ライフサイエンスコーパス: DHEA

1 DHEA accelerated impaired healing in an impaired healing

2 DHEA action involves induction of PPARalpha mRNA and pro

3 DHEA also increased miR-21 in primary human hepatocytes

4 DHEA and androstenedione are synthesized by the adrenals

5 DHEA and testosterone appear to interact and modulate th

6 DHEA did not alter the small number (<3%) of newly forme

7 DHEA directly inhibited human and murine Th17 cells, ind

8 DHEA dosing was flexible (100-400 mg/day).

9 DHEA increased androgen receptor, c-Fos, and c-Jun recru

10 DHEA increased c-Jun, but not c-Fos, protein expression

11 DHEA increased ERK1/2 and c-Src phosphorylation in a GPE

12 DHEA induced both PPARalpha mRNA and protein levels, as

13 DHEA is widely available as a dietary supplement without

14 DHEA levels were associated with increases in cortical t

15 DHEA promoted nuclear exclusion of FoxO1 that was blocke

16 DHEA reduced memory accuracy for emotional stimuli, and

17 DHEA regulates microglial inflammatory responses through

18 DHEA replacement could play a role in prevention and tre

19 DHEA showed no evidence of efficacy in SS.

20 DHEA stimulates axonal growth from specific populations

21 DHEA supplementation in older women, but not in men, imp

22 DHEA treatment of endothelial cells increased PKA activi

23 DHEA was previously shown to bind to the nerve growth fa

24 DHEA, like G-1, increased GPER and ERalpha36 mRNA and pr

25 DHEA-stimulated phosphorylation of FoxO1 was inhibited b

26 DHEA-sulfate (DHEA-S), DHEA, and 17beta-estradiol stimul

27 Randomization resulted in 14 DHEA and 14 placebo group subjects.

28 campal tissue (percentage conversion of [14C]DHEA to [14C]7alpha-hydroxyDHEA) was decreased selective

29 During hypoglycemia on day 2, DHEA prevented blunting of all neuroendocrine, autonomic

30 as higher in women with INSR mutations after DHEA than in women with PCOS and controls (874.2 [SE 242

31 ale scores was observed in 23 subjects after DHEA and in 13 subjects after placebo treatments.

32 tions were greater (P < 0.05) in women after DHEA than after placebo.

33 Based on intention-to-treat analyses, DHEA therapy compared with placebo induced significant d

34 collected from the ADHD patients to analyze DHEA and DHEA-S levels.

35 ion is common in patients with HIV/AIDS, and DHEA appears to be a useful treatment that is superior t

36 During the protein challenge, cortisol and DHEA declined over 5 h.

37 During OGTT, cortisol and DHEA increased after the third hour and began to show si

38 did protein, and it stimulated cortisol and DHEA.

39 dy tested the hypothesis that serum DHEA and DHEA-S are predictors of major coronary heart disease (C

40 metry to analyze baseline levels of DHEA and DHEA-S in the prospective population-based Osteoporotic

41 Both DHEA and DHEA-S levels were inversely associated with the age-adj

42 d from the ADHD patients to analyze DHEA and DHEA-S levels.

43 However, mice produce DHEA and DHEA-sulfate (DHEAS) in the fetal brain.

44 duction of dehydroepiandrosterone (DHEA) and DHEA sulfate in the adrenal reticularis is inversely cor

45 precursors dehydroepiandrosterone (DHEA) and DHEA-sulfate has evolved in humans.

46 creases in brain concentrations of DHEAS and DHEA after injection of DHEAS i.p. were attenuated by pr

47 9 +/- 0.1; peak: 12.7 +/- 0.9 microg/dL) and DHEA (baseline: 15.6 +/- 1.3; nadir: 11.2 +/- 1.0; peak:

48 E2 and DHEA-S levels were strong predictors of case status (C s

49 age) is associated with both performance and DHEA levels.

50 onship between disease/fibrosis severity and DHEA-S levels was not seen in patients with cholestatic

51 Serum testosterone and DHEA-S levels were not statistically significantly assoc

52 ral conversion of the weak adrenal androgens DHEA and androstenedione into the AR ligands testosteron

53 In the competitive affinity assay, DHEA-S specifically binds to aptamer molecules pre-hybri

54 GPER antagonist G-15 attenuated DHEA- and BSA-conjugated DHEA-stimulated pri-miR-21 tran

55 The association between DHEA and CHD risk remained significant after adjustment

56 The association between DHEA-S and severity of NAFLD persisted after adjusting f

57 DHEA/-S, evidence for an association between DHEA/-S levels and cardiovascular events is contradictor

58 trated a strong positive correlation between DHEA levels and performance on digit span forward/backwa

59 n disposition indexes did not differ between DHEA- and placebo-treated women, indicating that the sli

60 There was also an interaction between DHEA and testosterone on cortical thickness of the right

61 tudies have examined the interaction between DHEA- and testosterone-related cortical maturation in hu

62 n N,N'-(1,2-dihydroxyethylene)bisacrylamide (DHEA) cross-linked pNIPMAm inner shell.

63 or (S)-orteronel were identical for blocking DHEA formation from pregnenolone and for 17alpha-hydroxy

64 Furthermore, elevated blood DHEA-S levels at 12 h after treatment in the mouse may a

65 Both DHEA and DHEA-S levels were inversely associated with th

66 Both DHEA and testosterone have been reported in animal and i

67 nt of primary rat hepatocytes decreased both DHEA- and nafenopin-induced FACO activity in primary rat

68 d sex steroid synthesis and disordered brain DHEA production and thus provide phenotypic clues about

69 ined the timescale of neuronal activation by DHEA, using light-induced release of DHEA from targeted

70 the expansion of IL-10-producing T cells by DHEA.

71 and protein were significantly increased by DHEA.

72 hat androgen precursors such as cholesterol, DHEA and progesterone, as well as androgens are highly u

73 is strongly associated with low circulating DHEA-S.

74 ist G-15 attenuated DHEA- and BSA-conjugated DHEA-stimulated pri-miR-21 transcription.

75 In contrast, DHEA/-S showed no statistically significant association

76 oncentration and a reduction in the cortisol/DHEA-ratio in hair.

77 e and after 1 yr of treatment with 50 mg/day DHEA or P.

78 A "dose effect" of decreasing DHEA-S and incremental fibrosis stage was observed with

79 ulin), hirsutism [ie, dehydroepiandosterone (DHEA) and androstenedione], and hunger (ie, ghrelin).

80 an increase in the dehydroepiandrostendione (DHEA) concentration and a reduction in the cortisol/DHEA

81 Dehydroepiandrosterone (DHEA) administration has been shown to reduce accumulati

82 Dehydroepiandrosterone (DHEA) and testosterone are widely promoted as antiaging

83 Dehydroepiandrosterone (DHEA) is a neurosteroid with anxiolytic, antidepressant,

84 Dehydroepiandrosterone (DHEA) is a neurosteroid with potential effects on neurog

85 Dehydroepiandrosterone (DHEA) is a ubiquitous adrenal hormone with immunomodulat

86 Dehydroepiandrosterone (DHEA) is a weak androgen also used to elevate testostero

87 Dehydroepiandrosterone (DHEA) is an endogenous adrenal steroid hormone with cont

88 Dehydroepiandrosterone (DHEA) is the most abundant circulating steroid hormone i

89 Dehydroepiandrosterone (DHEA) is the most abundant steroid hormone and has been

90 Dehydroepiandrosterone (DHEA) regulates gene expression as a ligand for a G-prot

91 Dehydroepiandrosterone (DHEA), a 19-carbon precursor of sex steroids, is abundan

92 Dehydroepiandrosterone (DHEA), a C19 human adrenal steroid, activates peroxisome

93 ect of administering dehydroepiandrosterone (DHEA) on short-term memory.

94 ect of administering dehydroepiandrosterone (DHEA) on visual-spatial performance in postmenopausal wo

95 dogenous S1R agonist dehydroepiandrosterone (DHEA) as an FDA-approved model drug.

96 gnenolone (PREG) and dehydroepiandrosterone (DHEA) have been reported to improve memory in aged roden

97 ine GCF cortisol and dehydroepiandrosterone (DHEA) levels.

98 of osteoporosis, and dehydroepiandrosterone (DHEA), a ubiquitous steroid precusor, are reported to be

99 By contrast, dehydroepiandrosterone (DHEA) suppressed VZ cell proliferation in males, but not

100 erone (T), 75 mg/day dehydroepiandrosterone (DHEA), or placebo (P); and 57 elderly women were studied

101 se reactions to form dehydroepiandrosterone (DHEA) and androstenedione (Andro), respectively, critica

102 ne and SULT2A1 gene, dehydroepiandrosterone (DHEA) and its sulfated form (DHEA-S), and characteristic

103 adrenal sex hormone dehydroepiandrosterone (DHEA), which is present in serum mainly as the sulfate D

104 To determine if dehydroepiandrosterone (DHEA) replacement improves insulin secretion, insulin ac

105 gen and neurosteroid dehydroepiandrosterone (DHEA) is available as over-the-counter hormonal therapy

106 hat the neurosteroid dehydroepiandrosterone (DHEA), when administered preclinically, could suppress p

107 t, the production of dehydroepiandrosterone (DHEA) and DHEA sulfate in the adrenal reticularis is inv

108 sess the efficacy of dehydroepiandrosterone (DHEA) as a potential treatment.

109 ministration of oral dehydroepiandrosterone (DHEA) during episodes of repeated hypoglycemia can preve

110 m adrenal precursors dehydroepiandrosterone (DHEA) and DHEA-sulfate has evolved in humans.

111 echnology to release dehydroepiandrosterone (DHEA), a neurosteroid that promotes neurogenesis and neu

112 reductions in serum dehydroepiandrosterone (DHEA) concentrations may be involved in bone mineral den

113 , most significantly dehydroepiandrosterone (DHEA) and to a certain degree testosterone.

114 mutations underwent dehydroepiandrosterone (DHEA) challenge; serum androgens were measured every 30

115 Serum levels of sulfated DHEA (DHEA-S) were measured by enzyme-linked immunosorbent ass

116 glycemic clamp (2.9 mmol/L) following either DHEA (1,600 mg) or placebo.

117 ance test before and after 2 years of either DHEA or placebo.

118 mia were randomly assigned to receive either DHEA or placebo; 90% (69 of 77) of the DHEA patients and

119 docannabinoids, docosahexanoyl ethanolamide (DHEA) and eicosapentaenoyl ethanolamide (EPEA) by activa

120 ve oxygenated docosahexaenoyl ethanolamide- (DHEA) derived products that regulated leukocyte motility

121 ous infusion of DHEA-S (30 mg/kg; ANTE EUG + DHEA-S), 3) hyperinsulinemic hypoglycemia (2.8 +/- 0.1 m

122 E HYPO group versus the ANTE EUG, ANTE EUG + DHEA-S, and ANTE HYPO + DHEA-S groups (13 +/- 5 vs. 32 +

123 he ANTE HYPO versus the ANTE EUG, ANTE EUG + DHEA-S, and ANTE HYPO + DHEA-S groups (57 +/- 8 vs. 22 +

124 E HYPO group versus the ANTE EUG, ANTE EUG + DHEA-S, and ANTE HYPO + DHEA-S groups (P < 0.05).

125 Our data showed that exogenous DHEA significantly downregulated IGF-1 and its receptor

126 We find DHEA to be an effective treatment for midlife-onset majo

127 r Andro production from progesterone and for DHEA from pregnenolone, indicating a distributive charac

128 tor beta by CD4(+) T cells was necessary for DHEA-mediated EAE amelioration, as well as for direct do

129 ein phosphatase 2A (PP2A) is responsible for DHEA action, and protein phosphatase 1 might be involved

130 At baseline, mean +/- SD for DHEA versus placebo groups were Schirmer I tests 4.5 +/-

131 piandrosterone (DHEA) and its sulfated form (DHEA-S), and characteristics of attention-deficit/hypera

132 Four DHEA and one placebo group patient dropped out because o

133 ion was found between elevated levels of GCF DHEA and the severity of periodontitis.

134 rs2270112 demonstrated significantly higher DHEA-S levels than the G allele carriers.

135 In support, 7alpha-hydroxylated DHEA increases the immune response in mice with greater

136 n the ANTE HYPO group versus the ANTE HYPO + DHEA-S group (2.0 +/- 0.2 vs. 3.3 +/- 0.6 nmol/l; P < 0.

137 ANTE EUG, ANTE EUG + DHEA-S, and ANTE HYPO + DHEA-S groups (13 +/- 5 vs. 32 +/- 3, 38 +/- 7, and 29 +

138 ANTE EUG, ANTE EUG + DHEA-S, and ANTE HYPO + DHEA-S groups (57 +/- 8 vs. 22 +/- 5, 18 +/- 6, and 18 +

139 ANTE EUG, ANTE EUG + DHEA-S, and ANTE HYPO + DHEA-S groups (P < 0.05).

140 us infusion of DHEA-S (30 mg/kg; ANTE HYPO + DHEA-S).

141 he purpose of this study was to determine if DHEA-S could preserve counterregulatory responses during

142 te-mediated cleavage of the 1,2-diol bond in DHEA produced multiresponsive core/shell microgels with

143 l interfering RNA knockdown of PKA inhibited DHEA-stimulated phosphorylation of FoxO1.

144 In year 2, all participants took open-label DHEA (50 mg/d).

145 Finally we asked whether the EGF/LIF/DHEA-responsive stem cells had an increased potential fo

146 Like DHEA, GPER agonists G-1 and fulvestrant increased pri-mi

147 ted with a reduced risk (odds ratio per 1 ln[DHEA-S], 0.1; 95% confidence interval, 0.0-0.3; P = 0.00

148 cohorts in the advanced NAFLD group had low DHEA-S levels, with the majority in the hypoadrenal rang

149 ntal fibrosis stage was observed with a mean DHEA-S of 1.03 +/- 0.05, 0.96 +/- 0.07, 0.83 +/- 0.11, 0

150 Group 3 had significantly higher mean DHEA scores compared with group 1 (P <0.05); however, th

151 ery 30 min for 4 h after ingestion of 100 mg DHEA.

152 s substantial change in the hormonal milieu, DHEA administration produced no beneficial effects on co

153 Moreover, DHEA administration enhanced serum levels of DHEA, DHEAS

154 Neither DHEA nor low-dose testosterone replacement in elderly pe

155 We report that 10 nm DHEA increases primary miR-21 (pri-miR-21) transcription

156 1-fold) between PAPS and raloxifene, but not DHEA.

157 erature on vascular and metabolic actions of DHEA/-S, evidence for an association between DHEA/-S lev

158 Administration of DHEA in symptomatic mice induced regulatory CD4(+) T cel

159 We suggest that exogenous application of DHEA accelerates impaired wound repair, results which ma

160 To investigate the brain basis of DHEA's impact on emotion modulation, patients were admin

161 suggest that physiological concentrations of DHEA activate a GPER intracellular signaling cascade tha

162 Conversion of DHEA locally to downstream steroid hormones leads to est

163 effects were mediated by local conversion of DHEA to estrogen, acting through the estrogen receptor,

164 f DHEA administration and the correlation of DHEA levels and performance in the placebo condition to

165 were randomly assigned to receive 50 mg/d of DHEA or matching placebo for 6 months.

166 BNN27, a C17-spiroepoxy derivative of DHEA, was shown to have antiapoptotic properties via mec

167 ential of our nanosensor in the detection of DHEA-S and other small molecules in biomedical applicati

168 free, specific and quantitative detection of DHEA-S at clinically appropriate concentrations with an

169 can be measured to achieve the detection of DHEA-S.

170 en and women showed no significant effect of DHEA on body-composition measurements.

171 hodology that did not demonstrate effects of DHEA administration on episodic and short-term memory ta

172 ent demonstrated large beneficial effects of DHEA administration on Mental Rotation, Subject-Ordered

173 However, the effects of DHEA on human or murine pathogenic immune cells, such as

174 s, could completely eliminate the effects of DHEA on stem cell proliferation.

175 tion, coupled with the documented effects of DHEA's androgenic metabolites on visual-spatial performa

176 n vitro model to characterize the effects of DHEA, prolactin, 17beta-estradiol on insulin-growth fact

177 men with low levels of the sulfated form of DHEA and bioavailable testosterone and 57 elderly women

178 vide phenotypic clues about the functions of DHEA in mouse brain development.

179 8) plus simultaneous intravenous infusion of DHEA-S (30 mg/kg; ANTE EUG + DHEA-S), 3) hyperinsulinemi

180 8) with simultaneous intravenous infusion of DHEA-S (30 mg/kg; ANTE HYPO + DHEA-S).

181 In addition, we show that local injection of DHEA accelerates impaired healing in an ageing mouse col

182 s spectrometry to analyze baseline levels of DHEA and DHEA-S in the prospective population-based Oste

183 ression analyses demonstrated that levels of DHEA and its metabolites were positively related to cogn

184 Low serum levels of DHEA and its sulfate predict an increased risk of CHD, b

185 Levels of DHEA were positively correlated with attention as measur

186 tion significantly increases serum levels of DHEA, DHEAS, testosterone and estrone and substantially

187 DHEA administration enhanced serum levels of DHEA, DHEAS, testosterone, and estrone, and regression a

188 and Visual Search tasks and serum levels of DHEA, DHEAS, testosterone, estrone, and cortisol were me

189 th advanced NAFLD had lower plasma levels of DHEA-S than patients with mild NAFLD in both the initial

190 2-16.4; P = 0.001), whereas higher levels of DHEA-S were associated with a reduced risk (odds ratio p

191 stances (P = 0.03), whereas higher levels of DHEA-S were associated with lower right atrial pressure

192 Higher levels of E2 and lower levels of DHEA-S were associated with PAH in men.

193 is associated with low circulating levels of DHEA.

194 lation, patients were administered 400 mg of DHEA (N=14) or placebo (N=15) and underwent 3T fMRI whil

195 oglycemic clamps (2.9 mmol/L) with 800 mg of DHEA or placebo administered before each clamp.

196 was significantly reduced after 6 months of DHEA therapy compared with placebo (-1119 muU/mL per 2 h

197 Precursors of DHEA such as pregnenolone or six of its major metabolite

198 tion by DHEA, using light-induced release of DHEA from targeted DNA nanocapsules.

199 both sexes, and neither full replacement of DHEA (in elderly men and women) nor partial replacement

200 We conclude that 2 years of replacement of DHEA in elderly men and women does not improve insulin s

201 Although there have been multiple reports of DHEA's antidepressant and anxiolytic effects, no researc

202 ret the juxtaposition of the null results of DHEA administration and the correlation of DHEA levels a

203 The synthesis of DHEA and sex steroids, but not mouse glucocorticoids and

204 Six weeks of DHEA administration was associated with a significant im

205 essant medications.Intervention Six weeks of DHEA therapy, 90 mg/d for 3 weeks and 450 mg/d for 3 wee

206 Six weeks of DHEA treatment also was associated with significant impr

207 However, most studies on DHEA have been performed in rodents, and there is little

208 If 14 consecutive subjects on DHEA did not respond, a Phase III trial would be conside

209 effects of a four week regimen of 50 mg oral DHEA on performance on the digit span, verbal span, and

210 domized, double-blinded, pilot trial of oral DHEA (200 mg/day) versus placebo was conducted.

211 lled crossover design in which 50 mg of oral DHEA was administered daily in the drug condition to exp

212 n inside the DNA capsule prevents photocaged DHEA from activating neurons prematurely.

213 Compared with placebo, DHEA reduced activity in the amygdala and hippocampus, e

214 n subjects and influence the ratio of plasma DHEA:DHEA-S.

215 er, we observed processivity in pregnenolone/DHEA pulse-chase experiments.

216 However, mice produce DHEA and DHEA-sulfate (DHEAS) in the fetal brain.

217 and inhibitor studies suggest that the rapid DHEA-mediated increase in miR-21 involves a G-protein-co

218 On the basis of clinicians' ratings, DHEA was superior in the intent-to-treat analysis, where

219 Among the women, 27 received DHEA and 30 received placebo.

220 Among the men, 29 received DHEA, 27 received testosterone, and 31 received placebo.

221 in the placebo group, subjects who received DHEA for 2 years had an increase in plasma levels of sul

222 Women who received DHEA had an increase in BMD at the ultradistal radius.

223 ese data provide novel evidence for relative DHEA-S deficiency in patients with histologically advanc

224 tabolism, 112 elderly subjects with relative DHEA deficiency ingested a labeled mixed meal and underw

225 females with subcutaneous pellets releasing DHEA or 17-OH pregnenolone at a constant rate failed to

226 Despite restoring DHEA sulphate concentrations to values observed in young

227 DHEA-sulfate (DHEA-S), DHEA, and 17beta-estradiol stimulated keratinocyte and f

228 cortical thickness associated with salivary DHEA and testosterone levels in a longitudinal sample of

229 The concurrent reduction of serum DHEA levels and visual-spatial performance in this popul

230 This study tested the hypothesis that serum DHEA and DHEA-S are predictors of major coronary heart d

231 However, simultaneous DHEA-S infusion during antecedent hypoglycemia preserved

232 However, since DHEA tended to decrease insulin action, the change over

233 These unimNPs produced a steady DHEA release in vitro for over two months at pH7.4.

234 compound and its corresponding free steroid DHEA in brain within 1 h of injection.

235 orter, Mrp4, transports the sulfated steroid DHEA-s, and sulfated bile acids interact with Mrp4 with

236 Novel derivatives of the steroid DHEA 1, a known uncompetitive inhibitor of G6PD, were de

237 ch is present in serum mainly as the sulfate DHEA-S, is the most abundant steroid hormone in human bl

238 ly increased dehydroepiandrosterone sulfate (DHEA-S) and reduced estrone levels in KC patients compar

239 enal steroid dehydroepiandrosterone sulfate (DHEA-S) has been shown in several studies to oppose cort

240 vidence that dehydroepiandrosterone sulfate (DHEA-S) is involved in an organism's response to stress

241 osensor with dehydroepiandrosterone sulfate (DHEA-S), a small-molecule steroid hormone, as the target

242 DHEA-sulfate (DHEA-S), DHEA, and 17beta-estradiol stimulated keratinoc

243 estosterone, dehydroepiandrosterone sulfate [DHEA-S], and estradiol) influence cardiovascular disease

244 levels (E2, dehydroepiandrosterone-sulfate [DHEA-S], and testosterone) are associated with PAH in me

245 Serum levels of sulfated DHEA (DHEA-S) were measured by enzyme-linked immunosorbe

246 had an increase in plasma levels of sulfated DHEA by a median of 3.4 microg per milliliter (9.2 micro

247 57 elderly women with low levels of sulfated DHEA.

248 In summary, DHEA can acutely preserve a wide range of key neuroendoc

249 We report that systemic DHEA levels are strongly associated with protection agai

250 n to relate baseline levels of testosterone, DHEA-S, and estradiol to the incidence of CVD (coronary,

251 aloxifene, which is considerably larger than DHEA, can bind only to the unliganded (open) enzyme, whe

252 We conclude that DHEA may have acute effects to protect against hypoglyce

253 We conclude that DHEA stimulates phosphorylation of FoxO1 via PI 3-kinase

254 These results demonstrate that DHEA reduces activity in regions associated with generat

255 We demonstrate that DHEA regulates PPARalpha action by altering both the lev

256 However, research demonstrates that DHEA supplementation does not increase serum testosteron

257 s provide initial neuroimaging evidence that DHEA may be useful as a pharmacological intervention for

258 In the present study we hypothesized that DHEA may stimulate PI 3-kinase-dependent phosphorylation

259 Together these results indicate that DHEA oxidative metabolism produces potent novel molecule

260 Together, our data indicate that DHEA-activated TrkA signaling is a potent regulator of m

261 We previously reported that DHEA has opposing actions in endothelial cells to stimul

262 Here we show that DHEA reduces microglia-mediated inflammation in an acute

263 Here, we show that DHEA significantly increased the growth rates of human n

264 In this study, we show that DHEA suppressed peripheral responses from patients with

265 on visual-spatial performance, suggests that DHEA administration may enhance visual-spatial performan

266 This suggests that DHEA suppresses proliferation in males via a glucocortic

267 The DHEA-S-cortisol ratios during stress were significantly

268 gnificant differences were noted between the DHEA and placebo groups for dry eye symptoms, objective

269 the response rate was 56% (43 of 77) for the DHEA group versus 31% (21 of 68) for the placebo group.

270 the response rate was 62% (43 of 69) for the DHEA group, compared to 33% (21 of 64) for the placebo p

271 Hence, the DHEA-loaded, CTB-conjugated unimNPs represent an RGC/S1R

272 , estrone, and cortisol were measured in the DHEA and placebo conditions.

273 n the placebo drug condition, but not in the DHEA condition.

274 rformance on the visual-spatial tasks in the DHEA condition.

275 pliance with the intervention was 97% in the DHEA group and 95% in the placebo group.

276 sterone index and estradiol increased in the DHEA group only.

277 nsulin-like growth factor 1 increased in the DHEA group only.

278 ough 7 subjects met response criteria in the DHEA group, 5 met the criteria in the placebo group, and

279 +/- 0.7% after 2 y of supplementation in the DHEA group; however, in the placebo group, spine BMD was

280 ither DHEA or placebo; 90% (69 of 77) of the DHEA patients and 94% (64 of 68) of the placebo patients

281 ide prospective, empirical evidence that the DHEA-S level is increased by acute stress in healthy hum

282 acute stress in healthy humans and that the DHEA-S-cortisol ratio may index the degree to which an i

283 ssociate from P450 17A1 before conversion to DHEA.

284 aseline during year 2 after the crossover to DHEA.

285 conversion of 17alpha-hydroxypregnenolone to DHEA than toward the 17alpha-hydroxylation of pregnenolo

286 an insulin sensitivity index in response to DHEA compared with placebo (+1.4 vs -0.7, P = .005).

287 stimulation of ET-1 secretion in response to DHEA may determine whether DHEA supplementation improves

288 omoter activity and secretion in response to DHEA treatment was augmented by PI 3-kinase blockade and

289 efficiently by SULT2A1 in vitro, yet unlike DHEA, raloxifene is not sulfated in vivo.

290 ients with SS should avoid using unregulated DHEA supplements, since long-term adverse consequences o

291 Microarray analysis of cortisol- versus DHEA sulfate-producing adrenal tissue demonstrated that

292 nly to the unliganded (open) enzyme, whereas DHEA binds both the open and closed forms.

293 porter gene activity in this system, whereas DHEA treatment did not.

294 on in response to DHEA may determine whether DHEA supplementation improves or worsens cardiovascular

295 The objective was to determine whether DHEA supplementation in older adults improves BMD when c

296 oratory animals, but it is not known whether DHEA decreases abdominal obesity in humans.

297 Treatment of BAEC with DHEA inhibited transactivation of the ET-1 promoter repo

298 ntrations did not differ in men treated with DHEA or placebo.

299 helial cells (BAEC and HAEC), treatment with DHEA (100 nM) acutely enhanced phosphorylation of FoxO1.

300 rapidly dephosphorylated upon treatment with DHEA and nafenopin.