ライフサイエンスコーパス: metabolic disease

1 isioned drugs targeting this tissue to treat metabolic disease.

2 metabolism, and its dysregulation can cause metabolic disease.

3 e to treat symptoms and underlying causes of metabolic disease.

4 ciated with ccRCC, it can now be viewed as a metabolic disease.

5 rgets for combating diet-induced obesity and metabolic disease.

6 1) and demonstrate a role for these cells in metabolic disease.

7 utic approach for age-related sarcopenia and metabolic disease.

8 is population should target hypertensive and metabolic disease.

9 ies to enhance energy expenditure and combat metabolic disease.

10 ipogenic differentiation and obesity-related metabolic disease.

11 caemia and insulin resistance recapitulating metabolic disease.

12 lications for the development of obesity and metabolic disease.

13 to determine whether AsIII exposure affects metabolic disease.

14 w their perturbations contribute to systemic metabolic disease.

15 is associated with future cardiovascular and metabolic disease.

16 of surgery for the treatment of obesity and metabolic disease.

17 ical regulator of fetal programming of adult metabolic disease.

18 they are potential new targets for managing metabolic disease.

19 ific differences mediate the expressivity of metabolic disease.

20 parents may also contribute to their risk of metabolic disease.

21 ain susceptible to obesity-associated IR and metabolic disease.

22 strategies for the treatment of this common metabolic disease.

23 by long-term experiments in rodent models of metabolic disease.

24 r the prevention, and probably treatment, of metabolic disease.

25 adverse cardiovascular effects regardless of metabolic disease.

26 ulators and potential therapeutic targets of metabolic disease.

27 may be a risk factor for cardiovascular and metabolic disease.

28 re can protect from diet-induced obesity and metabolic disease.

29 st energy homeostasis and the development of metabolic disease.

30 esity and a potential therapeutic target for metabolic disease.

31 olling hypothalamic inflammation to mitigate metabolic disease.

32 crease the vulnerability to and even provoke metabolic disease.

33 birth weight, which is linked to subsequent metabolic disease.

34 isorders, cancer, cardiovascular disease and metabolic disease.

35 axis and beige-fat development in health and metabolic disease.

36 ntribute to the link of the E354Q variant to metabolic disease.

37 hy and inflammation, thereby contributing to metabolic disease.

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

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

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

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

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

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

44 function is relevant in both homeostasis and metabolic disease.

45 nimals against hypothermia and to counteract metabolic disease.

46 portant gap in the management of obesity and metabolic disease.

47 ointing to a key gap in our understanding of metabolic disease.

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

49 romising therapeutic target to fight against metabolic disease.

50 okine with complex roles in inflammation and metabolic disease.

51 of calories is important in the etiology of metabolic disease.

52 la and are accompanied by many indicators of metabolic disease.

53 development of microvascular dysfunction in metabolic disease.

54 tentially relevant for neurodegenerative and metabolic diseases.

55 ology and development of muscle diseases and metabolic diseases.

56 trategy to prevent or treat fructose-induced metabolic diseases.

57 t (HFD) predisposes offspring to obesity and metabolic diseases.

58 PK) is an established therapeutic target for metabolic diseases.

59 ects, paves the way for precision therapy of metabolic diseases.

60 this POP mixture could produce or exacerbate metabolic diseases.

61 is well established to significantly impact metabolic diseases.

62 creased risk of hepatic, cardiovascular, and metabolic diseases.

63 s, impaired neurodevelopment, and later life metabolic diseases.

64 been given to the role of micronutrients in metabolic diseases.

65 sing therapeutic target to treat obesity and metabolic diseases.

66 t as a new strategy in combating obesity and metabolic diseases.

67 oxidation whose plasma levels associate with metabolic diseases.

68 associated with a higher risk of developing metabolic diseases.

69 NaCT (SLC13A5), is a therapeutic target for metabolic diseases.

70 biomarkers for early diagnosis of dairy cow metabolic diseases.

71 d spiral that can lead to diabetes and other metabolic diseases.

72 ins robust diurnal rhythms and can alleviate metabolic diseases.

73 entral role in susceptibility to obesity and metabolic diseases.

74 th potent effects on systemic metabolism and metabolic diseases.

75 echanisms that link different POPs to common metabolic diseases.

76 ets for the treatment of obesity and related metabolic diseases.

77 ion tool for on-farm monitoring of dairy cow metabolic diseases.

78 for clinical treatment of obesity and other metabolic diseases.

79 and disruption of normal tissue functions in metabolic diseases.

80 is often associated with cardiovascular and metabolic diseases.

81 dian rhythm disruption increases the risk of metabolic diseases.

82 r, women maintain an elevated risk of cardio-metabolic diseases.

83 tic approach for prevention and treatment of metabolic diseases.

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

85 ng time, a promising preventive strategy for metabolic diseases.

86 s the cornerstone in first-line treatment of metabolic diseases.

87 n the context of obesity, diabetes and other metabolic diseases.

88 elevated inflammation and increased risk of metabolic diseases.

89 ted its application in the treatment of bone metabolic diseases.

90 o liver transplantation for the treatment of metabolic diseases.

91 steinemia is often associated with liver and metabolic diseases.

92 promising means of treating malignancies and metabolic diseases.

93 nifesting heterozygous cases in other inborn metabolic diseases.

94 ies targeted to diagnose, prevent, and treat metabolic diseases.

95 s and postulate sEH as a druggable target in metabolic diseases.

96 tant exposure and the increased incidence of metabolic diseases.

97 the treatment of obesity, diabetes and other metabolic diseases.

98 g pathways are commonly deregulated in human metabolic diseases.

99 as hAT, in the complex interwoven picture of metabolic diseases.

100 implicated in a range of cardiovascular and metabolic diseases.

101 ctious, neurodegenerative, inflammatory, and metabolic diseases.

102 mportance for developing strategies to treat metabolic diseases.

103 t well synchronized, individuals may develop metabolic diseases.

104 e tissue is linked to insulin resistance and metabolic diseases.

105 autoimmune, cardiovascular, infectious, and metabolic diseases.

106 nked to pathophysiological states, including metabolic diseases.

107 merous chronic infectious, inflammatory, and metabolic diseases.

108 rtant component of immune, inflammatory, and metabolic diseases.

109 F/Kit signalling as a therapeutic target for metabolic diseases.

110 tabolism and contributes to liver-associated metabolic diseases.

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

112 treating obesity-associated inflammatory and metabolic diseases.

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

114 tential impact in the understanding of human metabolic diseases.

115 ntly contribute to the growing prevalence of metabolic diseases.

116 t for gender dissimilarity in metabolism and metabolic diseases.

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

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

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

120 the etiology, development, and management of metabolic diseases.

121 creased risk of hepatic, cardiovascular, and metabolic diseases.

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

123 l progression and exacerbates development of metabolic diseases.

124 hlighted the significance of inflammation in metabolic diseases.

125 ut-related stimuli, but also in other common metabolic diseases.

126 apeutic targets for treatment of obesity and metabolic diseases.

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

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

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

130 context of infection, chronic inflammation, metabolic disease and cancer.

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

132 thods that will provide crucial insight into metabolic disease and how it may be treated by modulatin

133 ids in biological samples, plasma markers of metabolic disease and inflammation, and fecal microbiota

134 the identification of targets for preventing metabolic disease and its negative effects on health.

135 ssion of OSKM in vivo improves recovery from metabolic disease and muscle injury in older wild-type m

136 xpenditure and holds potential for combating metabolic disease and obesity.

137 e fusion can increase the susceptibility for metabolic disease and precede obesity and type 2 diabete

138 ide valuable insights into the links between metabolic disease and reproductive dysfunction.

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

140 logical connections between hypertension and metabolic disease and, most importantly, identify pathop

141 der with how these cell types play a role in metabolic disease and, perhaps, as targets for therapeut

142 great potential as a therapeutic target for metabolic diseases and cancer, development of LRH-1 modu

143 armacological inhibition in the treatment of metabolic diseases and cancer.

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

145 nvaluable insights into the understanding of metabolic diseases and may contribute to the development

146 relationship between the number of incident metabolic diseases and mortality risk.

147 It occasionally occurs in syndromic metabolic diseases and plurisystemic ciliopathies.

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

149 Metabolic diseases and the altered metabolic environment

150 immune cell phenotype and function in human metabolic diseases and, in parallel, of the effects of c

151 ations for the treatment of sleep disorders, metabolic disease, and cancer.

152 resident AT-LSK are one of the key point of metabolic disease, and could thus constitute a new promi

153 ystrophy, a condition associated with severe metabolic disease, and has also shown potential for the

154 Obesity is inherently a metabolic disease, and metabolic profiling has found wid

155 in conformation including neurodegeneration, metabolic diseases, and cancer.

156 Research suggests cardiovascular and metabolic diseases are influenced by psychological distr

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

158 The most studied NRs for treating metabolic diseases are the peroxisome proliferator-activ

159 und to be highly susceptible to diet-induced metabolic disease, as evidenced by impairments in glucos

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

161 plasma levels of sphingolipids contribute to metabolic disease, atherosclerosis, and insulin resistan

162 rmone (T3) exhibit therapeutic potential for metabolic disease but also exhibit undesired effects.

163 ex differences in the early origins of adult metabolic disease, but this has been little investigated

164 Work stress is a risk factor for cardio-metabolic diseases, but few large-scale studies have exa

165 een persistent organic pollutants (POPs) and metabolic diseases, but testable hypotheses regarding un

166 d fat impacts the development of obesity and metabolic diseases, but the potential for beneficial eff

167 tion of adiponectin exocytosis in health and metabolic disease by a combination of membrane capacitan

168 ber type specification and susceptibility to metabolic disease by folliculin interacting protein-1 (F

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

170 erent conditions including mitochondrial and metabolic disease, cancer, and neuromuscular degenerativ

171 ulates lifespan and reproduction, as well as metabolic diseases, cancer, and aging.

172 d PSCs (iPSCs) may have utility for modeling metabolic diseases caused by mutations in mitochondrial

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

174 Hypothyroidism, a metabolic disease characterized by low thyroid hormone (

175 ency is a rare, autosomal-recessive systemic metabolic disease characterized by severe combined immun

176 People who developed >/=1 metabolic disease component (hypertension, diabetes, dys

177 lover occurs into to peripheral tissues that metabolic diseases develop.

178 , aspirin use, smoking, body mass index, and metabolic diseases) did not differ significantly between

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

180 e development of high fat diet (HFD)-induced metabolic diseases due to enhanced anti-inflammation eng

181 ardiovascular diseases including obesity and metabolic disease, dyslipidemia, inflammation, atheroscl

182 te the development of obesity and associated metabolic diseases, emerging studies indicate that innat

183 ty, and mistimed sleep-increases the risk of metabolic diseases, especially obesity and T2DM.

184 inflammasomes, but also for treating common metabolic diseases for which effective therapies are cur

185 deficit of effects was associated with known metabolic disease genes.

186 xylase (ACC) inhibitors for the treatment of metabolic disease has been pursued by the pharmaceutical

187 of TRPC1 in adiposity and obesity-associated metabolic diseases has not yet been determined.

188 Diabetes mellitus, a chronic degenerative metabolic disease, has reached epidemic proportions in t

189 The rates of diabetes, obesity, and metabolic disease have reached epidemic proportions worl

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

191 es to the pathogenesis of cardiovascular and metabolic diseases; however, the molecular mechanisms th

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

193 Failure of this activity results in severe metabolic disease in humans.

194 duce heat, and could help combat obesity and metabolic disease in humans.

195 ves hepatocyte engraftment and correction of metabolic disease in mdr2 (-/-) mice.

196 may thus contribute to the increased risk of metabolic disease in O-GDM.

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

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

199 bacteria showed increased susceptibility to metabolic disease in the context of a high-fat diet.

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

201 ive, and painless point-of-care diagnosis of metabolic diseases in exhaled human breath.

202 of these enzymes have been linked to serious metabolic diseases in humans, and acetyl-CoA carboxylase

203 nd oxidative metabolism during the course of metabolic diseases in humans.

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

205 de problem associated with increased risk of metabolic diseases in the offspring.

206 ducibly associated with future risk of adult metabolic diseases including type 2 diabetes (T2D) and c

207 n of AMPK has been implicated in a number of metabolic diseases including type 2 diabetes mellitus an

208 aches to obesity, type 2 diabetes, and other metabolic diseases, including among only mildly obese or

209 n demonstrates beneficial effects in various metabolic diseases, including diabetes, and in bowel can

210 nflammation and in the pathogenesis of human metabolic diseases, including diabetes.

211 Worldwide epidemics of metabolic diseases, including liver steatosis, are assoc

212 ress has been shown to contribute to various metabolic diseases, including non-alcoholic fatty liver

213 contributes to the incidence and severity of metabolic diseases, including obesity and type 2 diabete

214 ays an important role in the pathogenesis of metabolic diseases, including obesity, diabetes, and ath

215 are at increased risk for cardiovascular and metabolic diseases, including obesity, high BP, diabetes

216 widely accepted that obesity and associated metabolic diseases, including type 2 diabetes, are intim

217 1 (mTORC1) signalling increases the risk for metabolic diseases, including type 2 diabetes.

218 Maternal metabolic diseases increase offspring risk for low birth

219 Our study marks the first time a human metabolic disease is induced in an experimental animal m

220 Obesity-linked metabolic disease is mechanistically associated with the

221 e pathogenesis or is rather a consequence of metabolic disease is not known.

222 tissue (BAT) to protect against obesity and metabolic disease is recognized, yet information about w

223 dence that the susceptibility to HFD-induced metabolic disease is similar in the 6J and 6N substrains

224 A susceptibility to metabolic diseases is associated with abdominal adipose

225 The worldwide prevalence of metabolic diseases is increasing, and there are global r

226 The battle against metabolic diseases, largely fueled by increased liver fa

227 d in cancer treatment increases the risk for metabolic disease later in life.

228 tern-style diet may be at increased risk for metabolic disease later in life.

229 T1 and other drug transporters implicated in metabolic diseases like gout, diabetes, and chronic kidn

230 No significant change in plasma metabolic disease markers over the study period was obse

231 treatment of homocystinuria and that ERT for metabolic diseases may not necessitate introduction of t

232 ulinemia, which is associated with aging and metabolic disease, may lead to defective protein homeost

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

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

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

236 nicotinamide riboside (NR), protects against metabolic disease, neurodegenerative disorders and age-r

237 Neither chronic systemic metabolic disease nor other retinal insults are required

238 Progressive metabolic disease on day-9 PET was associated with a sig

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

240 disruption of the circadian clock can cause metabolic diseases or exacerbate pathological states.

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

242 latory system or endocrine, nutritional, and metabolic diseases (P < 0.001).

243 In other metabolic diseases, pharmacotherapy is an accepted adjun

244 foetal tissue may have a mechanistic role in metabolic disease programming through interaction of the

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

246 and tested the hypothesis that diet-induced metabolic disease promotes retinopathy.

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

248 However, the relationship between Ubc13 and metabolic disease remains unclear.

249 ed with early life and with implications for metabolic disease resistance.

250 Metabolic diseases result from multiple genetic and envi

251 ink between location of fat accumulation and metabolic disease risk and depot-specific differences is

252 wer-body AT offers insight into the opposing metabolic disease risk associations between upper- and l

253 bdominal visceral fat is the specific cardio-metabolic disease risk factor.

254 to adulthood and may contribute to increased metabolic disease risk.

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

256 PERCIST was used, patients with progressive metabolic disease showed shorter OS (median, 4.7 mo) tha

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

258 g as a novel regulator of cardiovascular and metabolic disease states.

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

260 development and risk for obesity-associated metabolic disease such as T2D is unclear.

261 ding mortality rates and incidence of cardio-metabolic disease such as: (1) women consistently exhibi

262 thologies including chronic inflammatory and metabolic diseases such as atherosclerosis.

263 mal physiology and in the pathophysiology of metabolic diseases such as diabetes, and are thus of sig

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

265 linked impaired AMPK function to peripheral metabolic diseases such as diabetes.

266 lipid metabolism with implications in human metabolic diseases such as obesity and cancer, which dis

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

268 ive approach to the treatment of age-related metabolic diseases such as obesity and diabetes.

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

270 Metabolic diseases such as obesity and type 2 diabetes a

271 marks of muscular pathologies resulting from metabolic diseases such as obesity and type 2 diabetes.

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

273 lation of autophagy has been associated with metabolic diseases such as obesity, diabetes, or metabol

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

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

276 t and this neural network is associated with metabolic diseases, such as obesity.

277 ce predispose individuals to develop chronic metabolic diseases, such as type 2 diabetes and cardiova

278 ate, very few studies have directly compared metabolic disease susceptibility between NNT-deficient 6

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

280 Protoporphyria is a metabolic disease that causes excess production of proto

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

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

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

284 etary fatty acids, the link between FFA4 and metabolic diseases, the potential effects of the individ

285 B3 that could provide a new opportunity for metabolic disease therapy.

286 spite the substantial overlap of obesity and metabolic disease, there is heterogeneity with respect t

287 own to be highly susceptible to diet-induced metabolic disease, this notion stems primarily from comp

288 nisms of POPs that have been associated with metabolic diseases; three well-known POPs [2,3,7,8-tetra

289 core of many diseases ranging from inherited metabolic diseases to common conditions that are associa

290 l parameter in strain engineering as well as metabolic disease treatment.

291 ce greater derangements in redox homeostasis/metabolic disease upon HFD exposure.

292 the functional relevance of STS induction in metabolic disease, we showed that overexpression of STS

293 Cancer is also a metabolic disease where oncogenic signaling pathways reg

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

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

296 o the role of the fecal microbiota in cardio-metabolic disease with clear potential for prevention an

297 ted by HSPs could underlie susceptibility to metabolic disease with low aerobic capacity.

298 Obesity is a major risk factor for metabolic disease, with white adipose tissue (WAT) infla

299 ultiple disorders including inflammatory and metabolic diseases, yet relatively little is known regar

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