ライフサイエンスコーパス: glucose metabolism

1 d insulin secretion, adiposity, feeding, and glucose metabolism.

2 mpetitive endogenous RNAs in cholesterol and glucose metabolism.

3 idic because of low convective flow and high glucose metabolism.

4 health such as regulation of adipose tissue glucose metabolism.

5 describes how they impact islet biology and glucose metabolism.

6 ced metabolite from histidine, which impairs glucose metabolism.

7 ffecting the expression of genes involved in glucose metabolism.

8 und pregnancy-related physiologic changes in glucose metabolism.

9 ntricle at 8 d after TAC, indicating altered glucose metabolism.

10 ulators of inflammation as well as lipid and glucose metabolism.

11 inuum of metabolic disturbances in lipid and glucose metabolism.

12 tion of additional BCAAs will further impair glucose metabolism.

13 and tumor progression by reprogramming tumor glucose metabolism.

14 dependent on pathways inextricably linked to glucose metabolism.

15 ocesses, including the daily rhythm in human glucose metabolism.

16 ta3 antagonists for 1 month normalizes their glucose metabolism.

17 emed to play a role in regulating NKT cells' glucose metabolism.

18 ranscription factor in hepatic regulation of glucose metabolism.

19 A relevant role has been assigned to glucose metabolism.

20 ssive effects on both cell proliferation and glucose metabolism.

21 inating histone production, acetylation, and glucose metabolism.

22 tigate its effects on glucagon secretion and glucose metabolism.

23 increased weight gain with little effect on glucose metabolism.

24 nction, or expression of genes important for glucose metabolism.

25 eta-cell development, insulin secretion, and glucose metabolism.

26 tabolites as novel modulators of muscle cell glucose metabolism.

27 n increased FVIII synthesis or inhibition of glucose metabolism.

28 duct of this process, we examined changes in glucose metabolism.

29 ated the role of MALAT1 in regulating cancer glucose metabolism.

30 he renin-angiotensin system, and insulin and glucose metabolism.

31 play a role in regulating energy balance and glucose metabolism.

32 etite and decreases fat mass while improving glucose metabolism.

33 nism that partially underlies PF's effect on glucose metabolism.

34 y, shows that silencing SMS strongly impacts glucose metabolism.

35 ion, senescence, mitochondrial function, and glucose metabolism.

36 ic zebrafish further displayed dysfunctional glucose metabolism.

37 ly characterized for their role in lipid and glucose metabolism.

38 1 mediates the effects of insulin on hepatic glucose metabolism.

39 t in the intestine and to partially modulate glucose metabolism.

40 on is an important step in the regulation of glucose metabolism.

41 ort the concept of anticipatory budgeting on glucose metabolism.

42 FXR also regulates postprandial lipid and glucose metabolism.

43 acterized by insulin resistance and impaired glucose metabolism.

44 re of ATP-sensitive potassium channels after glucose metabolism.

45 adiposity, have been related to obesity and glucose metabolism.

46 king glycocalyx biology directly to cellular glucose metabolism.

47 genes associated with tumor development and glucose metabolism.

48 titians did not improve surrogate markers of glucose metabolism.

49 n the ileum and colon, modulated feeding and glucose metabolism.

50 glucose uptake and correspondingly increased glucose metabolism.

51 to nitric oxide (NO) signaling and impaired glucose metabolism.

52 inflammation, as well as improved lipid and glucose metabolism.

53 number of genes, including those involved in glucose metabolism.

54 roles in insulin secretion and consequently glucose metabolism.

55 ed protein which has recently been linked to glucose metabolism.

56 id, which is enabled by the reprogramming of glucose metabolism.

57 open up new ways to control food intake and glucose metabolism.

58 e decreased insulin signaling and disordered glucose metabolism.

59 ng tumorigenicity, sorafenib resistance, and glucose metabolism.

60 s beyond hepatic actions to exert control on glucose metabolism.

61 de evidence regarding a close interplay with glucose metabolism.

62 d, thus, obesity-associated deterioration of glucose metabolism.

63 ein through raised cellular intermediates of glucose metabolism.

64 insulin sensitivity, and measures of fasting glucose metabolism.

65 ing of the liver, including dysregulation of glucose metabolism.

66 from diet-induced obesity and its effects on glucose metabolism.

67 ated gene is implicated in the regulation of glucose metabolism.

68 FD-fed IgA-deficient mice have dysfunctional glucose metabolism, a phenotype that can be recapitulate

69 is increasing evidence that patients display glucose metabolism abnormalities before significant anti

70 An interaction between glucose metabolism abnormality and the WM dysconnectivit

71 at there is an exact proportionality between glucose metabolism and 2-FDG metabolism, called the lump

72 at there is an exact proportionality between glucose metabolism and 2-FDG metabolism, called the lump

73 anti-inflammatory activities, regulation of glucose metabolism and ability to stimulate fibroblast m

74 1 in mice with diet-induced obesity impaired glucose metabolism and AKT activation.

75 quired for its effect on insulin-independent glucose metabolism and AMPK activation.

76 allows for an identification of patterns of glucose metabolism and amyloid deposition related to the

77 Mttp-IKO mice exhibit improved hepatic glucose metabolism and augmented insulin signaling, with

78 restriction leads to a marked improvement in glucose metabolism and body-fat composition, including l

79 Glucose metabolism and calcium influx are involved in pr

80 m complications, including obesity, impaired glucose metabolism and cardiovascular disease, in both t

81 ransport, synaptic integrity and plasticity, glucose metabolism and cerebrovascular function.

82 T is distinct from WAT and BAT, with altered glucose metabolism and decreased insulin responsiveness.

83 ells (K(ATP)-GOF) also lose the link between glucose metabolism and excitation-induced insulin secret

84 or in which beta-cells were heterogeneous in glucose metabolism and GK kinetics were altered.

85 we show that HectH9 deficiency impedes tumor glucose metabolism and growth by HK2 inhibition.

86 ects of MCH on food intake, body weight, and glucose metabolism and highlight the relevance of SIRT1/

87 Mechanistically, mTORC1 engaged glucose metabolism and initiated a transcriptional progr

88 erimental evidence indicates that PFAS alter glucose metabolism and insulin secretion.

89 e SAT weight and further improved CL-induced glucose metabolism and insulin sensitivity in female obe

90 ApoJ) as a novel hepatokine targeting muscle glucose metabolism and insulin sensitivity through a low

91 hysiological links between circadian clocks, glucose metabolism and insulin sensitivity, and present

92 There are indications that glucose metabolism and insulin sensitivity, which are ge

93 Insulin plays a major role in glucose metabolism and its determination is of great val

94 ct of chitinase-3-like protein 1 (CHI3L1) on glucose metabolism and its underlying mechanisms in skel

95 cess functionally distinct from conventional glucose metabolism and leads to distinct metabolic requi

96 ein instability was associated with impaired glucose metabolism and lower glycolytic enzyme expressio

97 ul strategy in the prevention of the altered glucose metabolism and memory decline in these disorders

98 Silencing of HK-2 prevented increased glucose metabolism and MG formation.

99 Abnormal glucose metabolism and nonalcoholic fatty liver disease

100 property of the cancer phenotype is enhanced glucose metabolism and oxidative stress.

101 lpha can be a potential approach to modulate glucose metabolism and prevent diabetes.

102 sterone ((18)F-FFNP) PET/CT imaging of tumor glucose metabolism and progesterone receptor (PR) expres

103 C1 expression may contribute to dysregulated glucose metabolism and represents a novel biomarker and

104 Glucagon counters insulin's effects on glucose metabolism and serves as a rescue medicine in th

105 lude that PFKFB3 has a key role in mediating glucose metabolism and survival of NSCLC cells in respon

106 ning the effect of nitrate on adipose tissue glucose metabolism and the contribution of this tissue t

107 d, however, alter metabolic intermediates of glucose metabolism and those necessary for biosynthesis

108 H) is an important regulator of food intake, glucose metabolism, and adiposity.

109 vere human disorders resulting from abnormal glucose metabolism, and all previously described GSDs se

110 lucose-stimulated insulin secretion, hepatic glucose metabolism, and both adipose and pancreatic beta

111 ry nerves impacts pancreatic islet function, glucose metabolism, and diabetes onset, but how islet en

112 FXR and TGR5 are modulators of glucose metabolism, and FXR activity is reduced in norma

113 oss-sectional measures of amyloid-beta, tau, glucose metabolism, and grey matter degeneration in 15 c

114 records; measures of body fat, blood lipids, glucose metabolism, and inflammation were collected prio

115 ove measures of body fat, blood cholesterol, glucose metabolism, and inflammation.

116 e for NURR1 in governance of skeletal muscle glucose metabolism, and reveal a transcriptional link be

117 cell survival, vesicle/membrane trafficking, glucose metabolism, and stress responses.

118 sulin and glucagon exert opposing actions on glucose metabolism, and their secretion is classically v

119 ven the widespread use of 2-FDG PET to infer glucose metabolism, appreciating the potential limitatio

120 al, suggesting that the effects of MALAT1 on glucose metabolism are essential for its oncogenic activ

121 e impaired and both oxidative and glycolytic glucose metabolism are reduced.

122 We hypothesized that altered systemic glucose metabolism as a consequence of Mycobacterium tub

123 Most tumor cells reprogram their glucose metabolism as a result of mutations in oncogenes

124 es.Several metabolic factors affect cellular glucose metabolism as well as the innate inflammatory re

125 but less so with amyloid-beta deposition or glucose metabolism (assessed by positron emission tomogr

126 uitry (measured with PET imaging of cerebral glucose metabolism at baseline and at 6 and 12 months af

127 letal muscle lipid metabolism converges with glucose metabolism at the level of downstream RabGTPases

128 Expression levels of fatty acid oxidation, glucose metabolism, atrophy genes, and proteins as well

129 de novo cholesterol synthesis, fructose and glucose metabolism, basic amino acid metabolism, and bil

130 PC function, but not both, improves systemic glucose metabolism because of maintenance of AT regulato

131 eveals the mechanism by which YAP reprograms glucose metabolism, but also highlights the therapeutic

132 tion by RdCVF of glucose uptake in cones and glucose metabolism by aerobic glycolysis.

133 y factor 1 (IF1), a novel myokine, regulates glucose metabolism by AMPK and Akt dual pathways.

134 ation (tRES-HESP) corrected increased MG and glucose metabolism by increasing expression of Glo1 and

135 d that differential regulation of macrophage glucose metabolism by macrophage colony-stimulating fact

136 Glucose metabolism by positron emission tomography with

137 ated macrophages to D-mannose, which impairs glucose metabolism by raising intracellular mannose-6-ph

138 ally, CTRP6 regulates local inflammation and glucose metabolism by targeting macrophages and adipocyt

139 a mechanism by which alterations in cellular glucose metabolism can influence cellular inflammatory r

140 Regional LV glucose metabolism closely correlates with regional work

141 Therefore, abnormal glucose metabolism, cognitive impairment and widespread

142 for genes encoding other enzymes involved in glucose metabolism compared to follower cells.

143 ver, the obese KO mice demonstrated improved glucose metabolism compared with wild-type mice. Obese K

144 o how TIH, prevalent in people with impaired glucose metabolism, contributes to cardiovascular diseas

145 sting-like gene expression profile, improves glucose metabolism, de-represses lncRNAs and impairs mam

146 secretion from islet beta-cells is driven by glucose metabolism, depolarization of the cell membrane

147 neurodegenerative disorders of ageing, brain glucose metabolism deteriorates in a progressive, region

148 volved in various cellular processes such as glucose metabolism, development, stress resistance, and

149 ting evidence suggests that individuals with glucose metabolism disorders are susceptible to mortalit

150 We evaluated glucose metabolism disorders as a potential modifier by

151 gene-sets not only predicted reduced risk of glucose metabolism disorders but was also consistent wit

152 Glucose metabolism disorders may aggravate respiratory i

153 PET was used to measure cerebral glucose metabolism during 2 gait tasks, steering and str

154 eptor in skeletal-muscle AMPK activation and glucose metabolism during exercise, as well as unexpecte

155 The greater dependence on muscle glucose metabolism during increased oxygen demand may pr

156 he effect of maternal obesity on offspring's glucose metabolism during the perinatal period.

157 Downregulation of glucose metabolism, either by activation of the AHR, inh

158 utes to HCC development by regulating cancer glucose metabolism, enhancing glycolysis, and inhibiting

159 tion, apoptosis, inflammation, angiogenesis, glucose metabolism, erythropoiesis, and other physiologi

160 wever, we also reported that PF can increase glucose metabolism even in the absence of insulin in mus

161 se model whether early or late components of glucose metabolism, exemplified by fluorine 18 ((18)F) f

162 ly regulated a total of 237 DEGs involved in glucose metabolism, fatty acid oxidation, ion channels,

163 ired 30-50% of the cells to have near-normal glucose metabolism, fewer than cells with normal K(ATP)

164 tion, further supporting the significance of glucose metabolism for NKT cell function.

165 reveals that NKT cells use distinct arms of glucose metabolism for their survival and function.

166 Because of a shift in glucose metabolism from oxidative phosphorylation to lac

167 a differentiation trajectory that regulates glucose metabolism genes to determine the proliferative

168 In addition to its role in the regulation of glucose metabolism, glucagon has been described to promo

169 1 diabetes that are associated with altered glucose metabolism/glycolysis and report here that TG2 e

170 of RS was evaluated by monitoring body fat, glucose metabolism, gut hormones, gut microbiota, short-

171 mune cells in the regulation of postprandial glucose metabolism has not been fully elucidated.

172 xamining the effect of coffee consumption on glucose metabolism have been limited by the use of surro

173 in the 21st century, the need to understand glucose metabolism heightens.

174 Among genes involved in glucose metabolism, hexokinase domain containing 1 (HKDC

175 e therefore has a wide-ranging alteration in glucose metabolism: high [Ca(2+)](cytosol) activates PhK

176 glucose, demonstrating that acutely reduced glucose metabolism impairs cognition selectively in the

177 dehydrogenase (G6PD), an enzyme involved in glucose metabolism, improved survival in mouse models of

178 ocumented that 5-PAHSA primes adipocytes for glucose metabolism in a different way from insulin, prom

179 aster regulator of bioenergetics crucial for glucose metabolism in acute myeloid leukemia (AML), and

180 the existence of extensive reprogramming of glucose metabolism in AH.

181 In conclusion, D2R-OE(NAc) alters glucose metabolism in both sexes but drives robust weigh

182 arbon flux through pathways of oxidation and glucose metabolism in bovine hepatocytes exposed to incr

183 ach to exploit the consequences of increased glucose metabolism in cancer.

184 phosphate receptor-1 (S1PR1) expression and glucose metabolism in CD4(+) T cells as potential mechan

185 ing feeding circuits, energy expenditure and glucose metabolism in concert are currently being explor

186 isms underlying adropin's effects on hepatic glucose metabolism in DIO mice.

187 ntify a MAFG-lncRNA axis controlling hepatic glucose metabolism in health and metabolic disease.

188 bunit is required for metformin's control of glucose metabolism in hepatocytes.

189 Elevated glucose metabolism in immune cells represents a hallmark

190 The effects of dsi-RNA knockdown on glucose metabolism in intact mosquitoes were monitored u

191 We detected significant changes in cerebral glucose metabolism in key anorexia nervosa-related struc

192 e also show that STRIDE can be used to image glucose metabolism in many mouse tissues, including tumo

193 ons in overall body fat content and improved glucose metabolism in mice fed either regular chow or a

194 ect on metabolic flexibility or postprandial glucose metabolism in middle-aged overweight subjects.

195 e potential mechanisms by which PF increases glucose metabolism in muscle and liver cells independent

196 objectives were to measure insulin-sensitive glucose metabolism in neonatal lambs with IUGR and to de

197 ies have reported that EGFR signaling drives glucose metabolism in NSCLC cells; however, the precise

198 rmine the effects of BCAA supplementation on glucose metabolism in obese, prediabetic individuals.

199 est that BCAA supplementation did not impair glucose metabolism in obese, prediabetic subjects.

200 s bone formation in part through stimulating glucose metabolism in osteoblast lineage cells.

201 s study revealed different patterns of brain glucose metabolism in patients with severe and mild phen

202 s study revealed different patterns of brain glucose metabolism in patients with the severe and mild

203 plays an important role in the regulation of glucose metabolism in peripheral tissues.

204 males, spontaneous opioid withdrawal altered glucose metabolism in regions associated with reward and

205 BDNF may be a key factor mediating increased glucose metabolism in response to exercise, with implica

206 that the cyclin D1-HNF4alpha axis regulates glucose metabolism in response to feeding.

207 activation and highlights the importance of glucose metabolism in septic inflammation.

208 d key biomarkers of inflammation, lipid, and glucose metabolism in the blood of patients with moderat

209 cadian clock, GSIS, islet transcriptome, and glucose metabolism in the context of diet-induced obesit

210 , yet the role that these play in regulating glucose metabolism in the liver is still unclear.

211 s ever investigated the alterations of brain glucose metabolism in these subjects by means of [(18)F]

212 G PET/CT to investigate alterations in brain glucose metabolism in these subjects.

213 a major role in the dysregulation of hepatic glucose metabolism in type-2 diabetes(1-3), the mechanis

214 Glucose metabolism in vertebrate retinas is dominated by

215 We show here a new method of imaging glucose metabolism in vivo by MRI chemical shift imaging

216 These data reveal that increased platelet glucose metabolism in vivo contributes to increased plat

217 irect genetic evidence for the importance of glucose metabolism in Wnt-induced bone formation is lack

218 the genetic determinates of body weight and glucose metabolism in znt7-KO mice.

219 s and beta-cell function, indices of healthy glucose metabolism, in obese mice and obese, prediabetic

220 inopathy we found significant alterations in glucose metabolism including increased pyruvate, suggest

221 o assess whether CHADN could improve hepatic glucose metabolism independent of a change in insulin re

222 The correspondence between cerebral glucose metabolism (indexing energy utilization) and syn

223 We find that when glucose metabolism induces insulin secretion, it also in

224 nalysis of 27 plasma biomarkers representing glucose metabolism, inflammation, adipokines, endothelia

225 ts of high compared with low dairy intake on glucose metabolism, insulin sensitivity, and metabolic f

226 eritoneal glucose tolerance test (IPGTT) for glucose metabolism, insulin tolerance test (ITT), and hi

227 ention was not associated with any change in glucose metabolism: insulin secretion (mean difference,

228 ention was not associated with any change in glucose metabolism; insulin secretion (mean difference -

229 ve glycolysis which caused increased flux of glucose metabolism into lactate.

230 Decline in brain glucose metabolism is a hallmark of late-onset Alzheimer

231 which begs the question of whether targeting glucose metabolism is a viable approach to control MPhi

232 Precise modulation of hepatic glucose metabolism is crucial during the fasting and fee

233 in AD and amnestic mild cognitive impairment glucose metabolism is dramatically decreased, probably o

234 ical role remains controversial, and whether glucose metabolism is functionally different during full

235 estigated whether hypothalamic reactivity to glucose metabolism is impaired in AN.METHODSTwenty-four

236 Glucose metabolism is tightly regulated in healthy hepat

237 ven the widespread use of 2-FDG PET to infer glucose metabolism, it is relevant to appreciate the pot

238 lycemic dividing RMCs initiates intermediate glucose metabolism, leading to increased cytosolic UDP s

239 cance of estrogen hormones for regulation of glucose metabolism, little is known about the roles of e

240 Disturbance of glucose metabolism may be implicated in cognitive defici

241 ow subpopulations of beta-cells with altered glucose metabolism may impact islet function.

242 -strain loop area and compared with regional glucose metabolism measured by (18)F-fluorodeoxyglucose

243 sed flux of MG formation linked to increased glucose metabolism mediated by proteolytic stabilisation

244 Flux of glucose metabolism, MG formation and glycation and chang

245 studies in cells confirmed abnormalities in glucose metabolism, mitochondrial oxygen consumption, an

246 The improvement in glucose metabolism observed in an intraperitoneal glucos

247 and TGR5 activity contribute to the altered glucose metabolism observed in ICP.

248 Reprogrammed glucose metabolism of enhanced aerobic glycolysis (or th

249 AHL has a significant impact on the regional glucose metabolism of the auditory pathway.

250 Our purpose was to use PET to evaluate the glucose metabolism of the inferior colliculus (IC) and p

251 In addition, the lower glucose metabolism of these areas was associated with hi

252 tructure and function, body composition, and glucose metabolism on adult female and male Sprague Dawl

253 the findings suggest that familial abnormal glucose metabolism or a primary insulin signaling pathwa

254 Perturbation of glucose metabolism or disruption of Myc function or ster

255 should allow assessment of diseases in which glucose metabolism or storage is altered, for instance,

256 Glucose metabolism parameters including fasting glucose,

257 Both treatments had neutral effects on glucose metabolism parameters.

258 Notably, glucose metabolism pathway genes were important in vivo

259 glucose homeostasis; however, remodeling of glucose metabolism pathways pales compared with adaptati

260 benefit of lifestyle intervention to improve glucose metabolism post transplantation is unproven.

261 benefit of lifestyle intervention to improve glucose metabolism posttransplantation is unproven.

262 inal pyruvate levels coupled to dysregulated glucose metabolism prior to detectable optic nerve degen

263 deoxyglucose ((18)F-FDG) PET, which assesses glucose metabolism, provide valuable and complementary i

264 ism by which the gut microbiota can modulate glucose metabolism, providing a potential approach for t

265 pathophysiology (VBP) studies of blood flow, glucose metabolism, regional homogeneity, and amplitude

266 ysfunctions, we evaluated islet function and glucose metabolism regulation in DKO pigs.

267 Accordingly, glucose metabolism remained unaltered.

268 ole of lncRNAs in CRC metabolism, especially glucose metabolism remains largely unknown.

269 Glucose metabolism showed decline primarily in the sympt

270 oles for two dehydrogenase proteins in human glucose metabolism that may contribute to individual res

271 Thus, Glut1-mediated glucose metabolism through both lactate production and O

272 Here, we report that glucose metabolism through oxidative phosphorylation (OX

273 Therefore, tacrolimus affects glucose metabolism through the butyrate-associated GLP-1

274 y mutated or deleted in cancer and regulates glucose metabolism through the PI3K-AKT pathway.

275 gnancy and assess associations with maternal glucose metabolism throughout pregnancy.

276 This study links glucose metabolism to antiviral responses.

277 ecular pathways that respond to the state of glucose metabolism to drive the morula to blastocyst tra

278 dob) leads to a paradoxical up-regulation of glucose metabolism to favor hepatocellular carcinogenesi

279 myloids can be dissolved upon restoration of glucose metabolism to produce functional secreted FVIII.

280 allows a large minority of cells with normal glucose metabolism to promote glucose-stimulated [Ca(2+)

281 in-GHSR axis modulates insulin secretion and glucose metabolism using mouse models lacking ghrelin (G

282 erum bile acids, FXR and TGR5 in gestational glucose metabolism using mouse models.

283 n seven thalamic nuclei using fMRI and brain glucose metabolism using positron emission tomography (P

284 llular role in modulating insulin-stimulated glucose metabolism via AKT signaling.

285 stprandial interorgan crosstalk of lipid and glucose metabolism was evaluated, by determining postpra

286 lation of cells deficient in GK activity and glucose metabolism was imposed on the islet or in which

287 n of genes involved in insulin signaling and glucose metabolism was performed using specific arrays.

288 B1alpha and SH2B1delta in energy balance and glucose metabolism, we generated mice lacking these brai

289 e of these differentially abundant miRNAs on glucose metabolism, we transfected miR-20b-5p, a highly

290 Key enzymes involved in glucose metabolism were also increased after 12 and 24 h

291 Parameters of glucose metabolism were analyzed according to the oral m

292 Mitochondrial function and fatty acid and glucose metabolism were impaired in HF-patients compared

293 No significant differences in glucose metabolism were observed up to 20 weeks post-inj

294 ed inflammation or fibrosis, and insulin and glucose metabolism were unchanged.

295 Lactate is an end product of glucose metabolism, which serves metabolic and nonmetabo

296 T2 isoform is critical for insulin-regulated glucose metabolism, while the role of the AKT1 isoform r

297 mitochondria play a central role in coupling glucose metabolism with insulin secretion.

298 r tracer for Abeta and [(18)F]FDG tracer for glucose metabolism) with a novel analytical framework, w

299 (IGFs), specifically IGF1 and IGF2, promote glucose metabolism, with their availability regulated by

300 ring, there was a reduced change in cerebral glucose metabolism within the cognitive corticothalamic