Endocrinology

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Transcriptional Suppression of Type 1 Angiotensin II Receptor Gene Expression by Peroxisome Proliferator-Activated Receptor-γ in Vascular Smooth Muscle Cells*
Endocrinology - Tập 142 Số 7 - Trang 3125-3134 - 2001
Akira Sugawara, Kazuhisa Takeuchi, Akira Uruno, Yukio Ikeda, Shuji Arima, Masataka Kudo, Kazunori Sato, Yoshihiro Taniyama, Sadayoshi Ito
Androgen-Dependent Regulation of Androgen Nuclear Receptor in the Rat Ventral Prostate*
Endocrinology - Tập 110 Số 6 - Trang 1926-1932 - 1982
Jean‐Paul Blondeau, Etienne‐Emile Baulieu, P Röbel
Foxl3, a Target of miR-9, Stimulates Spermatogenesis in Spermatogonia During Natural Sex Change in <i>Monopterus albus</i>
Endocrinology - Tập 157 Số 11 - Trang 4388-4399 - 2016
Yu Gao, Dan Jia, Qing Hu, Dapeng Li
Transdifferentiation of Differentiated Ovary into Functional Testis by Long-Term Treatment of Aromatase Inhibitor in Nile Tilapia
Endocrinology - Tập 155 Số 4 - Trang 1476-1488 - 2014
Lina Sun, Xiaolong Jiang, Qing‐Ping Xie, Jing Yuan, Baofeng Huang, Wenjing Tao, Linyan Zhou, Yoshitaka Nagahama, Deshou Wang
Females with differentiated ovary of a gonochoristic fish, Nile tilapia, were masculinized by long-term treatment with an aromatase inhibitor (Fadrozole) in the present study. The reversed gonads developed into functional testes with fertile sperm. The longer the fish experienced sex differentiation, the longer treatment time was needed for successful sex reversal. Furthermore, Fadrozole-induced sex reversal, designated as secondary sex reversal (SSR), was successfully rescued by supplement of exogenous 17β-estradiol. Gonadal histology, immunohistochemistry, transcriptome, and serum steroid level were analyzed during SSR. The results indicated that spermatogonia were transformed from oogonia or germline stem cell-like cells distributed in germinal epithelium, whereas Leydig and Sertoli cells probably came from the interstitial cells and granulosa cells of the ovarian tissue, respectively. The transdifferentiation of somatic cells, as indicated by the appearance of doublesex- and Mab-3-related transcription factor 1 (pre-Sertoli cells) and cytochrome P450, family 11, subfamily B, polypeptide 2 (pre-Leydig cells)-positive cells in the ovary, provided microniche for the transdifferentiation of germ cells. Decrease of serum 17β-estradiol was detected earlier than increase of serum 11-ketotestosterone, indicating that decrease of estrogen was the cause, whereas increase of androgen was the consequence of SSR. The sex-reversed gonad displayed more similarity in morphology and histology with a testis, whereas the global gene expression profiles remained closer to the female control. Detailed analysis indicated that transdifferentiation was driven by suppression of female pathway genes and activation of male pathway genes. In short, SSR provides a good model for study of sex reversal in teleosts and for understanding of sex determination and differentiation in nonmammalian vertebrates.
Thyrotropin-Releasing Hormone (TRH): Distribution in Hypothalamic and Extrahypothalamic Brain Tissues of Mammalian and Submammalian Chordates
Endocrinology - Tập 95 Số 3 - Trang 854-862 - 1974
Ivor M.D. Jackson, Seymour Reichlin
Growth Hormone Release in the Rat: Effects of Somatostatin and Thyrotropin- Releasing Factor
Endocrinology - Tập 97 Số 5 - Trang 1151-1156 - 1975
Marvin R. Brown, Wylie Vale
Myostatin Gene Deletion Prevents Glucocorticoid-Induced Muscle Atrophy
Endocrinology - Tập 148 Số 1 - Trang 452-460 - 2007
H. Gilson, Olivier Schakman, Lydie Combaret, Pascale Lause, Luc Grobet, Didier Attaix, Jean‐Marie Ketelslegers, Jean‐Paul Thissen
Dexamethasone Impairs Growth Hormone (GH)-Stimulated Growth by Suppression of Local Insulin-Like Growth Factor (IGF)-I Production and Expression of GH- and IGF-I-Receptor in Cultured Rat Chondrocytes*
Endocrinology - Tập 139 Số 7 - Trang 3296-3305 - 1998
Christian Jux, Kathrin Leiber, Ulrike Hügel, Werner Blum, Claes Ohlsson, Günter Klaus, Otto Mehls
Increased Bone Turnover and Possible Accelerated Fracture Healing in a Murine Model With an Increased Circulating C-Type Natriuretic Peptide
Endocrinology - Tập 156 Số 7 - Trang 2518-2529 - 2015
Eri Kondo, Akihiro Yasoda, Toshihito Fujii, Kazumasa Nakao, Yui Yamashita, Yoriko Ueda-Sakane, Naotetsu Kanamoto, Masako Miura, Hiroshi Arai, Masashi Mukoyama, Nobuya Inagaki, Kazuwa Nakao
Recent studies have revealed that C-type natriuretic peptide (CNP) is a potent stimulator of endochondral bone growth. Nevertheless, the effect of CNP on bone turnover has not yet been well studied. To elucidate this issue, we investigated the bone phenotype of a mouse model with elevated plasma CNP concentrations (SAP-CNP-Tg mice) in the present study. Microcomputed tomography (CT) analysis revealed less bone in femurs, but not in lumber vertebrae, of young adult SAP-CNP-Tg mice than that of wild-type mice. Bone histomorphometry of the tibiae from 8-week-old SAP-CNP-Tg mice showed enhanced osteoblastic and osteoclastic activities, in accordance with elevated serum levels of osteocalcin and tartrate-resistant acid phosphatase-5b, respectively. Next we performed an open and stabilized femoral fracture using 8-week-old SAP-CNP-Tg mice and compared the healing process with age-matched wild-type mice. An immunohistochemical study revealed that CNP and its receptors, natriuretic peptide receptor-B and natriuretic peptide clearance receptor, are expressed in hard calluses of wild-type mice, suggesting a possible role of CNP/natriuretic peptide receptor-B signaling in fracture repair, especially in bone remodeling stage. On micro-CT analysis, a rapid decrease in callus volume was observed in SAP-CNP-Tg mice, followed by a generation of significantly higher new bone volume with a tendency of increased bone strength. In addition, a micro-CT analysis also showed that bone remodeling was accelerated in SAP-CNP-Tg mice, which was also evident from increased serum osteocalcin and tartrate-resistant acid phosphatase-5b levels in SAP-CNP-Tg mice at the remodeling stage of fracture repair. These results indicate that CNP activates bone turnover and remodeling in vivo and possibly accelerates fracture healing in our mouse model.
C-Type Natriuretic Peptide as a New Regulator of Food Intake and Energy Expenditure
Endocrinology - Tập 151 Số 8 - Trang 3633-3642 - 2010
Megumi Inuzuka, Naohisa Tamura, Nobuko Yamada, Goro Katsuura, Naofumi Oyamada, Daisuke Taura, Takuhiro Sonoyama, Yasutomo Fukunaga, Kousaku Ohinata, Masakatsu Sone, Kazuwa Nakao
The physiological implication of C-type natriuretic peptide (CNP) including energy metabolism has not been elucidated, because of markedly short stature in CNP-null mice. In the present study we analyzed food intake and energy expenditure of CNP-null mice with chondrocyte-targeted CNP expression (CNP-Tg/Nppc−/− mice), in which marked skeletal dysplasia was rescued, to investigate the significance of CNP under minimal influences of skeletal phenotypes. In CNP-Tg/Nppc−/− mice, body weight and body fat ratio were reduced by 24% and 32%, respectively, at 20 wk of age, and decreases of blood glucose levels during insulin tolerance tests were 2-fold exaggerated at 17 wk of age, as compared with CNP-Tg/Nppc+/+ mice. Urinary noradrenalin excretion of CNP-Tg/Nppc−/− mice was greater than that of CNP-Tg/Nppc+/+ mice by 28%. In CNP-Tg/Nppc−/− mice, rectal temperature at 1600 h was higher by 1.1 C, and uncoupling protein-1 mRNA expression in the brown adipose tissue was 2-fold increased, which was canceled by propranolol administration, as compared with CNP-Tg/Nppc+/+ mice. Oxygen consumption was significantly increased in CNP-Tg/Nppc−/− mice compared with that in CNP-Tg/Nppc+/+ mice. Food intake of CNP-Tg/Nppc−/− mice upon ad libitum feeding and refeeding after 48 h starvation were reduced by 21% and 61%, respectively, as compared with CNP-Tg/Nppc+/+ mice. This study unveiled a new aspect of CNP as a molecule regulating food intake and energy expenditure. Further analyses on precise mechanisms of CNP actions would lead to the better understanding of the significance of the CNP/guanylyl cyclase-B system in food intake and energy expenditure.
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