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ENDOCRINE JOURNAL is a long-established, open-access, peer-reviewed online journal. It publishes peer-reviewed research articles across various aspects of basic, translational, and clinical endocrinology. ENDOCRINE JOURNAL provides an opportunity to share your ideas, concepts, and scientific observations in any area of endocrinology. Manuscripts can be submitted as original articles, notes, rapid communications, or review articles. We have a fast review and editorial decision system, with a particular focus on rapid, genuine scientific publications that are frequently cited. Please refer to the link for author guidelines.

ENDOCRINE JOURNAL 是一本开放获取、同行评议的在线期刊，历史悠久。该杂志在基础、转化和临床内分泌学等多个领域发表同行评议的研究文章。ENDOCRINE JOURNAL 为您提供了一个交流您在内分泌学各个领域的想法、概念和科学观察的机会。手稿可以作为原始文章、注释、快速通信或评论文章提交。我们拥有快速的审稿和编辑决策系统，并特别关注快速、真实的科学出版物，这些出版物通常被广泛引用。请通过链接获取作者指南。

Endocrine Journal

This article aims to understand the isolated effect of maternal thyroid-stimulating hormone (TSH), free thyroxine (FT4) and antithyroid peroxidase antibodies (TPOAb) in early pregnancy on gestational diabetes mellitus (GDM). Based on a birth cohort, pregnant women presented to maternity hospitals for the first antenatal care from Nov 2008 to Oct 2010 were invited to participate in the study. A self-administered questionnaire was asked to complete to collect data on socio-economic variables, previous adverse pregnancy outcomes, method of conception, previous endocrinic and metabolic diseases, and pregnancy-related anxiety in 1st trimester of the index pregnancy. Pre-pregnancy BMI was measured. Serum samples were collected, and TSH, FT4 and TPOAb were assayed. GDM was confirmed from medical records screened on 24–28 gestational weeks by using oral glucose tolerance test (OGTT). The prevalence of isolated subclinical hypothyroidism, hypothyroidemia and positive TPOAb in early pregnancy was 2.0%, 2.0% and 12.8%. Prevalence of GDM in women with the isolated sub-clinical hypothyroidism, hypothyroxinemia and positive TPOAb was 2.9%, 2.8% and 3.1%, respectively, which were all higher than that detected in euthyroidism women (1.2%). Women with isolated positive TPOAb had significantly higher TSH and lower FT4 level compared with euthyroidism women. It was found that isolated positive TPOAb in early pregnancy increased the risk of GDM, adjusted RR and 95%CI being 2.541(1.037–6.226). No significant relationships were identified between isolated sub-clinical hypothyroidism or hypothyroxinemia with GDM. In conclusion, isolated thyroid autoimmunity, represented by positive TPOAb, in early pregnancy were associated with GDM independent of TSH and FT4.

Kun Huang

Yeqing Xu

Shuangqin Yan

Tao Li

Yuanhong Xu

Peng Zhu

Fangbiao Tao

Endocr J

Isolated effect of maternal thyroid-stimulating hormone, free thyroxine and antithyroid peroxidase antibodies in early pregnancy on gestational diabetes mellitus: a birth cohort study in China

Forkhead transcription factors of the FoxO family have important roles in cellular proliferation, apoptosis, differentiation and stress resistance. FoxO proteins also play important roles in metabolism of complex organisms. FoxO1 regulates glucose and lipid metabolism in liver, as well as preadipocyte, myoblast and vascular endothelial cell differentiation. In the hypothalamus, FoxO controls food intake. In this chapter, we review the role of FoxO in pancreatic β cells. Pancreatic β cells secrete insulin to maintain the plasma glucose levels in a strict physiological range. Defects of β cell function cause diabetes. The expression pattern of FoxO1 during pancreatic organogenesis is similar to that of Pdx1, Nkx2.2 and Pax4, transcription factors known to be critical for β cell development. FoxO1 is expressed in a subset of pancreatic duct cells, in which insulin and/or Pdx1 are occasionally expressed. FoxO1 inhibits β cell proliferation through suppression of Pdx1 by competing with FoxA2 and protects against β cell failure induced by oxidative stress through NeuroD and MafA induction. Thus, a series of FoxO1 studies in pancreas suggested that FoxO1 plays important roles in pancreatic β cell differentiation, neogenesis, proliferation and stress resistance. Genetic or pharmacological manipulation of FoxO can be used to prevent β cell failure or aid in the differentiation of uncommitted endocrine progenitors into β cells for transplantation.

Tadahiro KITAMURA

Yukari IDO KITAMURA

Role of FoxO Proteins in Pancreatic .BETA. Cells

To explore the role of NF-κB activation in the development of insulin resistance and investigate whether or not that the inhibition of NF-κB activation by PDTC will improve the insulin resistance of L6 cells exposed to H2O2. L6 cells were treated with H2O2, PDTC or both H2O2 and PDTC for 4 hours. The uptake of glucose with stimulation of insulin, the expression of P38-MAPK, p- P38-MAPK, NF-κBp65, p- NF-κBp65, IRS-1, IRS-2, p-IRS-2, PI3K, IκBα, p- IκBα, caspase-8 and GLUT4, the production of ROS, TNF-α, IL-6 and IL-1β as well as the apoptosis rate of L6 cells were determined and compared in L6 treated with H2O2 alone or both H2O2 and PDTC. Compared with the L6 cells treated with H2O2 alone, the L6 cells treated with both H2O2 and PDTC showed (1) significantly lower production of ROS, TNF-α, IL-6 and IL-1β; (2) significantly decreased expression of P38-MAPK, p- P38-MAPK and NF-κBp65, p- NF-κBp65, p- IκBα and caspase-8; (3) significantly lower rate of apoptosis; (4) significantly higher expression of IRS-2, p-IRS-2 (Tyr 612), PI3K and GLUT4; (5) significantly higher uptake of glucose with stimulation of insulin; (6) significantly increased expression of Bcl2 and decreased ratio of Bax to Bcl2. Based on the findings of the present study, inhibition of NF-κB activation by PDTC would improve the insulin resistance of L6 cells exposed to H2O2.

Fengyang Xie

Jian Zhu

Baolian Hou

Yuan Wang

Fanzhu Meng

Zhixing Ren

Shuping Ren

Inhibition of NF-&amp;kappa;B activation improves insulin resistance of L6 cells

抑制NF-κB激活改善L6细胞的胰岛素抵抗

The target of this study was to explore the role of mitochondria mediated apoptosis and inflammation in cisplatin-induced testicular damage and to evaluate the ameliorative effect of resveratrol. Adult male Wistar rats were randomly allocated to 4 groups. Group I (Control) received normal saline, Group II (Resveratrol) received resveratrol (50 mg/kg/day), Group III (Cisplatin) received cisplatin (7.5 mg/kg/week, i.p.) and Group IV (Resveratrol + Cisplatin) received resveratrol and cisplatin in the same regimen of treatment. Treatment with resveratrol in Groups II and IV started 48h before cisplatin injection and continued for further 4 successive weeks. Cisplatin-treated rats showed reduced body weight, absolute testes weight and sperm count, motility and viability. On the other hand, cisplatin treatment increased the percentage of sperm abnormalities. It also decreased serum testosterone level, mitochondrial membrane potential while, increased cytochrome C liberation from the mitochondria into the cytosol. The activities of caspase-3 & -9 were increased. The level of TNF-α, IL-6 and Bax were increased whereas Bcl-2 was decreased. Oxidative stress markers were found to increase with a concomitant reduction in the antioxidant enzymes and GSH levels. These results were confirmed by immunohistochemical and histopathological analysis. Contrary to all these results, there were improvements in cisplatin induced testicular damage through attenuation of mitochondria mediated apoptosis, inflammation, and oxidative stress owing to resveratrol pretreatment. Thus, resveratrol, as a potential therapeutic agent, may hold promise in preventing mitochondria mediated apoptosis and inflammation in cisplatin-induced testicular damage in rats.

Hamdy A.A. Aly

Basma G. Eid

Cisplatin induced testicular damage through mitochondria mediated apoptosis, inflammation and oxidative stress in rats: impact of resveratrol

顺铂通过线粒体介导的凋亡、炎症和氧化应激诱导大鼠睾丸损伤：白藜芦醇的影响

Liwen Zheng

Changjie Zhang

Lele Liao

Zhijie Hai

Xin Luo

Haoliang Xiao

Knockdown of Gfi1 increases BMSCs exosomal &lt;i&gt;miR-150-3p&lt;/i&gt; to inhibit osteoblast ferroptosis in steroid-induced osteonecrosis of the femoral head through BTRC/Nrf2 axis

敲低Gfi1通过BTRC/Nrf2轴增加BMSCs外泌体miR-150-3p以抑制类固醇诱导的股骨头坏死中成骨细胞铁死亡

The mean height is taller in males than in females, except for early teens. In this regard, previous studies have revealed that (1) distribution of the mean adult heights in subjects with disorders accompanied by discordance between sex chromosome complement and bioactive sex steroids and in control subjects (the British height standards) indicates that, of the ~12.5 cm of sex difference in the mean adult height, ~9 cm is accounted for by the difference in the sex chromosome complement and the remaining ~3.5 cm is explained by the dimorphism in sex steroids (primarily due to the growth-promoting effect of gonadal androgens); (2) according to the infancy-childhood-puberty growth model, the sex difference in the childhood growth function produces height differences of ~1 cm in childhood and 8-10 cm at 18-20 years of age, whereas the sex difference in the pubertal growth function yields height difference of ~4.5 cm at 18-20 years of age; and (3) SHOX expression and methylation analyses using knee cartilage tissues and cultured chondrocytes have shown lower SHOX expression levels in female samples than in male samples and methylation patterns consistent with partial spreading of X-inactivation affecting SHOX in female samples. These findings suggest that small but persistent sex difference in SHOX expression dosage leads to the variation in the sex steroid independent childhood growth function, thereby yielding the sex difference in height which remains small in childhood but becomes obvious in adulthood.

Tsutomu Ogata

Atsushi Hattori

Maki Fukami

&lt;i&gt;SHOX&lt;/i&gt; and sex difference in height: a hypothesis

<i>SHOX</i>与身高性别差异：一种假设

Anti-thyroglobulin antibodies (TgAb) and/or anti-thyroid peroxidase antibodies (TPOAb) positivity at baseline is a risk marker for thyroid immune-related adverse events (thyroid-irAEs) in anti-programmed cell death-1 antibody (PD-1-Ab) treatment; however, it is unknown if TgAb and TPOAb titers are associated with clinical characteristics of thyroid-irAEs. Among 586 patients treated with PD-1-Ab at Nagoya University Hospital between 2 November 2015 and 30 September 2021, 57 patients developed thyroid-irAEs (thyrotoxicosis [n = 38]; hypothyroidism without prior thyrotoxicosis {isolated hypothyroidism} [n = 19]) in whom thyroid function, and TgAb and TPOAb titers were determined at baseline and at the onset. The changes in TgAb (median, 54.8 vs. 0.2 IU/mL; p = 0.002) and TPOAb titers (31.6 vs. 0 IU/mL; p = 0.032) from baseline to onset of developing thyroid-irAEs were greater in patients with thyrotoxicosis than patients with isolated hypothyroidism. Higher TgAb and TPOAb titers, and the TgAb titer at baseline were associated with an earlier onset of thyrotoxicosis and higher peak free thyroxine levels, respectively. Twenty-eight patients who developed hypothyroidism after thyrotoxicosis had higher TgAb (54.5 vs. 10.7 IU/mL; p = 0.011) and TPOAb titers at baseline (46.1 vs. 9.0 IU/mL; p < 0.001) and greater changes in TgAb (61.7 vs. 7.8 IU/mL; p = 0.025) and TPOAb titers (52.8 vs. –0.8 IU/mL; p < 0.001) than patients who did not develop hypothyroidism. The TgAb titer at baseline and changes in the TgAb and TPOAb titers were greater in patients with thyrotoxicosis than patients with isolated hypothyroidism, suggesting that the magnitude of the thyroid autoimmune response reflects the clinical types of thyroid-irAEs.

Ayana Yamagami

Shintaro Iwama

Tomoko Kobayashi

Xin Zhou

Yoshinori Yasuda

Takayuki Okuji

Masaaki Ito

Tetsushi Izuchi

Masahiko Ando

Takeshi Onoue

Takashi Miyata

Mariko Sugiyama

Daisuke Hagiwara

Hidetaka Suga

Ryoichi Banno

Hiroshi Arima

Changes in TgAb and TPOAb titers are greater in thyrotoxicosis than isolated hypothyroidism induced by PD-1 blockade

PD-1阻断诱导的甲状腺毒症中TgAb和TPOAb滴度变化大于孤立性甲状腺功能减退症

Glutamic acid decarboxylase (GAD) is an enzyme that catalyzes the conversion of glutamic acid into γ-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the central nervous system (CNS). GAD is widely expressed in the CNS and pancreatic β-cells. GABA produced by GAD plays a role in regulating insulin secretion in pancreatic islets. Anti-GAD antibody is an established marker of type 1 diabetes mellitus (T1DM) and is also associated with stiff-person syndrome (SPS) and several other neurological disorders, including ataxia, cognitive impairment, limbic encephalitis, and epilepsy, collectively referred to as GAD antibody-spectrum disorders (GAD-SD). We report the case of a 17-year-old male patient who developed GAD-SD and T1DM after allogeneic hematopoietic cell transplantation (HCT). He presented with memory disorders, including feelings of déjà vu, accompanied by vomiting and headaches, and exhibited abnormal brain magnetic resonance imaging and electroencephalogram results. In addition to elevated fasting plasma glucose and glycated hemoglobin levels, markedly elevated anti-GAD antibody levels were detected in the serum and cerebrospinal fluid. Based on these findings, the patient was diagnosed with GAD-SD and T1DM and treated with methylprednisolone, followed by multiple daily insulin injections. We also reviewed previously reported cases of GAD-SD following HCT and multiple positive islet-related antibodies.

Shinichiro Sano

Taemi Ogura

Takayuki Takachi

Yuki Murai

Yasuko Fujisawa

Kenichiro Watanabe

Masaki Yoshimura

Glutamic acid decarboxylase antibody-spectrum disorders and type 1 diabetes mellitus in a patient following allogenic hematopoietic cell transplantation with review of literature

谷氨酸脱羧酶抗体谱疾病与异基因造血细胞移植后患者的1型糖尿病：文献综述

Adolescent and young adult (AYA, 15-39 years old) patients with papillary thyroid carcinoma (PTC) experience significant psychological distress and place great importance on obtaining information regarding the disease; however, their demands remain unmet. We aimed to investigate clinicopathological and molecular features of PTC in AYA patients and compare them to those of PTC in older patients (≥40 years). This retrospective study enrolled 1,677 patients diagnosed with PTC from January 2018 to December 2022, with 400 AYA patients and 1,277 older adults. At the time of diagnosis, AYA patients with PTC had higher rates of presentation in females, larger tumor size (>2.0 cm), lymphatic vessel invasion, chronic thyroiditis, clinical lymph node metastasis, and pathologic lymph node metastasis, but lower rates of multifocality and extrathyroidal extension compared with PTC in older adults. The two groups had no significant differences regarding surgical method and distant metastasis. The prevalences of BRAF p.V600E and TERT promoter mutations of PTC were significantly lower in AYA patients (69.1% vs. 82.6% and 1.3% vs. 18.8%, respectively; both p < 0.001). In conclusion, PTC in AYA patients differed from PTC in older patients. Particularly, BRAF p.V600E and TERT promoter mutations in AYA with PTC were less frequently observed than in older adults.

Van Phu Thang Nguyen

Hirokazu Kurohama

Yuko Akazawa

Thi Ngoc Anh Nguyen

Katsuya Matsuda

Yuki Matsuoka

Zhanna Mussazhanova

Kenichi Yokota

Shinya Satoh

Hiroyuki Yamashita

Thi Nhung Nguyen

Yerkerzhan Sailaubekova

Masahiro Nakashima

Clinicopathological and molecular characteristics of papillary thyroid carcinoma in adolescent and young adult patients

青少年和年轻成人乳头状甲状腺癌的临床病理和分子特征

Abbreviation	Endocr J
Journal Impact	1.33
Quartiles(Global)	ENDOCRINOLOGY & METABOLISM(Q4)

ISSN	0918-8959, 1348-4540
h-index	83

Publication Information	Publisher: Japan Endocrine Society，Publishing cycle: Bimonthly，Journal Type: journal，Open Access Journals: No
Basic data	Year of publication: 1993，Proportion of original research papers: 85.38%，Self Citation Rate:0.00%， Gold OA Rate: 98.35%
Average review cycle	网友分享经验：平均1.5月
Average recruitment ratio	网友分享经验：约75%

Endocrine Journal

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