseases and previously at another eye center.

139 ation of the genetic underpinnings of common metabolic diseases and traits, highlighting the inherent

140 mice are resistant to diet-induced obesity, metabolic disease, and circadian disruption associated w

141 es to additional threats, such as allergens, metabolic disease, and other pathogens.

142 of feeding behavior is necessary to prevent metabolic disease, and thus it is imperative that molecu

143 isease, cholestatic liver disease, endocrine/metabolic diseases, and hematologic/lymphoproliferative

144 inal microbiome contribute to development of metabolic diseases, and recent advances, such as the eff

145 Chronic inflammation in many infectious and metabolic diseases, and some cancers, is accompanied by

146 CI, 0.65-1.12]) after adjustment for chronic metabolic diseases, antibiotic use during middle adultho

147 vity is limited and food supply is abundant, metabolic diseases are becoming a serious epidemic.

148 Metabolic diseases are increasing among adolescents with

149 n major depressive disorder (MDD) and cardio-metabolic diseases are still poorly understood.

150 for myriad neurological, cardiovascular and metabolic diseases as well as for cancer and immunomodul

151 ers, to include common neurodegenerative and metabolic diseases, as well as cancer.

152 d arthritis and inflammatory bowel disease), metabolic diseases (atherosclerosis, diabetes and obesit

153 uption of this molecular clock can result in metabolic disease but its potential regulation by immune

154 based diets has been linked to lower risk of metabolic diseases but the effect on abdominal fat distr

155 fects in the mucus layer have been linked to metabolic diseases, but previous studies predominantly i

156 is important for understanding mechanisms of metabolic diseases, but structural organization of mitoc

157 factors contributing to the pathogenesis of metabolic diseases, but the molecular regulators that dr

158 agonists could also improve obesity-related metabolic disease by increasing brown adipose tissue (BA

159 flammation in chronic inflammatory or cardio-metabolic diseases by generating a feed-forward loop bet

160 Inflammatory and metabolic diseases can originate during early-life and h

161 metabolic pathways and connected with human metabolic diseases, central nervous system diseases, and

162 Type 2 diabetes is a chronic metabolic disease characterized by pancreatic beta-cell

163 ith T2D (n = 153) from German population and metabolic disease cohorts.

164 ose tissue (WAT) - a key contributor in many metabolic diseases - contributes about one fourth of a h

165 s 2 (SARS-CoV-2) and an existing pandemic of metabolic disease driven by obesity.

166 estern lifestyle is linked to autoimmune and metabolic diseases, driven by changes in diet and gut mi

167 ondrial disorders are genetically determined metabolic diseases due to a biochemical deficiency of th

168 s of glycosylation (CDG) are a group of rare metabolic diseases, due to impaired protein and lipid gl

169 n registry and network for Intoxication type Metabolic Diseases (E-IMD).

170 e interventions to limit the transmission of metabolic disease from the obese mother to her infant ar

171 ce of inborn errors in 1901, a vast array of metabolic diseases has been identified and characterized

172 The incidence of diabetes, obesity, and metabolic diseases has reached an epidemic status worldw

173 kyl substances (PFASs) may increase risk for metabolic diseases; however, epidemiologic evidence is l

174 ave a greater risk for childhood obesity and metabolic diseases; however, the underlying biological m

175 ) gene to be associated with reduced risk of metabolic diseases (hypertriglyceridemia, obesity, type

176 Mid-life metabolic disease (ie, obesity, diabetes, and prediabete

177 pregnancy (ICP) can predispose offspring to metabolic disease in adulthood, likely due to a combinat

178 to induce ATM accumulation, and to transfer metabolic disease in control mice.

179 sity confers significant risk for developing metabolic disease in obesity whereas preferential expans

180 Poor maternal diet can lead to metabolic disease in offspring, whereas maternal exercis

181 ween maternal obesity and the development of metabolic disease in offspring.

182 nd hypertriglyceridemia, which can result in metabolic disease in susceptible women.

183 ervention in pregnancy to reduce features of metabolic disease in the offspring of hypercholanemic mo

184 tionale for how NAC can prevent the onset of metabolic disease in the offspring of mothers who consum

185 ratio with CPT1A-cg00574958, and the risk of metabolic diseases in 3 populations (Genetics of Lipid L

186 However, its role in metabolic diseases in adolescents is not well-studied.

187 lationships between gut microbiota, BAs, and metabolic diseases in both genders.

188 eutic targets that may effectively alleviate metabolic diseases in humans as they do in animal models

189 ngal communities and inspect their impact on metabolic diseases in humans.

190 spose to the development of inflammatory and metabolic diseases in later life.

191 netically higher testosterone is harmful for metabolic diseases in women but beneficial in men.

192 idney disease, obstructive sleep apnoea, and metabolic disease including diabetes and obesity.

193 nd their dysfunctions, which lead to several metabolic diseases including obesity or type 2 diabetes.

194 with an increased risk of developing chronic metabolic diseases including obesity, non-alcoholic fatt

195 e, and less invasive therapeutic options for metabolic disease, including inhibitors of TGF-beta sign

196 /IL-22 were linked to established markers of metabolic disease, including insulin sensitivity.

197 a potential cell source for the treatment of metabolic disease, including type 2 diabetes.

198 ghlighted the gut microbiota's importance in metabolic disease, including Type II Diabetes Mellitus (

199 ASH is associated with many widely occurring metabolic diseases, including obesity and type 2 diabete

200 as been linked to the development of chronic metabolic diseases, including obesity, hepatic steatosis

201 1 (mTORC1) signalling increases the risk for metabolic diseases, including type 2 diabetes.

202 ith clinical data, which shows that mid-life metabolic disease increases VCID risk, particularly in f

203 connect immune-mediated skin conditions and metabolic diseases, independent of confounding factors.

204 is may be a potential therapeutic target for metabolic disease intervention.

205 Obesity-linked metabolic disease is mechanistically associated with the

206 n adipose tissue mechanics and their role in metabolic disease is poorly defined.

207 there is any uncharted backyard left in the metabolic disease landscape.

208 tion of the carotid body plays a key role in metabolic diseases like type 2 diabetes.

209 al novel therapeutic strategies for treating metabolic diseases linked to lipotoxicity.

210 Susceptibility to metabolic diseases may be influenced by mitochondrial ge

211 Cardiovascular-metabolic disease, microscopic misdiagnosis, and delay i

212 This new concept of metabolic disease modeling by somatic genome editing cou

213 Several metabolic disease models have shown that dysregulation o

214 g and genetic ablation of miR-128-1 in mouse metabolic disease models result in increased energy expe

215 Nonetheless, many metabolic disease models still depend upon laborious ger

216 uptions of the circadian clock can result in metabolic diseases, mood disorders, and accelerated agin

217 24) by imPERCIST5 than in those with stable metabolic disease (n = 7) or partial metabolic response

218 iagnostic and prognostic tool in obesity and metabolic diseases needs to be further evaluated.

219 new avenues for therapeutic intervention in metabolic disease, neurodegeneration, and aging.

220 ciated with pathogenesis of inflammatory and metabolic diseases, neurodegeneration and malignancies.

221 Using middle-aged mice, we modeled metabolic disease (obesity/prediabetes) via chronic high

222 s play a key role in the increased programed metabolic disease of HFD-exposed offspring.

223 /-) mice to recover from cachexia, an immune-metabolic disease of muscle wasting that impairs fitness

224 A number of genetic and metabolic diseases of adulthood causing spinal cord atro

225 The genetic and metabolic diseases of adulthood causing spinal cord sign

226 ncluding cancer, cardiovascular disease, and metabolic diseases of the liver and kidney.

227 issue mechanics, and delineate the impact of metabolic disease on the mechanical properties of adipos

228 to the potential impact of mitochondrial and metabolic diseases on the function of stem and/or germ c

229 have been approved to date, most of them for metabolic disease or oncology, and more than 10 potentia

230 Nonmetabolic responders (n = 6) (stable metabolic disease or progressive disease) showed a media

231 enrolled healthy newborns and children with metabolic diseases or hearing loss (106 participants tot

232 se (CMR), partial metabolic response, stable metabolic disease, or progressive metabolic disease.

233 w that some of the inflammatory ATM inducing metabolic disease, originate from resident AT-LSK.

234 In other metabolic diseases, pharmacotherapy is an accepted adjun

235 t (HFD) feeding further exacerbates the K2KO metabolic disease phenotype.

236 y) subject to obesogenic challenges exhibits metabolic disease phenotypes in skeletal muscle; sarcome

237 ve of metastases were considered progressive metabolic disease (PMD).

238 may be associated with an increased risk of metabolic diseases, possibly due to stimulation of gluco

239 and may provide mechanistic insight into the metabolic disease predisposition in individuals with FA.

240 ate relative to the lean state and underlies metabolic disease progression.

241 reticulum (ER) stress, both of which promote metabolic disease progression.

242 may also serve as potential therapeutics for metabolic disease; rather than disrupt ADS lyase, compou

243 o FA phenotypes and the links between FA and metabolic disease remain poorly understood.

244 effective treatments for obesity and related metabolic disease remains a challenge.

245 s no consensus on the implications of PAE on metabolic disease risk in adults.

246 sence of which is associated with lower host metabolic disease risk.

247 ental to understanding their contribution to metabolic disease risk.

248 influence islet biology and consequentially metabolic disease risk.

249 el studies in rodents have shown TRF reduces metabolic disease risks by maintaining metabolic homeost

250 seases, including cognitive decline, cancer, metabolic disease, sarcopenia and frailty.

251 potential target to resolve obesity related metabolic diseases; SCD1 deficiency causes endoplasmic r

252 erformed population studies to elucidate the metabolic disease seen in the clinical cohort.

253 that this method will be useful in assessing metabolic disease states and developing therapies to imp

254 uided treatment of type 2 diabetes and other metabolic disease states in vivo in humans.

255 bstrates when studying GNG in the context of metabolic disease states.

256 in hepatic function, which in turn result in metabolic disease such as hepatosteatosis later in life.

257 ption factor that confers protection against metabolic diseases such as atherosclerosis by targeting

258 ffected by acquired autoimmune disorders and metabolic diseases such as diabetes mellitus.

259 ognized and heavily pursued for treatment of metabolic diseases such as diabetes, but also obesity, i

260 ping effective therapeutic interventions for metabolic diseases such as insulin resistance, NAFLD, an

261 shown its effectiveness in the treatment of metabolic diseases such as obesity and diabetes via regu

262 Loss of sleep is associated with metabolic diseases such as obesity and diabetes, cardiov

263 n populations suggest links between AIF1 and metabolic diseases such as obesity and diabetes, such as

264 s has been investigated for the treatment of metabolic diseases such as obesity and type 2 diabetes (

265 Metabolic diseases such as obesity and type 2 diabetes a

266 ion in skeletal muscle being associated with metabolic diseases such as obesity and type II diabetes,

267 abolism and hence are therapeutic targets in metabolic diseases such as type 2 diabetes and non-alcoh

268 The global prevalence of metabolic diseases such as type 2 diabetes mellitus, ste

269 lin resistance being a major risk factor for metabolic diseases such as type 2 diabetes.

270 unfolding paradigm in which old age, chronic metabolic disease (such as obesity, type 2 diabetes, and

271 This concept is especially relevant to metabolic diseases, such as chronic kidney disease (CKD)

272 is may contribute to the interaction between metabolic diseases, such as diabetes and altered brain f

273 bute to their increased risk for adult onset metabolic diseases, such as diabetes and obesity.

274 ure studies of their roles in development of metabolic diseases, such as obesity and type 2 diabetes.

275 is and non-inflammatory pain as well as with metabolic diseases, such as osteoporosis.

276 rnal HFD-induced inflammation contributes to metabolic disease susceptibility of the offspring via al

277 ely to be an epiphenomenon in the context of metabolic disease than a key determinant.

278 Diabetes is a chronic metabolic disease that causes blood glucose (BG) concent

279 an efficacy of drugs targeting BAT to treat metabolic disease that is at the same time higher and su

280 RATIONALE: Early vascular changes in metabolic disease that precipitate the development of ca

281 Diabetes mellitus is a lifelong metabolic disease that requires frequent subcutaneous in

282 (multimorbidity), such as cardiovascular and metabolic diseases, that share the same pathways of acce

283 visceral adipose tissue with obesity-related metabolic diseases, the distribution of lipids between t

284 with GLP-1 stimulatory activity as potential metabolic disease therapeutics.

285 way and provide another focus for cancer and metabolic disease therapies.

286 circulation are promising new approaches for metabolic disease therapy, but neither approach alone ca

287 ed the hypothesis that early in the onset of metabolic diseases there is a decline in serum levels of

288 examine mucus function in mouse models with metabolic disease to distinguish these factors.

289 her VAT or SAT amount among subjects free of metabolic diseases to identify possible contributing met

290 tion of beta3-AR agonists as a treatment for metabolic disease.TRIAL REGISTRATIONClinicaltrials.gov N

291 The metabolic disease type 2 diabetes (T2D) is a risk factor

292 f the association between glycine and cardio-metabolic diseases using genetic approaches.

293 sal effects of dietary intake on the risk of metabolic diseases, we performed meta-analysis, CPT1A tr

294 PT1A methylation, hence reducing the risk of metabolic diseases, whereas FAT intake inhibits CPT1A me

295 h partial metabolic response and progressive metabolic disease, which is the best predictor of the CT

296 biota plays a role in the pathophysiology of metabolic diseases, which include nonalcoholic fatty liv

297 ty and insulin resistance can lead to severe metabolic diseases, while calorie-restricted (CR) diets

298 and protein, is an important risk factor for metabolic diseases with significant familial aggregation

299 lpha, a potential drug target for cancer and metabolic diseases, with its three ligands.

300 -induced obesity are associated with various metabolic diseases, yet the underlying mechanisms remain