ライフサイエンスコーパス: glucose metabolism

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

2 gulate glucose uptake and insulin-stimulated glucose metabolism.

3 R logic gate" to tightly regulate energy and glucose metabolism.

4 FXR also regulates postprandial lipid and glucose metabolism.

5 in renal tubular cells and reprogramming of glucose metabolism.

6 r of energy homeostasis, including lipid and glucose metabolism.

7 roliferation and survival, angiogenesis, and glucose metabolism.

8 Dietary proteins are important modulators of glucose metabolism.

9 s in age and amyloid-beta-related changes in glucose metabolism.

10 riance and amyloid-beta-related increases in glucose metabolism.

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

12 between amyloid-beta deposition and regional glucose metabolism.

13 ion of Glut1 and hexokinase 2, and decreased glucose metabolism.

14 xis, without affecting energy expenditure or glucose metabolism.

15 recovery of HS/PCs, thrombocyte numbers, or glucose metabolism.

16 and this gene might be involved in abnormal glucose metabolism.

17 ed nuclear receptor which controls lipid and glucose metabolism.

18 er insulin action or directly modify hepatic glucose metabolism.

19 fects on top of MC4R deficiency on lipid and glucose metabolism.

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

21 gh intrinsic cellular factors that reprogram glucose metabolism.

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

23 idize fatty acids and enhanced dependence on glucose metabolism.

24 lementary spatial information of the altered glucose metabolism.

25 is is reversed by inhibition of Akt, mTOR or glucose metabolism.

26 nd peripheral levels to mediate appetite and glucose metabolism.

27 le Tconv cell proliferation mainly relied on glucose metabolism.

28 current local and remote changes in regional glucose metabolism.

29 hem to regulate cholesterol, fatty acid, and glucose metabolism.

30 h AKT2 more important for insulin-stimulated glucose metabolism.

31 itive measures, brain amyloid deposition and glucose metabolism.

32 lso differed substantially in terms of their glucose metabolism.

33 tributes to systemic insulin sensitivity and glucose metabolism.

34 ally, we calculated years lived with healthy glucose metabolism.

35 active oxygen species (ROS) owing to altered glucose metabolism.

36 e treatment of metabolic disorders involving glucose metabolism.

37 ctivity, kidney structure, and regulation of glucose metabolism.

38 diet alone in adequately suppressing cardiac glucose metabolism.

39 A was also identified as being important for glucose metabolism.

40 sulin from pancreatic beta cells to regulate glucose metabolism.

41 testinal barrier, systemic inflammation, and glucose metabolism.

42 5-AG can deliver complementary insights into glucose metabolism.

43 complications extending far beyond impaired glucose metabolism.

44 analyses highlighted enrichment in lipid and glucose metabolism.

45 induced clearance of plasma uridine improves glucose metabolism.

46 in resistance, as well as, on feto-placental glucose metabolism.

47 for the production of acetate directly from glucose metabolism.

48 hanisms that contribute toward this improved glucose metabolism.

49 established cause of monogenic disorders of glucose metabolism.

50 nase (AMPK) is a key sensor and regulator of glucose metabolism.

51 e metabolism, cardiac septum development and glucose metabolism.

52 eased insulin signaling, and improved global glucose metabolism.

53 de distribution, body weight regulation, and glucose metabolism.

54 estigated its potential nutrigenetic role in glucose metabolism.

55 ion is necessarily associated with disturbed glucose metabolism.

56 atio of oxygen and carbohydrate (lactate and glucose) metabolism.

57 n+/-standard deviation) 1235+/-810 in normal glucose metabolism, 1109+/-748 in prediabetes, and 937+/

58 an+/-standard deviation) 3.4+/-2.8 in normal glucose metabolism, 3.0+/-2.7 in prediabetes, and 2.3+/-

59 Ppargamma, a central regulator of lipid and glucose metabolism, acting as its transcriptional co-act

60 g was shown to reduce bodyweight and improve glucose metabolism after the 56-week period of this tria

61 -1 as a result of electrical activity, while glucose metabolism alone is insufficient to depolarize t

62 Glucose metabolism also influenced the acute phase of in

63 ated that BEZ also has beneficial effects on glucose metabolism, although the underlying mechanisms o

64 rescribed dose, on measures of potassium and glucose metabolism.Among African-American adults with pr

65 1 in mice with diet-induced obesity impaired glucose metabolism and AKT activation.

66 e (PI3K) pathway regulates multiple steps in glucose metabolism and also cytoskeletal functions, such

67 pound B positron emission tomography imaging glucose metabolism and amyloid-beta deposition, we teste

68 cific to brain regions showing age-invariant glucose metabolism and amyloid-beta-related hypermetabol

69 to regulate a novel gene network involved in glucose metabolism and appetite control, suggesting a po

70 porter 1-mediated glucose influx that drives glucose metabolism and ATP production, which led to incr

71 effects of exendin-4 on the control of blood glucose metabolism and beta-cell mass.

72 es and suggest a connection between cellular glucose metabolism and Borrelia-induced cytokine product

73 some antiinflammatory approaches may affect glucose metabolism and cardiovascular health.

74 mproved glucose-dependent insulin secretion, glucose metabolism and cholesterol metabolism, compared

75 Because thiamine regulates intracellular glucose metabolism and corrects for multiple damaging ef

76 gic function for IKKepsilon in reprogramming glucose metabolism and driving progression in PDAC.

77 To investigate whether abnormal glucose metabolism and duration of diabetes mellitus (DM

78 g to a CREB-dependent increase in astrocytic glucose metabolism and elevated lactate export.

79 Abnormal glucose metabolism and enhanced oxidative stress acceler

80 omponents related to intramyocellular lipid, glucose metabolism and fiber size in soleus and gastrocn

81 In MCI with SNAP, sustained glucose metabolism and gray matter volume were associate

82 was associated with impaired feto-placental glucose metabolism and growth.

83 eding were related to altered feto-placental glucose metabolism and growth.

84 G influence its concentration via effects on glucose metabolism and handling.

85 lipid cycling in WAT and improved whole-body glucose metabolism and hepatic insulin sensitivity in co

86 worse memory performance, lower hippocampal glucose metabolism and increased levels of cerebrospinal

87 Sirt2-deficient mammary tumor cells altered glucose metabolism and inhibited malignant growth.

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

89 ere we show that HIF-1alpha is important for glucose metabolism and insulin action in skeletal muscle

90 control over GCK activation and, therefore, glucose metabolism and insulin secretion through regulat

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

92 bed in children; however, in adult patients, glucose metabolism and insulin sensitivity are essential

93 plementation for patients with T2DM improves glucose metabolism and insulin sensitivity.

94 pocampal memory formation is limited by both glucose metabolism and insulin signaling.

95 an important regulator of insulin-stimulated glucose metabolism and lipid oxidation, with relevance t

96 the mechanisms governing insulin resistance, glucose metabolism and lipogenesis in juvenile fish fed

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

98 1b(+) MNPs play crucial roles in maintaining glucose metabolism and net energy balance.

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

100 ype mice, which was largely due to increased glucose metabolism and reduced inflammation in skeletal

101 more insulin sensitive with increased muscle glucose metabolism and resistant to diet-induced obesity

102 f amyloid and regional tauopathy on cerebral glucose metabolism and subsequent memory decline.

103 binding protein (CREB) is a key regulator of glucose metabolism and synaptic plasticity that is canon

104 Baseline glucose metabolism and task-specific changes can be quan

105 idate a novel approach to assessing baseline glucose metabolism and task-specific changes in a single

106 murine pancreatic beta-cells, which improved glucose metabolism and the adaptation of beta-cells to o

107 al molecular mechanism for the governance of glucose metabolism and the control of hepatic lipid accu

108 r understanding the regulatory mechanisms of glucose metabolism and treatment of T2D.

109 llular 1,3-BPG levels in response to altered glucose metabolism and underscore the potential for chem

110 total body irradiation showed alterations in glucose metabolism and, when challenged with HFD, marked

111 ify a crucial link among oncogene signaling, glucose metabolism, and cytoplasmic p53, which may poten

112 ceptor (GLP-1R) is a key regulator of normal glucose metabolism, and exogenous GLP-1R agonist therapy

113 ose tissue (WAT), FGF21 regulates aspects of glucose metabolism, and in susceptible WAT depots, it ca

114 sociated with anxiety-like behavior, altered glucose metabolism, and insulin resistance in male offsp

115 ted fat load on insulin sensitivity, hepatic glucose metabolism, and lipid metabolism in humans.

116 ioactivity was taken as a surrogate index of glucose metabolism, and markers of thyroid function were

117 combining 2-deoxy-D-glucose, which inhibits glucose metabolism, and metformin, which inhibits oxygen

118 ting circadian regulation of energy balance, glucose metabolism, and postprandial inflammatory respon

119 ose, to map regional cerebral blood flow and glucose metabolism, and with [(11)C]-isoaminobutyric aci

120 r exercise-mediated changes in cardiomyocyte glucose metabolism are important for physiological cardi

121 way, dysregulated tumor pHe and upregulated glucose metabolism are linked tightly and their relative

122 MC4R effects on energy expenditure and glucose metabolism are primarily mediated by the G prote

123 We aimed to use decline in PCC glucose metabolism as a proxy for the development and pr

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

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

126 Regional differences in glucose metabolism between the highest and lowest metabo

127 We further found differences in glucose metabolism between the primary PDTX and distant

128 cted longitudinal changes in body weight and glucose metabolism biomarkers among women with prior ges

129 us japonicus, can activate AMPK and modulate glucose metabolism both in vitro and in vivo.

130 This production is independent of glucose metabolism but requires sodium/glucose cotranspo

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

132 posttranslational activation of GCK enhances glucose metabolism by approximately 35%.

133 r data suggest that BEZ may improve impaired glucose metabolism by augmenting hepatic mitochondrial p

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

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

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

137 Taken together, our results indicate that glucose metabolism changed during the course of HSV infe

138 Cancer cells display altered glucose metabolism characterized by a preference for aer

139 triggered by decreased whole-brain cerebral glucose metabolism (CMRglc) has not been resolved by pre

140 ce developed insulin resistance with reduced glucose metabolism compared to that in wild-type mice.

141 ing EML4-ALK rearrangements displayed higher glucose metabolism compared with EML4-ALK-negative NSCLC

142 ated apolipoproteins in de novo lipogenesis, glucose metabolism, complement activation, blood coagula

143 thus demonstrate that adaptive responses in glucose metabolism contribute to macrophage migratory ac

144 Restoration of central regulation of glucose metabolism could be a promising therapeutic targ

145 F-FDG injection) to measure changes in tumor glucose metabolism (DeltaSUVmax).

146 ed neurodegeneration status (temporoparietal glucose metabolism determined by fluorodeoxyglucose F 18

147 d NASH-related phenotypes in mice, including glucose metabolism disorders, lipid accumulation and enh

148 Accordingly, alterations in glucose metabolism, divergences in free fatty acids and

149 p-regulated genes involved in DNA repair and glucose metabolism, down-regulated proteolysis and prote

150 lammatory signaling, insulin resistance, and glucose metabolism driven by an HFD can be modified by a

151 nhibition of T cell Akt/mTORC1 signaling and glucose metabolism drives T cell dysfunction.

152 Here, we investigate the changes of glucose metabolism during epithelial mesenchymal transit

153 r study sheds new light on the regulation of glucose metabolism during major developmental transition

154 al glucose uptake, brain insulin may improve glucose metabolism during systemic hyperinsulinemia.

155 lusion:PPM1K rs1440581 may affect changes in glucose metabolism during weight loss, and this effect i

156 In comparison with glucose metabolism, early-phase (11)C-DED and (11)C-PiB

157 ompanied by beta-cell dysfunction in fat and glucose metabolism, enhancing their risk of type 2 diabe

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

159 ondary, but participating, role of GLUT2 and glucose metabolism for GLP-1 secretion via an amplifying

160 aphy) and ND (hippocampal volume or cortical glucose metabolism from AD-vulnerable regions).

161 Pnpla2, AdipoQ, Fasn) adipogenic genes, and glucose metabolism genes (Glut4, Irs1).

162 d to induction of two proteins important for glucose metabolism, Glut1 and Hexokinase 2 (HXK2).

163 Defective glucose metabolism has been identified as a feature of A

164 Robust preference for fermentative glucose metabolism has motivated domestication of the bu

165 Sequential metabolic enzymes in glucose metabolism have long been hypothesized to form m

166 des or directly promote selected pathways of glucose metabolism have suggested opportunities for futu

167 26 genes showed that mostly genes related to glucose metabolism, immune system and development were d

168 n of a GCK optical biosensor and potentiates glucose metabolism, implicating rises in cytoplasmic Ca(

169 used FDG-PET to measure resting state brain glucose metabolism in 131 DOC patients to identify objec

170 To investigate, we examined glucose metabolism in 18-mo-old transgenic mice with mus

171 ween gut microbiota, insulin resistance, and glucose metabolism in 3 inbred mouse strains with differ

172 t oversupply of retinol would further impair glucose metabolism in a mouse model of diet-induced insu

173 hese changes influence systemic immunity and glucose metabolism in a whole-body integrative and a neu

174 HFD did not affect body weight or glucose metabolism in atERalphaKO- compared to control m

175 on spatial organization and isoform-specific glucose metabolism in cells.

176 that IGF2 controls bone growth by regulating glucose metabolism in chondrocytes.

177 Consequently, targeting of EGFR-driven glucose metabolism in combination with pharmacological s

178 el EML4-ALK-HIF1alpha-HK2 cascade to enhance glucose metabolism in EML4-ALK-positive NSCLC.

179 fat diet on glucose tolerance and hepatocyte glucose metabolism in female offspring.

180 (ii) MP increased whole-brain glucose metabolism in HC but not in CA; and group by cha

181 significant role in the acute regulation of glucose metabolism in healthy humans and render the oxyt

182 zation of metabolic enzymes participating in glucose metabolism in human cells.

183 Multiple-tracer approaches for investigating glucose metabolism in humans usually involve the adminis

184 Metabolic analysis showed that YC-1 shifted glucose metabolism in hypoxic cells from anaerobic glyco

185 secretion, oxygen consumption, and [U-(13)C]glucose metabolism in islets isolated from the pancrease

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

187 related protein 1 (LRP1) regulates lipid and glucose metabolism in liver and adipose tissue.

188 relevant, multienzyme metabolic complex for glucose metabolism in living human cells.

189 T, we measured differences in regional brain glucose metabolism in males and females following morphi

190 oxygen utilization, energy homeostasis, and glucose metabolism in mammalian cells.

191 ical assays to measure changes in myocardial glucose metabolism in mice subjected to acute and chroni

192 nteraction and synergy in regulating hepatic glucose metabolism in mice.

193 pentose phosphate pathway is a key route of glucose metabolism in most organisms, providing NADPH fo

194 in basal and stimulated states, and improved glucose metabolism in obesity- and diabetes-prone C57BL/

195 also increased insulin-stimulated whole body glucose metabolism in old mice, which could be attribute

196 Glucokinase (GCK) controls the rate of glucose metabolism in pancreatic beta cells, and its act

197 To assess reductions of cerebral glucose metabolism in Parkinson's disease (PD) with 18F-

198 lin resistance with significant increases in glucose metabolism in peripheral organs.

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

200 strate that HIF-1alpha is a key regulator of glucose metabolism in skeletal muscle by directly contro

201 pose tissues may therefore affect whole-body glucose metabolism in the absence of an effect on body w

202 Elevated glucose metabolism in the availability of oxygen, a phen

203 at risk for Alzheimer's disease show reduced glucose metabolism in the brain.

204 ationship between Wnt signaling and neuronal glucose metabolism in the cellular context.

205 al stimulation was associated with increased glucose metabolism in the cingulate and prefrontal brain

206 analyses identified elevated and imbalanced glucose metabolism in the Igf2 null mouse.

207 transcriptional upregulation of effectors of glucose metabolism in the kidney.

208 PD participants showed reduced glucose metabolism in the occipital and inferior parieta

209 A reduction in glucose metabolism in the posterior cingulate cortex (PC

210 ucose metabolism was reduced with age, while glucose metabolism in the precuneus was maintained acros

211 Diabetes is associated with impaired glucose metabolism in the presence of excess insulin.

212 but, rather, correlates with suppression of glucose metabolism in the tricarboxylic acid cycle.

213 layed distinctly different patterns of brain glucose metabolism in their homecage, including areas as

214 e the potential to provide information about glucose metabolism in tumor tissue.

215 Strikingly, directly comparing lactate and glucose metabolism in vivo indicated that lactate's cont

216 rate that it is possible to measure cerebral glucose metabolism in vivo with sub-second time resoluti

217 ulin resistance and beta-cell dysfunction in glucose metabolism in youth with prediabetes, the relati

218 ween greater iron stores and disturbances in glucose metabolism, including increased risk of type 2 d

219 for the lifetime risk of developing impaired glucose metabolism, including prediabetes, as are data f

220 s with subthreshold amyloid, suggesting that glucose metabolism increases before decreasing in the co

221 Adequate suppression of cardiac glucose metabolism increases the interpretability and di

222 hat although acute inhibition of EGFR-driven glucose metabolism induces only minimal cell death, it l

223 g in AgRP neurons is important in regulating glucose metabolism, insulin signaling in POMC neurons co

224 Impaired glucose metabolism is a substantial burden on population

225 Therefore, modulation of hepatic glucose metabolism is an important target for antidiabet

226 Liver glucose metabolism is dependent on glucokinase activity.

227 We have asked whether glucose metabolism is enhanced by either a fall in intra

228 geted therapies (e.g. PLX-4032/vemurafenib), glucose metabolism is reduced, and cells increase mitoch

229 er, a neglected but very important branch of glucose metabolism is the hexosamine biosynthesis pathwa

230 examine the impact of "breakfast" on hepatic glucose metabolism later in the same day.

231 d CO adipose tissue, including components of glucose metabolism, lipid droplet trafficking, and cytos

232 termined the effects of the miR-29 family on glucose metabolism, lipid metabolism, and insulin respon

233 studies indicated that shizukaol F modulates glucose metabolism mainly by AMPKa phosphorylation activ

234 mutant cells exhibit a profound reliance on glucose metabolism, malate-aspartate shuttle deregulatio

235 eless, their positive influence on lipid and glucose metabolism may have potential in the control of

236 regulates many important pathways, including glucose metabolism, membrane mechanical stability, and c

237 status (oral glucose tolerance test; normal glucose metabolism [n=1269], prediabetes [n=335], or T2D

238 ugh concomitant Pten deletion normalizes the glucose metabolism of Ad/N1ICD mice, it dramatically acc

239 PDXs reproduced the glucose metabolism of the parental tumors and therefore

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

241 Chemical inhibition of glucose metabolism or glucose deprivation substantially

242 d exposure to mild cold may lead to improved glucose metabolism or prevent the development of obesity

243 in T2DM (B=-184 [-297 to -71]) versus normal glucose metabolism (P for trend=0.001).

244 2DM (B=-0.61 [-0.97 to -0.25]) versus normal glucose metabolism (P for trend=0.001).

245 Both treatments had neutral effects on glucose metabolism parameters.

246 au), (11)C-PiB (amyloid-beta) and (18)F-FDG (glucose metabolism) positron emission tomography, apolip

247 KO mice had improved insulin sensitivity and glucose metabolism, possibly secondary to the effects of

248 ogenesis, and glucose transporter 1-mediated glucose metabolism promoted Tfh cell responses.

249 Glucose metabolism promotes insulin secretion in beta-ce

250 T versus NGT is in line with the compromised glucose metabolism reflected in impaired beta-cell funct

251 ention in the highest compared to the lowest glucose metabolism regions defined in young adults (T =

252 Here, we show that glucose metabolism regulates pro-inflammatory NF-kappaB

253 Here, the authors show that glucose metabolism regulates pro-inflammatory responses

254 shift in bioenergetics and in activation of glucose-metabolism regulating Akt/AMPK/p70S6 kinase path

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

256 tested whether and how life-long changes in glucose metabolism relate to amyloid-beta deposition and

257 gh early and life-long regional variation in glucose metabolism relates to the regional vulnerability

258 In vivo analysis of hepatic glucose metabolism revealed that the hepatic glucokinase

259 proteins involved in nucleotide metabolism, glucose metabolism, ribosome biogenesis, and phosphoryla

260 S: The gut microbiota affects host lipid and glucose metabolism, satiety, and chronic low-grade infla

261 [U-(13)C]glucose metabolism showed a twofold increase in alanine

262 eural control of hepatic functions including glucose metabolism.SIGNIFICANCE STATEMENT A growing body

263 ion becomes dysregulated (ie, uncoupled from glucose metabolism) so that insulin secretion persists i

264 n %-hyperemia (laser-Doppler flowmetry), and glucose metabolism status (oral glucose tolerance test;

265 tagonize the physiological actions of GIP in glucose metabolism, subcutaneous abdominal adipose tissu

266 Results show that (i) CA had lower baseline glucose metabolism than HC in frontal cortex including a

267 e transcription of several key regulators of glucose metabolism that contain HREs, suggesting a role

268 cells versus xenografts reveals differential glucose metabolism that could reflect distinct tumor mic

269 unlike celastrol, has beneficial effects on glucose metabolism that occur independently of its lepti

270 ime, establish a vital role of FAK in cancer glucose metabolism through alterations in the OXPHOS-to-

271 nd suggest a model for regulation of hepatic glucose metabolism through interdependent FoxO/FoxA bind

272 gnals and Foxp3 balance mTORC1 signaling and glucose metabolism to control the proliferation and supp

273 n in early development and cancer depends on glucose metabolism to fuel macromolecule biosynthesis.

274 uded that M. leprae could modulate host cell glucose metabolism to increase the cellular reducing pow

275 uirements and found an increased reliance on glucose metabolism to sustain PIK3CA mutant cell prolife

276 To assess the contribution of glucose metabolism to the regional vulnerability to amyl

277 ween the rs1440581 PPM1K genetic variant and glucose-metabolism traits during weight loss.The rs14405

278 We measured brain glucose metabolism using PET and [(18)F]FDG both at base

279 We assessed glucose metabolism, ventricular function and remodeling,

280 ated insulin resistance and deterioration of glucose metabolism via altered neurocircuit functions.

281 co-controls CNS glucose sensing and systemic glucose metabolism via regulation of glucose uptake acro

282 Cerebral glucose metabolism was assessed with positron emission t

283 cose metabolism were found such that frontal glucose metabolism was reduced with age, while glucose m

284 al mechanisms mediating these effects, brain glucose metabolism was studied in a subset of monkeys (n

285 an adipokine that plays a role in lipid and glucose metabolism, was identified as the most significa

286 In line with ghrelin's proposed role in glucose metabolism, we find decreased glucose-stimulated

287 e phospholipid metabolism regulates systemic glucose metabolism, we perturbed choline/ethanolamine ph

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

289 in age and amyloid-beta-dependent changes in glucose metabolism were found such that frontal glucose

290 Anthropometrics and biomarkers of glucose metabolism were investigated in a observational

291 aragangliomas often exhibit dysregulation of glucose metabolism, which is also driven by mutations in

292 is increased expression of genes involved in glucose metabolism, which led to chronic degenerative ch

293 n oncogenic function of YAP in reprogramming glucose metabolism, while the underlying mechanism remai

294 lysis and more specifically FAK-reprogrammed glucose metabolism will disrupt the bioenergetic and bio

295 This work links glucose metabolism with cartilage development and provid

296 maging disease-specific patterns of regional glucose metabolism with PET and (18)F-FDG allows for a h

297 Inhibition of glucose metabolism with the GLUT4 inhibitor ritonavir el

298 as an important counterregulatory hormone in glucose metabolism, with actions opposing those of insul

299 taken for 3 mo, on measures of potassium and glucose metabolism, with measures collected from frequen

300 cretion, and expression of genes involved in glucose metabolism, without impacting the basal oxygen c