Endocrine journalPub Date : 2025-01-06Epub Date: 2024-10-23DOI: 10.1507/endocrj.EJ24-0401
Nami Suzuki, Jaeduk Yoshimura Noh, Ai Kozaki, Natsuko Watanabe, Ai Yoshihara, Miho Fukushita, Masako Matsumoto, Hideyuki Imai, Shigenori Hiruma, Masahiro Ichikawa, Masakazu Koshibu, Akiko Sankoda, Rei Hirose, Toshu Inoue, Kiminori Sugino, Koichi Ito
{"title":"Incidence of the postpartum diagnosis of thyroid eye disease in relation to thyroid function in Graves' disease.","authors":"Nami Suzuki, Jaeduk Yoshimura Noh, Ai Kozaki, Natsuko Watanabe, Ai Yoshihara, Miho Fukushita, Masako Matsumoto, Hideyuki Imai, Shigenori Hiruma, Masahiro Ichikawa, Masakazu Koshibu, Akiko Sankoda, Rei Hirose, Toshu Inoue, Kiminori Sugino, Koichi Ito","doi":"10.1507/endocrj.EJ24-0401","DOIUrl":"10.1507/endocrj.EJ24-0401","url":null,"abstract":"<p><p>It has been reported that Graves' disease (GD) sometimes improves spontaneously during pregnancy, although exacerbation of GD during postpartum period or relapse of hyperthyroidism caused by GD might occur. This study aimed to investigate the incidence of postpartum diagnosis of thyroid eye disease (TED) in relation to thyroid dysfunction. This retrospective cross-sectional study enrolled 11,104 deliveries from the patients with GD between January 2004 and August 2022. Within the 12-month postpartum period, 72 patients (0.65%) were diagnosed with TED. The thyroid function of the 72 patients comprised 9 remission, 13 continued antithyroid medicine, and 50 thyroid dysfunction; 30 newly diagnosed GD, 1 hypothyroidism, and 19 relapse/recurrence of GD. In the 49 patients with thyroid dysfunction, no difference was observed in the median values of thyroid-stimulating hormone (TSH) receptor antibody (TRAb) and TSH receptor stimulating antibody between the TED diagnosis and the development of hyperthyroidism. However, when the patients were classified into the newly developed GD and relapse/recurrence of GD groups, the difference became significant and the TRAb level was high in the newly developed GD (16.1 vs. 5.0 IU/L, p < 0.0001, and 15.0 vs. 6.0 IU/L, p = 0.0003). Thyroid dysfunction preceded TED diagnosis in more than half of the patients and the median time for each event was 6.5 vs. 8.1 months. The active phase TED was observed in 8 of the 72 patients. Of the 72 patients newly diagnosed with TED in postpartum, two-thirds were accompanied by thyroid dysfunction and 8 of them were in active phase.</p>","PeriodicalId":11631,"journal":{"name":"Endocrine journal","volume":" ","pages":"103-113"},"PeriodicalIF":1.3,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11778393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142497219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Association between non-high-density lipoprotein cholesterol and type 2 diabetes: a systematic review and meta-analysis of cohort studies.","authors":"Mengqi Han, Yue Shen, Xin Guo, Cheng Hong, Xincan Ji, Haoyang Guo, Yuelong Jin, Hui Yuan","doi":"10.1507/endocrj.EJ24-0189","DOIUrl":"10.1507/endocrj.EJ24-0189","url":null,"abstract":"<p><p>Non-high-density lipoprotein cholesterol (non-HDL), a more readily available and reliable lipid parameter, is unclear in its association with type 2 diabetes (T2D). Previous studies assessing the relationship between non-HDL and T2D risk remains inconsistent results. We performed a meta-analysis to systematically evaluate this association. The PubMed, EMBASE, Medline, Web of Science, and Cochrane Library databases were systematically searched to find articles on \"non-HDL\" and \"T2D\" from inception to December 6, 2023. A random-effects model was used to calculate the effect estimates and 95% confidence intervals. Subgroup analyses and univariate Meta-regression were performed to explore sources of heterogeneity. The main exposure and outcome were non-HDL and T2D, respectively, in the general population. A total of 8 studies included 251,672 participants who met the inclusion criteria for this study. Meta-analysis showed that higher non-HDL increased the risk of T2D compared with the lower non-HDL group (total effect size: 1.16; 95% CI 1.079-1.251, p < 0.001). Subgroup analyses and Meta-regression of the association between non-HDL and T2D were not affected by region, proportion of men, sample size, or adjustment for confounders (including BMI, hypertension, waist circumference, and family history of diabetes). Higher non-HDL may be associated with an increased risk of T2D. Large prospective cohort studies are needed to validate these findings, and further studies are required in order to elucidate the underlying pathophysiologic mechanisms underlying the association between non-HDL and T2D.</p>","PeriodicalId":11631,"journal":{"name":"Endocrine journal","volume":" ","pages":"43-51"},"PeriodicalIF":1.3,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11778345/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142307381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Inhibition of mmu_circ_0009303 improves metabolic dysfunction-associated steatotic liver disease by regulating lipid metabolism and oxidative stress.","authors":"Ju Zhou, Wu Li, Xiaowei Chi, Dingchun Li, Chunxia Yang, Zhiwen Duan","doi":"10.1507/endocrj.EJ24-0008","DOIUrl":"10.1507/endocrj.EJ24-0008","url":null,"abstract":"<p><p>Circular RNAs (circRNAs) play an important role in regulating inflammation and oxidative stress during the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD); however, the underlying mechanism is unclear. This study aimed to determine the role of mmu_circ_0009303 in MASLD. We used a bioinformatics approach to identify potential targets and established an in vitro model of MASLD. Oil red O staining, cell transfection and dual-luciferase reporter assay were used to determine the role of mmu_circ_0009303. The results indicated that the mmu_circ_0009303 expression was significantly increased in the MASLD model both in vitro and in vivo and was associated with oxidative stress levels and inflammation. Moreover, bioinformatics analyses revealed that miRNA-182-5p and Foxo3 are targets of mmu_circ_0009303 and miRNA-182-5p, respectively. In the in vitro MASLD model, mmu_circ_0009303 promoted fat deposition in NCTC1469 cells, which was induced by free fatty acid (FFA) through the regulation of miRNA-182-5p/Foxo3. The expression of miRNA-182-5p and Forkhead box O3 (Foxo3) was associated with mmu_circ_0009303 expression in the liver of mice with MASLD, which was induced by a high-fat diet. Furthermore, mmu_circ_0009303 may be involved in regulating the expression of lipid metabolism-related regulatory proteins, such as CPT1A, SLC27A4, ACBD3, SREBP1, FAS, PPARα, and PPARγ. Taken together, mmu_circ_0009303 promotes oxidative stress, inflammation, and excessive fat accumulation in NCTC1469 cells induced by FFA through the regulation of miRNA-182-5p/Foxo3 and lipid metabolism-related regulatory proteins. These findings provide a potential target for the treatment of MASLD.</p>","PeriodicalId":11631,"journal":{"name":"Endocrine journal","volume":" ","pages":"79-91"},"PeriodicalIF":1.3,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11778371/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142497220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Endocrine journalPub Date : 2025-01-01DOI: 10.1507/endocrj.EJ20241105
Kazuwa Nakao
{"title":"Celebrating the 100<sup>th</sup> anniversary of the Japan Endocrine Society: reflecting on my 50 years of hormone research.","authors":"Kazuwa Nakao","doi":"10.1507/endocrj.EJ20241105","DOIUrl":"10.1507/endocrj.EJ20241105","url":null,"abstract":"","PeriodicalId":11631,"journal":{"name":"Endocrine journal","volume":"72 1","pages":"1-21"},"PeriodicalIF":1.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11776489/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Endocrine journalPub Date : 2025-01-01DOI: 10.1507/endocrj.EJ20241021
Mari Suzuki Hotta
{"title":"In celebration of 100 exciting years of the Japan Endocrine Society.","authors":"Mari Suzuki Hotta","doi":"10.1507/endocrj.EJ20241021","DOIUrl":"https://doi.org/10.1507/endocrj.EJ20241021","url":null,"abstract":"","PeriodicalId":11631,"journal":{"name":"Endocrine journal","volume":"72 2","pages":"123-130"},"PeriodicalIF":1.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143078741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Ghrelin-LEAP2 interactions along the stomach-liver axis.","authors":"Katsuya Sakai, Yuki Nakazato, Yuki Shiimura, Weidong Zhang, Masamitsu Nakazato","doi":"10.1507/endocrj.EJ24-0543","DOIUrl":"https://doi.org/10.1507/endocrj.EJ24-0543","url":null,"abstract":"<p><p>Ghrelin produced in the stomach promotes food intake and GH secretion, and acts as an anabolic peptide during starvation. Ghrelin binds to the growth hormone secretagogue receptor, a G protein-coupled receptor (GPCR), whose high-resolution complex structures have been determined in the apo state and when bound to an antagonist. Anamorelin, a low-molecular-weight ghrelin agonist, has been launched in Japan for the treatment of cancer cachexia, and its therapeutic potential has attracted attention due to the various biological activities of ghrelin. In 2019, liver-expressed antimicrobial peptide (LEAP2), initially discovered as an antimicrobial peptide produced in the liver, was identified to be upregulated in the stomach of diet-induced obese mice after vertical sleeve gastrectomy. LEAP2 binds to the GHSR and antagonizes ghrelin's activities. The serum concentrations of human LEAP2 are positively correlated with body mass index, body fat accumulation, and fasting serum concentrations of glucose and triglyceride. Serum LEAP2 elevated and ghrelin reduced in obesity. Ghrelin and LEAP2 regulate body weight, food intake, and GH and blood glucose concentrations, and other physiological phenomena through their interactions with the same receptor, GHSR.</p>","PeriodicalId":11631,"journal":{"name":"Endocrine journal","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Intragenic duplication of PHEX in a girl with X-linked hypophosphatemia: a case report with review of literature.","authors":"Kazuhisa Akiba, Keiko Matsubara, Atsushi Hattori, Maki Fukami","doi":"10.1507/endocrj.EJ24-0355","DOIUrl":"https://doi.org/10.1507/endocrj.EJ24-0355","url":null,"abstract":"<p><p>Over 70 intragenic copy-number variations (CNVs) of PHEX have been identified in patients with X-linked hypophosphatemia (XLH). However, the underlying mechanism of these CNVs has been poorly investigated. Furthermore, although PHEX undergoes X chromosome inactivation (XCI), the association between XLH in women with heterozygous PHEX variants and skewed XCI remains unknown. In this study, we determined the precise genomic structure and the XCI status of a girl with XLH who showed short stature and bowing of the legs at 2 years old. Laboratory tests revealed low levels of serum phosphate and elevated levels of alkaline phosphatase and fibroblast growth factor 23. Multiplex ligation-dependent probe amplification and targeted long-read sequencing revealed that she carried a 24.6-kb intragenic duplication of PHEX. The duplication was tandemly aligned in a head-to-tail orientation. The duplication breakpoints shared a 2-bp microhomology, indicating that this CNV resulted from a replication-based error. Trio sequencing results showed that the duplication was a de novo CNV that occurred on the paternally-derived allele. DNA methylation analysis demonstrated random XCI. A literature review of 12 previously reported cases of intragenic CNVs of PHEX revealed that the deletions/duplications can be ascribed to replication-based errors. Our findings and those of previous studies indicate that XLH-causative CNVs in PHEX predominantly arise from replication-based errors. Thus, the genomic region surrounding PHEX may be vulnerable to replication-based errors during gametogenesis or early embryogenesis. Our study provides supporting evidence that heterozygous PHEX variants can lead to XLH in women with random XCI.</p>","PeriodicalId":11631,"journal":{"name":"Endocrine journal","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Endocrine journalPub Date : 2024-12-07DOI: 10.1507/endocrj.EJ23-0723
Lou-Yan Ma, Song-Fang Liu, Zheng-Quan Ma, Ya-Gang Guo, Mo Li, Yuan Gao, Yu-Ting Wen, Yu Niu, Hai-Xia Sui, Bao-Shan Li, Ya Li, Ya-Li Lv, Yao Huang, Jia-Jia Zhai
{"title":"Liraglutide improves cognition function in streptozotocin-induced diabetic rats by downregulating β-secretase and γ-secretase and alleviating oxidative stress in HT-22 cells.","authors":"Lou-Yan Ma, Song-Fang Liu, Zheng-Quan Ma, Ya-Gang Guo, Mo Li, Yuan Gao, Yu-Ting Wen, Yu Niu, Hai-Xia Sui, Bao-Shan Li, Ya Li, Ya-Li Lv, Yao Huang, Jia-Jia Zhai","doi":"10.1507/endocrj.EJ23-0723","DOIUrl":"https://doi.org/10.1507/endocrj.EJ23-0723","url":null,"abstract":"<p><p>Diabetes has been regarded as an independent risk factor for Alzheimer's disease (AD). Liraglutide could improve cognition in AD mouse models, but its precise mechanism remains unclear. In this study, we used STZ-induced diabetic rats and HT-22 cells to investigate the effects of liraglutide. The MWM test, MTT assay, ELISA, western blot, and immunofluorescence were used in this research. Diabetic rats induced by STZ displayed a longer escape latency and entered the target zone less frequently (p < 0.05) in the MWM test. Intraperitoneal injection of liraglutide improved the cognition of diabetic rats (p < 0.05) and reduced Aβ42 expression in the hippocampus (p < 0.05). In vivo experiments showed that HT-22 cell viability decreased in the HG group, but liraglutide (100 nmol/L and 1 μmol/L) enhanced HT-22 cell viability (p < 0.05). Oxidative stress markers were upregulated in HT-22 cells in the HG group, while liraglutide treatment significantly reduced these markers (p < 0.05). Western blot and immunofluorescence analyses demonstrated increased levels of Aβ, BACE1, and γ-secretase in HT-22 cells in the HG group (p < 0.05), whereas these levels were reduced in the liraglutide treatment group (p < 0.05). These effects were reversed by the nuclear factor kappa B (NF-κB) and extracellular signal-regulated kinase 1/2 (ERK1/2) inhibitors (p < 0.05). These findings suggest that liraglutide improved the cognition of diabetic rats and might exert its protective effects by reducing oxidative stress, downregulating BACE1 and γ-secretase expression, and decreasing Aβ deposition via the NF-κB and ERK1/2 pathways.</p>","PeriodicalId":11631,"journal":{"name":"Endocrine journal","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Glutamic acid decarboxylase antibody-spectrum disorders and type 1 diabetes mellitus in a patient following allogenic hematopoietic cell transplantation with review of literature.","authors":"Shinichiro Sano, Taemi Ogura, Takayuki Takachi, Yuki Murai, Yasuko Fujisawa, Tsutomu Ogata, Kenichiro Watanabe, Masaki Yoshimura","doi":"10.1507/endocrj.EJ24-0457","DOIUrl":"https://doi.org/10.1507/endocrj.EJ24-0457","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":11631,"journal":{"name":"Endocrine journal","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142779608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The role of oxidative stress, glucocorticoid receptor and ARMC5 in lipid metabolism.","authors":"Yosuke Okuno, Atsunori Fukuhara, Iichiro Shimomura","doi":"10.1507/endocrj.EJ24-0177","DOIUrl":"10.1507/endocrj.EJ24-0177","url":null,"abstract":"<p><p>Lipid metabolism includes lipogenesis, lipolysis, and cholesterol metabolism and it exerts a wide range of biological effects. We previously found novel roles of adipocyte oxidative stress in diet-induced obesity, adipocyte glucocorticoid receptor in Cushing syndrome, and ARMC5 in adrenocortical cells. Using genetically modified mice in which oxidative stress was eliminated or augmented specifically in adipose tissues, we have been able to elucidate that obesity-induced oxidative stress inhibited healthy adipose expansion and ameliorated insulin sensitivity. Using adipocyte-specific glucocorticoid receptor knockout mice, we found that glucocorticoids also inhibited healthy adipose expansion and decreased insulin sensitivity. This was partly due to the transcriptional upregulation of ATGL. We identified ARMC5 as a novel ubiquitin E3 ligase of full-length SREBF, a master regulator of lipid metabolism. In adrenocortical cells, ARMC5 suppresses SREBF2 activity, and loss of ARMC5 may lead to cholesterol accumulation and the development of primary bilateral macronodular adrenal hyperplasia.</p>","PeriodicalId":11631,"journal":{"name":"Endocrine journal","volume":" ","pages":"1097-1101"},"PeriodicalIF":1.3,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11778357/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141455982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}