Journal of Endocrinology最新文献_第8页

Blocking FGF23 signaling improves the growth plate of mice with X-linked hypophosphatemia. 阻断FGF23信号通路可改善x连锁低磷血症小鼠的生长。

IF 4 3区医学

Journal of Endocrinology Pub Date : 2023-09-01 DOI: 10.1530/JOE-23-0025

Rocío Fuente, Eva-Maria Pastor-Arroyo, Nicole Gehring, Patricia Oro Carbajosa, Laura Alonso-Durán, Ivan Zderic, James Tapia-Dean, Ahmad Kamal Hamid, Carla Bettoni, Fernando Santos, Carsten A Wagner, Isabel Rubio-Aliaga

{"title":"Blocking FGF23 signaling improves the growth plate of mice with X-linked hypophosphatemia.","authors":"Rocío Fuente, Eva-Maria Pastor-Arroyo, Nicole Gehring, Patricia Oro Carbajosa, Laura Alonso-Durán, Ivan Zderic, James Tapia-Dean, Ahmad Kamal Hamid, Carla Bettoni, Fernando Santos, Carsten A Wagner, Isabel Rubio-Aliaga","doi":"10.1530/JOE-23-0025","DOIUrl":"https://doi.org/10.1530/JOE-23-0025","url":null,"abstract":"Fibroblast growth factor 23 (FGF23) is a phosphaturic hormone. X-linked hypophosphatemia (XLH) is the most prevalent inherited phosphate wasting disorder due to mutations in the PHEX gene, which cause elevated circulating FGF23 levels. Clinically, it is characterized by growth impairment and defective mineralization of bones and teeth. Treatment of XLH is challenging. Since 2018, neutralizing antibodies against FGF23 have dramatically improved the therapy of XLH patients, although not all patients fully respond to the treatment, and it is very costly. C-terminal fragments of FGF23 have recently emerged as blockers of intact FGF23 signaling. Here, we analyzed the effect on growth and bone of a short 26 residues long C-terminal FGF23 (cFGF23) fragment and two N-acetylated and C-amidated cFGF23 peptides using young XLH mice (Phex C733RMhda mice). Although no major changes in blood parameters were observed after 7 days of treatment with these peptides, bone length and growth plate structure improved. The modified peptides accelerated the growth rate probably by improving growth plate structure and dynamics. The processes of chondrocyte proliferation, death, hypertrophy, and the cartilaginous composition in the growth plate were partially improved in young treated XLH mice. In conclusion, these findings contribute to understand the role of FGF23 signaling in growth plate metabolism and show that this may occur despite continuous hypophosphatemia.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":"259 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10332725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Fibroblast growth factor 10 alleviates acute lung injury by inhibiting excessive autophagy via Nrf2. 成纤维细胞生长因子10通过Nrf2抑制过度自噬减轻急性肺损伤。

IF 4 3区医学

Journal of Endocrinology Pub Date : 2023-09-01 DOI: 10.1530/JOE-23-0095

Shuai Huang, Yincong Xue, Wanying Chen, Mei Xue, Lei Miao, Li Dong, Hao Zuo, Hezhi Wen, Xiong Lei, Zhixiao Xu, Meiyu Quan, Lisha Guo, Yawen Zheng, Zhendong Wang, Li Yang, Yuping Li, Chengshui Chen

{"title":"Fibroblast growth factor 10 alleviates acute lung injury by inhibiting excessive autophagy via Nrf2.","authors":"Shuai Huang, Yincong Xue, Wanying Chen, Mei Xue, Lei Miao, Li Dong, Hao Zuo, Hezhi Wen, Xiong Lei, Zhixiao Xu, Meiyu Quan, Lisha Guo, Yawen Zheng, Zhendong Wang, Li Yang, Yuping Li, Chengshui Chen","doi":"10.1530/JOE-23-0095","DOIUrl":"https://doi.org/10.1530/JOE-23-0095","url":null,"abstract":"Acute lung injury (ALI) is associated with an increased incidence of respiratory diseases, which are devastating clinical disorders with high global mortality and morbidity. Evidence confirms that fibroblast growth factors (FGFs) play key roles in mediating ALI. Mice were treated with LPS (lipopolysaccharide: 5 mg/kg, intratracheally) to establish an in vivo ALI model. Human lung epithelial BEAS-2B cells cultured in a corresponding medium with LPS were used to mimic the ALI model in vitro. In this study, we characterized FGF10 pretreatment (5 mg/kg, intratracheally) which improved LPS-induced ALI, including histopathological changes, and reduced pulmonary edema. At the cellular level, FGF10 pretreatment (10 ng/mL) alleviated LPS-induced ALI accompanied by reduced reactive oxygen species (ROS) accumulation and inflammatory responses, such as IL-1β, IL-6, and IL-10, as well as suppressed excessive autophagy. Additionally, immunoblotting and co-immunoprecipitation showed that FGF10 activated nuclear factor erythroid-2-related factor 2 (Nrf2) signaling pathway via Nrf2 nuclear translocation by promoting the interaction between p62 and keap1, thereby preventing LPS-induced ALI. Nrf2 knockout significantly reversed these protective effects of FGF10. Together, FGF10 protects against LPS-induced ALI by restraining autophagy via p62-Kelch-like ECH-associated protein 1 (Keap1)-Nrf2 signaling pathway, implying that FGF10 could be a novel therapy for ALI.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":"259 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10047244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Neural gut-to-brain communication for postprandial control of satiation and glucose metabolism. 神经肠-脑通讯对餐后饱腹感和葡萄糖代谢的控制。

IF 4 3区医学

Journal of Endocrinology Pub Date : 2023-09-01 DOI: 10.1530/JOE-22-0320

Leonie Cabot, Juliet Erlenbeck-Dinkelmann, Henning Fenselau

{"title":"Neural gut-to-brain communication for postprandial control of satiation and glucose metabolism.","authors":"Leonie Cabot, Juliet Erlenbeck-Dinkelmann, Henning Fenselau","doi":"10.1530/JOE-22-0320","DOIUrl":"https://doi.org/10.1530/JOE-22-0320","url":null,"abstract":"The brain is tuned to integrate food-derived signals from the gut, allowing it to accurately adjust behavioral and physiological responses in accordance with nutrient availability. A key element of gut-to-brain communication is the relay of neural cues via peripheral sensory neurons (PSN) which harbor functionally specialized peripheral endings innervating the muscular and mucosal layers of gastrointestinal (GI) tract organs. In this review, we detail the properties of GI tract innervating PSN and describe their roles in regulating satiation and glucose metabolism in response to food consumption. We discuss the complex anatomical organization of vagal and spinal PSN subtypes, their peripheral and central projection patterns, and describe the limitations of unselective lesion and ablation approaches to investigate them. We then highlight the recent identification of molecular markers that allow selective targeting of PSN subtypes that innervate GI tract organs. This has facilitated accurately determining their projections, monitoring their responses to gut stimuli, and manipulating their activity. We contend that these recent developments have significantly improved our understanding of PSN-mediated gut-to-brain communication, which may open new therapeutic windows for the treatment of metabolic disorders, such as obesity and type 2 diabetes.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":"258 3","pages":""},"PeriodicalIF":4.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9937860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Pro-resolving role of glucagon in lipopolysaccharide-induced mice lung neutrophilia. 胰高血糖素在脂多糖诱导小鼠肺中性粒细胞增多症中的促溶解作用。

IF 4 3区医学

Journal of Endocrinology Pub Date : 2023-09-01 DOI: 10.1530/JOE-22-0196

Daniella Bianchi Reis Insuela, Maximiliano Ruben Ferrero, Amanda da Silva Chaves, Diego de Sá Coutinho, Nathalia Dos Santos Magalhães, Ana Carolina Santos de Arantes, Adriana Ribeiro Silva, Patrícia Machado Rodrigues E Silva, Marco Aurélio Martins, Vinicius Frias Carvalho

{"title":"Pro-resolving role of glucagon in lipopolysaccharide-induced mice lung neutrophilia.","authors":"Daniella Bianchi Reis Insuela, Maximiliano Ruben Ferrero, Amanda da Silva Chaves, Diego de Sá Coutinho, Nathalia Dos Santos Magalhães, Ana Carolina Santos de Arantes, Adriana Ribeiro Silva, Patrícia Machado Rodrigues E Silva, Marco Aurélio Martins, Vinicius Frias Carvalho","doi":"10.1530/JOE-22-0196","DOIUrl":"https://doi.org/10.1530/JOE-22-0196","url":null,"abstract":"Prior research demonstrated that glucagon has protective roles against inflammation, but its effect on the resolution of inflammation remains elusive. Using in vitro and in vivo approaches, this study aimed to investigate the pro-resolving potential of glucagon on pulmonary neutrophilic inflammation caused by lipopolysaccharide. Lipopolysaccharide induced an increase in the proportions of neutrophils positives to glucagon receptor (GcgR) in vitro. In addition, lipopolysaccharide induced an increase in the neutrophil accumulation and expression of GcgR by the inflammatory cells in the lungs, however, without altering glucagon levels. Intranasal treatment with glucagon, at the peak of neutrophilic inflammation, reduced the neutrophil number in the bronchoalveolar lavage (BAL), and lung tissue within 24 h. The reduction of neutrophilic inflammation provoked by glucagon was accompanied by neutrophilia in the blood, an increase in the apoptosis rate of neutrophils in the BAL, enhance in the pro-apoptotic Bax protein expression, and decrease in the anti-apoptotic Bcl-2 protein levels in the lung. Glucagon also induced a rise in the cleavage of caspase-3 in the lungs; however, it was not significant. Glucagon inhibited the levels of IL-1β and TNF-α while increasing the content of pro-resolving mediators transforming growth factor (TGF-β1) and PGE2 in the BAL and lung. Finally, glucagon inhibited lipopolysaccharide-induced airway hyper-reactivity, as evidenced by the reduction in lung elastance values in response to methacholine. In conclusion, glucagon-induced resolution of neutrophilic inflammation by promoting cessation of neutrophil migration and a rise of neutrophil apoptosis and the levels of pro-resolving mediators TGF-β1 and PGE2.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":"259 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10285061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Recycling glucocorticoids: therapeutic implications of the 11β-HSD1 enzyme system. 循环糖皮质激素:11β-HSD1酶系统的治疗意义。

IF 4 3区医学

Journal of Endocrinology Pub Date : 2023-09-01 DOI: 10.1530/JOE-22-0289

Kevin H Tsai, Mark S Cooper

{"title":"Recycling glucocorticoids: therapeutic implications of the 11β-HSD1 enzyme system.","authors":"Kevin H Tsai, Mark S Cooper","doi":"10.1530/JOE-22-0289","DOIUrl":"https://doi.org/10.1530/JOE-22-0289","url":null,"abstract":"Endogenous glucocorticoids and commonly used oral glucocorticoids have the property of existing in an inactive and active form in vivo. The inactive form can be converted back to the active form, or 'recycled' in cells and tissues that express the 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) enzyme. This recycling provides an important contribution to the action of glucocorticoids. This review examines the literature relating to the importance of 11β-HSD1 activity during glucocorticoid treatment, with an emphasis on studies examining bone and joint disease and the ability of glucocorticoids to suppress inflammatory damage in models of arthritis. Animal models with global or selective deletion of 11β-HSD1 have determined the extent to which this recycling is important in normal physiology and during treatment with oral glucocorticoids. These studies demonstrate that 11β-HSD1-mediated recycling of inactive glucocorticoids has a substantial action and indeed is responsible for the majority of the effects of orally administered glucocorticoids on a range of tissues. Importantly, the anti-inflammatory actions of glucocorticoids appear largely through this mechanism such that mice that lack 11β-HSD1 are resistant to the anti-inflammatory actions of glucocorticoids. The recognition that to a large extent the circulating inactive counterpart of these glucocorticoids is more important to anti-inflammatory effects than the active glucocorticoid presents novel opportunities to more selectively target glucocorticoids to tissues or to reduce the likely side effects.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":"258 3","pages":""},"PeriodicalIF":4.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9914592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Postmenopausal osteoporosis coexisting with sarcopenia: the role and mechanisms of estrogen. 绝经后骨质疏松伴骨骼肌减少症:雌激素的作用及机制。

IF 4 3区医学

Journal of Endocrinology Pub Date : 2023-09-01 DOI: 10.1530/JOE-23-0116

Lingyun Lu, Li Tian

引用次数: 0

Islet cells in human type 1 diabetes: from recent advances to novel therapies - a symposium-based roadmap for future research. 人类1型糖尿病中的胰岛细胞：从最新进展到新疗法——基于研讨会的未来研究路线图。

IF 4 3区医学

Journal of Endocrinology Pub Date : 2023-08-31 Print Date: 2023-09-01 DOI: 10.1530/JOE-23-0082

James Cantley, Decio Laks Eizirik, Esther Latres, Colin M Dayan

引用次数: 0

Mineralocorticoid receptor signalling in primary aldosteronism. 原发性醛固酮增多症中的盐皮质激素受体信号传导。

IF 4 3区医学

Journal of Endocrinology Pub Date : 2023-08-28 Print Date: 2023-09-01 DOI: 10.1530/JOE-22-0249

Jun Yang, Morag J Young, Timothy Cole, Peter J Fuller

引用次数: 0

RISING STARS: The heat is on: how does heat exposure cause pregnancy complications? 新星：高温：高温是如何导致妊娠并发症的？

IF 4 3区医学

Journal of Endocrinology Pub Date : 2023-08-25 Print Date: 2023-09-01 DOI: 10.1530/JOE-23-0030

Caitlin S Wyrwoll

{"title":"RISING STARS: The heat is on: how does heat exposure cause pregnancy complications?","authors":"Caitlin S Wyrwoll","doi":"10.1530/JOE-23-0030","DOIUrl":"10.1530/JOE-23-0030","url":null,"abstract":"The incidence and severity of heatwaves are increasing globally with concomitant health complications. Pregnancy is a critical time in the life course at risk of adverse health outcomes due to heat exposure. Dynamic physiological adaptations, which include altered thermoregulatory pathways, occur in pregnancy. If heat dissipation is ineffective, maternal and neonate health outcomes can be compromised. Indeed, epidemiological studies and animal models reveal that exposure to heat in pregnancy likely elicits an array of health complications including miscarriage, congenital anomalies, low birth weight, stillbirth, and preterm birth. Despite these associations, the reasons for why these complications occur are unclear. An array of physiological and endocrine changes in response to heat exposure in pregnancy likely underpin the adverse health outcomes, but currently, conclusive evidence is sparse. Accompanying these fundamental gaps in knowledge is a poor understanding of what exact climatic conditions challenge pregnant physiology. Moreover, the overlay of thermoregulatory-associated behaviours such as physical activity needs to be taken into consideration when assessing the risks to human health and identifying critical populations at risk. While the health impacts from heat are largely preventable through strategic interventions, for the related clinical practice, public health, and policy approaches to be effective, the gaps in basic science understanding urgently need to be addressed.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":"259 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2023-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10646462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Exercise prevents obesity by reducing gut-derived inflammatory signals to brown adipocytes in mice. 运动通过减少小鼠棕色脂肪细胞的肠道炎症信号来预防肥胖。

IF 4 3区医学

Journal of Endocrinology Pub Date : 2023-08-22 Print Date: 2023-09-01 DOI: 10.1530/JOE-23-0123

Daiana Araujo Santana-Oliveira, Henrique Souza-Tavares, Aline Fernandes-da-Silva, Flavia Maria Silva-Veiga, Gustavo Casimiro-Lopes, Patricia Cristina Lisboa, Carlos Alberto Mandarim-de-Lacerda, Vanessa Souza-Mello

{"title":"Exercise prevents obesity by reducing gut-derived inflammatory signals to brown adipocytes in mice.","authors":"Daiana Araujo Santana-Oliveira, Henrique Souza-Tavares, Aline Fernandes-da-Silva, Flavia Maria Silva-Veiga, Gustavo Casimiro-Lopes, Patricia Cristina Lisboa, Carlos Alberto Mandarim-de-Lacerda, Vanessa Souza-Mello","doi":"10.1530/JOE-23-0123","DOIUrl":"10.1530/JOE-23-0123","url":null,"abstract":"Gut dysbiosis impairs nonshivering thermogenesis (NST) in obesity. The antiobesogenic effects of exercise training might involve the modulation of gut microbiota and its inflammatory signals to the brown adipose tissue (BAT). This study evaluated whether high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) prevent overweight through reduced gut-derived inflammatory signals to BAT in high-fat-fed mice. Sixty male C57BL/6 mice (3 months old) comprised six experimental groups: control (C) diet group, C diet + HIIT (C-HIIT) group, C diet + MICT (C-MICT) group, high-fat (HF) diet group, HF diet + HIIT (HF-HIIT) group, and HF diet + MICT (HF-MICT) group. The protocols lasted for 10 weeks. HIIT and MICT restored body mass, mitigated glucose intolerance, and prevented hyperinsulinemia in HF-trained groups. A chronic HF diet caused dysbiosis, but HIIT and MICT prevented gut dysbiosis and preserved tight junction (TJ) gene expression. HF-HIIT and HF-MICT groups exhibited a similar pattern of goblet cell distribution, agreeing with the decreased plasma lipopolysaccharide concentrations and interscapular BAT (iBAT) Lbp-Cd14-Tlr4 expression. The lowered Nlrp3 and Il1β in the HF-HITT and HF-MICT groups complied with iBAT thermogenic capacity maintenance. This study shows reliable evidence that HIIT and MICT prevented overweight by restoring the diversity of the gut microbiota phyla and TJ gene expression, thereby reducing inflammatory signals to brown adipocytes with preserved thermogenic capacity. Both exercise modalities prevented overweight, but HIIT rescued Zo-1 and Jam-a gene expression, exerting more potent anti-inflammatory effects than MICT (reduced LPS concentrations), providing a sustained increase in thermogenesis with 78% less distance traveled.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":"259 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2023-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10420161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0