ライフサイエンスコーパス: gonadal

1 on of leukemic stem cells (LSCs) can utilize gonadal adipose tissue (GAT) as a niche to support their

2 ty were reduced, respectively, 75 and 70% in gonadal adipose tissue (GAT), 90 and 80% in subcutaneous

3 n of genes involved in metabolic pathways in gonadal adipose tissue of WT and APNko, but this effect

4 hat chemotherapy-resistant CD36+ LSCs co-opt gonadal adipose tissue to support their metabolism and s

5 ing blood glucose concentrations and greater gonadal adiposity (in females).

6 intrauterine growth restriction (IUGR) with gonadal, adrenal, and bone marrow failure, predispositio

7 hormone is disrupted most often, followed by gonadal, adrenal, and thyroid hormones, leading to abnor

8 lism, and action) and at all relevant sites (gonadal, adrenal, intratumoral) simultaneously at the ti

9 Assessment of gonadal and adrenal function (particularly if high index

10 mechanism that is influenced by circulating gonadal and adrenal hormones.

11 Cases of gonadal and extragonadal primary were included in the na

12 etal macrophages are associated with nascent gonadal and mesonephric vasculature during the initial p

13 measured reproductive-related morphological, gonadal and molecular changes during the entire life his

14 ment to Caenorhabditis elegans postembryonic gonadal and pharyngeal BMs.

15 ions with discrepancies between chromosomal, gonadal and phenotypic sex.

16 profound influence of TSD on male pituitary-gonadal and pituitary-thyroid axis hormones characterize

17 her TSD affects the course of male pituitary-gonadal and pituitary-thyroid axis related hormones duri

18 mouse models that allow distinction between gonadal and sex chromosome effects.

19 oatrophy with approximately 90% reduction in gonadal and subcutaneous white adipose tissue and brown

20 The 3 main types are called somatic, gonadal, and gonosomal mosaicism, which differ in terms

21 Gonadal androgen suppression (castration via orchiectomy

22 Suppression of gonadal androgens by medical or surgical castration rema

23 ators of the pituitary-thyroid and pituitary-gonadal axes.

24 s associated with the hypothalamic-pituitary-gonadal axis (HPG axis) in fish had become a conventiona

25 n, suppression of the hypothalamic-pituitary-gonadal axis appears to be a principal contributor, with

26 The hypothalamic-pituitary-gonadal axis controls puberty and reproduction and is ti

27 ditions impairing the hypothalamic-pituitary-gonadal axis during paediatric or pubertal life may resu

28 e following: (a) the hypothalamic-pitutitary-gonadal axis in female FHMs, where aromatase inhibition

29 role in regulating the hypothalamo-pituitary-gonadal axis in vivo through the activation of nNOS in n

30 lic information to the hypothalamo-pituitary-gonadal axis is mediated by leptin receptors on AgRP neu

31 The hypothalamic-pituitary-gonadal axis is of relevance in many processes related t

32 the activation of the hypothalamic-pituitary-gonadal axis is unclear.

33 es to orchestrate the hypothalamus-pituitary-gonadal axis physiology.

34 ent of the estrogenic hypothalamic-pituitary-gonadal axis regulation in females showed that leptin ac

35 rly activation of the hypothalamic-pituitary-gonadal axis results in central precocious puberty.

36 educed activity of the hypothalamo-pituitary-gonadal axis such as delayed puberty, hypothalamic ameno

37 r of the adult female hypothalamus-pituitary-gonadal axis, is paradoxically produced by neurons in th

38 regulate the mammalian hypothalamo-pituitary gonadal axis, may be involved in the seasonal control of

39 modifications to the hypothalamic-pituitary-gonadal axis.

40 e many aspects of the hypothalamic-pituitary-gonadal axis.

41 vate and maintain the hypothalamic-pituitary-gonadal axis.

42 rine system along the hypothalamus-pituitary-gonadal axis; however, most studies address either devel

43 otein, is the most abundant component in the gonadal BM, where it facilitates type IV collagen remova

44 d higher responses than women, likely due to gonadal cancer-testis-antigen expression.

45 diagnosis, and treatment of infertility and gonadal cancers, and in efforts to augment human and ani

46 c division is involved in the acquisition of gonadal cell fates.

47 hway to suppress endogenous mobile elements, gonadal cell TE landscapes can still dramatically change

48 , a portion of excessive early-stage somatic gonadal cells are found to originate from early-stage ge

49 We have previously shown that somatic gonadal cells are required for male GSC specification an

50 We find excessive early-stage somatic gonadal cells in E(z) mutant testes, which originate fro

51 In Drosophila, Nup107 knockdown in somatic gonadal cells resulted in female sterility, whereas male

52 KN-1 localizes to the plasma membrane of all gonadal cells, with apical and lateral bias.

53 ansposable elements (TEs) from mobilizing in gonadal cells.

54 by mixing ZW (female) and ZZ (male) cells in gonadal chimeras, or by altering oestrogen levels of ZW

55 Drosophila Piwi is the founding member of a gonadal clade of Argonaute proteins that serve as silenc

56 ines and discovered dynamic TE landscapes in gonadal cultures that were defined by a subset of active

57 This effect is partially dependent on gonadal DAF-16/FOXO activity.

58 e cancer survivors, but endocrine effects of gonadal damage are likewise central to long-term health

59 m the testes of wild-type mice and mice with gonadal defects due to disruption of the genes Mlh3, Hor

60 Subordinates experience gonadal development if separated from the queen.

61 zooplankton to the diet, somatic growth and gonadal development of whitefish.

62 actor 1 (Nr5a1, Sf-1) expression in the male gonadal development pathway, post sex determination, imp

63 us to study sex-specific gene expression and gonadal development.

64 ermal development and normally timed somatic gonadal development.

65 MRT1 is an essential sex-linked regulator of gonadal differentiation in avians, and that it likely ac

66 t, expression of thermoresponsive genes, and gonadal differentiation in fathead minnows, Pimephales p

67 In mice, Dmrt1 is required for male gonadal differentiation in somatic cells and germ cells

68 etermination, implies a vital role in testis gonadal differentiation.

69 l (E2) during embryonic development prior to gonadal differentiation.

70 of WwTW effluent exposure on reproduction or gonadal disruption in roach down the female germ line an

71 es a DAF-1/TGFbetaR signaling cascade in the gonadal distal tip cell (DTC), the germline stem cell ni

72 Increased gonadal DNA methylation changes following nicotine reexp

73 mal markers of airway reactivity, and global gonadal DNA methylation changes in F2 offspring in a sex

74 s are being examined in relation to parental gonadal dose, reconstructed using questionnaire and meas

75 opituitarism, obesity, diabetes mellitus, or gonadal dysfunction between survivors and siblings.

76 to identify genes that contribute to primary gonadal dysfunction.

77 Patients with 46,XY gonadal dysgenesis (GD) exhibit genital anomalies, which

78 varian atrophy syndrome in Drosophila called gonadal dysgenesis (GD).

79 XX female gonadal dysgenesis (XX-GD) is a rare, genetically hetero

80 ic problems including nephropathy, blastoma, gonadal dysgenesis and genital discordance.

81 nd generated XY(DMY-) mutants to investigate gonadal dysgenesis in medaka.

82 ovel mutant that is useful for investigating gonadal dysgenesis in phenotypic female patients with th

83 Mutations in human SRY cause gonadal dysgenesis leading to XY female development (Swy

84 Mutations in SRY cause 46 XY gonadal dysgenesis with female somatic phenotype (Swyer

85 Mutations in SRY cause gonadal dysgenesis with female somatic phenotype.

86 he gene, MAP3K1, are a common cause of 46,XY gonadal dysgenesis, accounting for 15-20% of cases [Ostr

87 ed dogs with XY chromosomal sex but complete gonadal dysgenesis, which is classified as 78, XY disord

88 ive comorbidities and hypothalamic-pituitary-gonadal dysregulation.

89 ecific genetic effects as well as downstream gonadal effects.

90 y sexual characteristics, but did not affect gonadal end points or inhibit ability to court females.

91 females was not solely reflective of absent gonadal estrogen, as chronically ovariectomized Kiss1r K

92 ssion but did not affect Sox9 mRNA levels in gonadal explants.

93 d outperformed gonadal expression levels and gonadal expression correlations in predicting germ cell-

94 Our method outperformed gonadal expression levels and gonadal expression correla

95 nt relationship to Sex-lethal is revealed by gonadal expression of RBP9, providing a maternal fail-sa

96 as a tightly timely and spatially controlled gonadal expression pattern.

97 regulatory landscape of genes with distinct gonadal expression patterns.

98 that hypodermal expression, but not somatic gonadal expression, of lin-28 is sufficient for restorin

99 al dwarfism, extreme insulin resistance, and gonadal failure and identified compound heterozygous fra

100 Transfusional iron overload and gonadal failure are addressed, followed by options for f

101 ressed in this chapter, including fertility, gonadal failure, erectile dysfunction, and menstrual iss

102 ower mRNA expression of PIK3R1 and PIK3CB in gonadal fat and liver respectively.

103 Gonadal fat develops postnatally, whereas subcutaneous f

104 Robustly enhanced lipolysis was found in gonadal fat of Adipoq(-/-) dams.

105 Female myonectin-deficient mice had larger gonadal fat pads and developed mild insulin resistance w

106 Our studies also implicate microRNAs in gonadal feedback control of gonadotropin synthesis and s

107 exual maturity had altered susceptibility to gonadal feminization and an impaired capacity to reprodu

108 There was no difference in the severity of gonadal feminization in roach derived from either WwTW e

109 g hormone (FSH) is an essential regulator of gonadal function and fertility.

110 udy suggests that FGF23 and Klotho influence gonadal function and testicular mineral ion homeostasis

111 known to regulate sexual differentiation and gonadal function in mammals.

112 Preservation of gonadal function is an important priority for the long-t

113 Laboratory-evaluated impaired gonadal function was found in 24.3% of female and 55.6%

114 anscription factor with an essential role in gonadal function.

115 drugs can adversely affect hypothalamic and gonadal functioning.

116 Therefore, we analyzed gonadal functions in survivors of HL.

117 nd histologically similar to the more common gonadal GCTs.

118 rming an ectopic niche similar to the native gonadal germ cell niche.

119 roliferation, survival and expression of the gonadal germline program as marked by MVH.

120 efish activity levels as well as somatic and gonadal growth all peaked during the summer, coinciding

121 and altered expression of key regulators of gonadal growth and steroidogenesis.

122 dymal white adipose tissue (eWAT) and female gonadal gWAT.

123 e sets indicative of teleost brain-pituitary-gonadal-hepatic (BPGH) axis function indicated that WWTP

124 ced AGD index and gonadal weight, changes in gonadal histology and altered expression of key regulato

125 or arrested egg deposition with no observed gonadal histopathology.

126 dence from animal studies indicates that the gonadal hormone 17beta-estradiol (E(2)) impacts the stru

127 nation of underlying genetic differences and gonadal hormone exposure.

128 cluding social partners, circadian cues, and gonadal hormone fluctuations.

129 ted status, suggesting that dysregulation of gonadal hormone function may be a characteristic trait o

130 adult brain function in males independent of gonadal hormone influence.

131 neurotrophic and angiogenic growth factors, gonadal hormone receptors, and neurotransmitters such as

132 to characterize the chemical composition and gonadal hormone regulation of these sexually dimorphic C

133 Together, these data indicate a stress and gonadal hormone responsive nucleus that is unique to fem

134 dimorphism have emphasized the importance of gonadal hormones and cell-autonomous influences in mamma

135 central nervous system (CNS) factors, genes, gonadal hormones and receptors, genitalia, and social/en

136 Here, we review the mechanisms by which gonadal hormones and sex chromosome complement each cont

137 c stress and the underlying contributions of gonadal hormones and sex chromosomes.

138 e organizational and activational effects of gonadal hormones and to genes on the sex chromosomes.

139 Gonadal hormones are linked to mechanisms that govern ap

140 These gonadal hormones are produced by the hypothalamic-pituit

141 These data show that gonadal hormones are required for maintaining sex-typica

142 Although these actions of gonadal hormones are well supported, the possibility tha

143 y and provide a potential mechanism by which gonadal hormones could regulate the maturation of the as

144 Among evolocumab-treated patients, gonadal hormones did not change from baseline to week 52

145 Here, we report that manipulations of gonadal hormones do significantly alter the maturation o

146 ned for a female phenotype unless exposed to gonadal hormones during a perinatal sensitive period.

147 specting the breadth and depth of the impact gonadal hormones have on brain functioning and its rich

148 discriminable, suggesting opposite roles for gonadal hormones in influencing male and female olfactor

149 tivity are sexually dimorphic or affected by gonadal hormones in the MePD.

150 ffects of stress, where the rapid decline of gonadal hormones in women combined with cellular aging p

151 Rats were used to determine how sex and gonadal hormones influence choices between small, immedi

152 The influence of gonadal hormones on multiple sclerosis (MS) is not well

153 printed genes is most likely attributable by gonadal hormones rather than by sex chromosome complemen

154 largely been attributed to modulation by the gonadal hormones testosterone and estradiol.

155 data provide a substantive mechanism linking gonadal hormones to cellular excitability and anhedonia-

156 y circuits was used to test contributions of gonadal hormones to sex differences in vHPC afferents.

157 d gonadectomies to test the contributions of gonadal hormones to this stress response.

158 , cortisol, adrenocorticotropic hormone, and gonadal hormones were analyzed at baseline and week 52.

159 An emerging hypothesis is that fluctuating gonadal hormones, especially estrogen, in the menstrual

160 adverse effects were observed in steroid or gonadal hormones, even at very low LDL-C levels.

161 itary males independent of pheromonal input, gonadal hormones, opponents, or social context.

162 s were not the consequence of the actions of gonadal hormones, we induced gonadal sex reversal to alt

163 al to hippocampal function and influenced by gonadal hormones.

164 ces in risky decision making are mediated by gonadal hormones.

165 RFR1 is regulated by perinatal but not adult gonadal hormones.

166 ry thyroid (HPT), and hypothalamic-pituitary-gonadal (HPG) axes and review the evidence for selected

167 ary-adrenal (HPA) and hypothalamic-pituitary-gonadal (HPG) axes in underlying some of these complex i

168 s are produced by the hypothalamic-pituitary-gonadal (HPG) axis and have been shown to determine sex

169 syndrome (PCOS) is a hypothalamic-pituitary-gonadal (HPG) axis disorder.

170 s associated with the hypothalamic-pituitary-gonadal (HPG) axis in female fathead minnows, specifical

171 The hypothalamic-pituitary-gonadal (HPG) axis is a key biological system required f

172 ral components of the hypothalamic-pituitary-gonadal (HPG) axis.

173 itary development and hypothalamic-pituitary-gonadal (HPG) function in adulthood.

174 h have focused on the hypothalamic-pituitary-gonadal (HPG)-axis and reproduction, but other effects h

175 nt, suggesting that sex hormones act via the gonadal-hypophyseal axis.

176 Cancer treatment can cause gonadal impairment.

177 Gonadal intact Dmp1-ERalpha(-/-) female mice had no sign

178 rce of niche Dpp, but instead is required in gonadal intermingled cells (ICs, the progenitor cells of

179 or extrinsic factors, we generated models of gonadal intersex by mixing ZW (female) and ZZ (male) cel

180 riptional analysis of hypothalamic-pituitary-gonadal-liver axis revealed negligible effects.

181 We show that gonadal macrophages are derived from primitive yolk-sac

182 the skeletal framework from initial to final gonadal maturation and use elemental mass ratios in bone

183 eract while PGCs are en route to the somatic gonadal mesoderm, and previous studies have shown that C

184 e in an identical manner to vertebrate aorta-gonadal-mesonephros (AGM) HSCs.

185 to detect germ cell-specific expression from gonadal microarray data.

186 The embryonic gonadal microenvironment has recently been shown to dete

187 Adrenal and gonadal mitochondrial metabolic activity requires electr

188 ing also act downstream of lin-28 in somatic gonadal morphogenesis and fertility.

189 We propose that the abnormal somatic gonadal morphogenesis of lin-28(lf) hermaphrodites resul

190 8 is sufficient for restoring normal somatic gonadal morphology in lin-28(lf) mutants.

191 d fertility associated with abnormal somatic gonadal morphology.

192 t the potential impact of assessing parental gonadal mosaicism has not been considered.

193 abolished in mutants, indicating a defective gonadal negative feedback control.

194 Somatic gonadal niche cells control the survival, differentiatio

195 fore, defines a secondary role for planarian gonadal niche cells in promoting GSC differentiation.

196 n germ cells, which are enwrapped by somatic gonadal niche cells, are freed into the body cavity, the

197 atic chimeras and stem cell competitions for gonadal niches.

198 ment, is not dependent on the genetic sex of gonadal or neural crest cells, and may be blocked by rep

199 rmone receptors are expressed in various non-gonadal organs.

200 ones regulate the morphogenesis of these non-gonadal organs.

201 with biological effects on metamorphosis and gonadal phenotypes, respectively, that were observed in

202 de-differentiate toward their common adrenal-gonadal precursor cell type.

203 involving the fusion of clusters of somatic gonadal precursor cells (SGPs) and their ensheathment of

204 primordial germ cells (PGCs) towards somatic gonadal precursor cells (SGPs).

205 mscribed by guidance signals towards somatic gonadal precursor cells (SGPs).

206 Somatic gonadal precursor cells and germ cells fail to prolifera

207 sets differential cell affinity for somatic gonadal precursors to specify stromal intermingled cells

208 ments dihydrotestosterone synthesis from non-gonadal precursors.

209 The simple Caenorhabditis elegans gonadal primordium, which contains two somatic gonad pre

210 from WT1(+) somatic progenitor pools in the gonadal primordium.

211 g of beta-catenin and variable expression of gonadal receptors and both CYP11B1 and CYP11B2.

212 The molecular expression of CYP11B2 and gonadal receptors in adenomas were also explored.

213 way, and expressed LHCGR and GNRHR, encoding gonadal receptors, at levels that were more than 100 tim

214 ich up-regulated dio3 expression and induced gonadal regression.

215 product of which plays an important role in gonadal responsiveness to FSH.

216 Expression of Sry in the gonadal ridge activates a Sox9-dependent gene regulatory

217 in a cellular model of the rat embryonic XY gonadal ridge) was reduced by 2-fold relative to wild-ty

218 ertoli cell differentiation in the embryonic gonadal ridge, is initiated by SRY, a Y-encoded architec

219 the differential effects of male and female gonadal secretions (commonly referred to as sex hormones

220 Using a mouse model that segregates gonadal sex (ovaries and testes) from chromosomal sex (X

221 cs" mixture during embryonic days 8 to 14 of gonadal sex determination and the incidence of adult ons

222 distinct between germ cells at the onset of gonadal sex determination at embryonic day 13 (E13) and

223 3) following ancestral exposure during fetal gonadal sex determination.

224 ar, the thermosensitive genetic triggers for gonadal sex differentiation are largely unknown.

225 ally dimorphic expression pattern, preceding gonadal sex differentiation, and is capable of respondin

226 embryonic expression, preceding the onset of gonadal sex differentiation.

227 the best candidate master regulator of avian gonadal sex differentiation.

228 ne (ESR2) polymorphism rs2978381, one of two gonadal sex hormone genes, significantly mitigate the ne

229 Female gonadal sex hormones are responsible for this sexual dim

230 ctively, these studies establish that female gonadal sex hormones underlie the sexual dimorphic diffe

231 , known as B6.Y (POS) mice, commonly undergo gonadal sex reversal and develop as phenotypic females.

232 Gonadal sex reversal did not alter the sexually dimorphi

233 the actions of gonadal hormones, we induced gonadal sex reversal to alter the hormonal environment o

234 arrying a Cys342Tyr substitution displays XY gonadal sex reversal with variable expressivity.

235 DMRT1 also maintains male gonadal sex: its loss, even in adults, can trigger sexua

236 secreted VPR-1 MSPd acts at least in part on gonadal sheath cell precursors in L1 to early L2 stage h

237 y aspects of developmental arrest of the non-gonadal soma [1, 4, 5].

238 at expresses Neo controlled by the zebrafish gonadal soma derived factor (gsdf) promoter.

239 to be expressed sex-specifically in the non-gonadal soma of hermaphrodites.

240 shut off TRA-1 expression in the entire non-gonadal soma, suggesting that somatic sexual differentia

241 ntally is regulated differently from the non-gonadal soma: daf-18/PTEN acts non-autonomously within t

242 First, gonadal somatic cell-targeting Amhr2-Cre mice were cross

243 for transplantation of PGCs aggregated with gonadal somatic cells and showed that reconstituted ovar

244 fficient to promote a male identity in adult gonadal somatic cells suggests that the sexual identity

245 demonstrate the presence of a functional non-gonadal somatic piRNA pathway in the adult fat body that

246 cells outside the gonads, the role of a non-gonadal somatic piRNA pathway is not well characterized.

247 Declines in the gonadal-somatic index (GSI) and increased mortality were

248 However, this was dependent on the gonadal status of the male housing partner, since those

249 eing paired with a male, irrespective of his gonadal status, increased female weight.

250 that Drosophila p53 is selectively active in gonadal stem cells after exposure to stressors that dest

251 reproductive axis is primarily regulated by gonadal steroid and circadian cues, but the starvation-s

252 n regressed oviducts (P<0.001) demonstrating gonadal steroid control, typical of an oviduct and egg s

253 Severe gonadal steroid deficiency induces bone loss in adult me

254 Part of the sex difference, but not the gonadal steroid dependence, resulted from differential p

255 ostaglandin signal to mate and show that the gonadal steroid DHP modulates mRNA levels of the putativ

256 In mice, we used gonadectomy to eliminate gonadal steroid hormone-dependent expression of AVP in t

257 Circulating gonadal steroid hormones are thought to modulate a wide

258 data suggest that dSTACs functionally mimic gonadal steroid hormones, enabling sirtuins to transduce

259 Gonadal steroid increases and fluctuations during peri-p

260 r identity and sex difference in response to gonadal steroid manipulations, but care is needed in our

261 o gel group) after suppression of endogenous gonadal steroid production experienced a profound decrea

262 serelin acetate, which suppresses endogenous gonadal steroid production, and were randomized to treat

263 and reproductive axes, but the existence of gonadal steroid-sensitive neuronal crosstalk remains und

264 er observed that exogenous RFRP-3 suppresses gonadal steroidogenesis and mating behavior in NMRs give

265 Examination of adrenal and gonadal steroidogenesis showed no defects in Tspo(-/-) m

266 (Dose-Response of Gonadal Steroids and Bone Turnover in Men; NCT00114114).

267 on/development in NMRs, we quantified plasma gonadal steroids and GnRH-1- and kisspeptin-immunoreacti

268 receptor (AR), suggesting changing levels of gonadal steroids during puberty directly modulate the so

269 At puberty, gonadal steroids have stimulatory effects on the activat

270 During sensitive periods in utero, gonadal steroids help organize biological sex difference

271 findings demonstrate that direct actions of gonadal steroids in GHRH neurons modulate growth and pub

272 We found that a primary effect of gonadal steroids in the highly sexually dimorphic preopt

273 Gonadal steroids modulate CNS plasticity, including phre

274 Gonadal steroids modulate growth hormone (GH) secretion

275 We examined here whether gonadal steroids modulated the excitability of kisspepti

276 acetate to suppress endogenous production of gonadal steroids, and anastrazole to suppress conversion

277 Pharmacological inhibition of Dnmts mimicked gonadal steroids, resulting in masculinized neuronal mar

278 ing inhibitory circuit and its modulation by gonadal steroids.

279 the gonads begins with fate specification of gonadal supporting cells into either ovarian pre-granulo

280 ustained testicular endocrine function, with gonadal testosterone production, as well as exocrine fun

281 atic bud initiation lags behind the onset of gonadal testosterone synthesis by about three days.

282 If gonadal tissue is spared-as in somatic genomic mosaicism

283 ntal mass ratios in bone, muscle, liver, and gonadal tissue to determine the fluxes and fates of sele

284 s by depleting body reserves and building up gonadal tissue.

285 duces robust wasting of adipose, muscle, and gonadal tissues that are distant from the tumor, phenoty

286 dhesion system that connects the uterine and gonadal tissues through their juxtaposed BMs at the site

287 pregnenolone, is synthesized in adrenal and gonadal tissues to initiate steroid synthesis by catalyz

288 In gonadal tissues, the Piwi-interacting (piRNA) pathway pr

289 omparative evaluation of long-term renal and gonadal toxicity is crucial to decisions regarding futur

290 of HL provides well-grounded information on gonadal toxicity of currently used treatment regimens an

291 both germ cells and somatic cells complicate gonadal transcriptome studies.

292 mal ovarian phenotype but with a "male-like" gonadal transcriptome.

293 Further, most neomales had gonadal transcriptomes similar to that of regular males.

294 I-III ovarian, I-II extragonadal, or stage I gonadal tumors with subsequent recurrence) received thre

295 s, hematologic malignancies, carcinomas, and gonadal tumors.

296 and adulthood included reduced AGD index and gonadal weight, changes in gonadal histology and altered

297 FD) gained 56% less body weight and 74% less gonadal white adipose tissue (WAT) than WT mice.

298 n reduction of body mass, total fat, size of gonadal white adipose tissue, and interscapular brown ad

299 RNA levels were significantly lower in iBAT, gonadal white adipose tissue, and livers of ppHF dams.

300 t VEGFA expression was lower in inguinal and gonadal white adipose tissues of ESR1 total body knockou