Journal of Endocrinology最新文献_第3页

Bidirectional crosstalk between bone and muscle: the role of RANKL pathway in osteosarcopenia. 骨骼与肌肉之间的双向串扰：RANKL通路在骨肉疏松症中的作用。

IF 3.4 3区医学

Journal of Endocrinology Pub Date : 2024-07-18 Print Date: 2024-09-01 DOI: 10.1530/JOE-24-0093

Soo Yeon Jang, Kyung Mook Choi

引用次数: 0

Does glucose-dependent insulinotropic polypeptide receptor blockade as well as agonism have a role to play in management of obesity and diabetes? GIPR 阻断和激动作用在肥胖症和糖尿病的治疗中都能发挥作用吗？

IF 3.4 3区医学

Journal of Endocrinology Pub Date : 2024-07-15 Print Date: 2024-08-01 DOI: 10.1530/JOE-23-0339

Ryan A Lafferty, Peter R Flatt, Victor A Gault, Nigel Irwin

{"title":"Does glucose-dependent insulinotropic polypeptide receptor blockade as well as agonism have a role to play in management of obesity and diabetes?","authors":"Ryan A Lafferty, Peter R Flatt, Victor A Gault, Nigel Irwin","doi":"10.1530/JOE-23-0339","DOIUrl":"10.1530/JOE-23-0339","url":null,"abstract":"Recent approval of the dual glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) receptor agonist, tirzepatide, for the management of type 2 diabetes mellitus (T2DM) has reinvigorated interest in exploitation of GIP receptor (GIPR) pathways as a means of metabolic disease management. However, debate has long surrounded the use of the GIPR as a therapeutic target and whether agonism or antagonism is of most benefit in management of obesity/diabetes. This controversy appears to be partly resolved by the success of tirzepatide. However, emerging studies indicate that prolonged GIPR agonism may desensitise the GIPR to essentially induce receptor antagonism, with this phenomenon suggested to be more pronounced in the human than rodent setting. Thus, deliberation continues to rage in relation to benefits of GIPR agonism vs antagonism. That said, as with GIPR agonism, it is clear that the metabolic advantages of sustained GIPR antagonism in obesity and obesity-driven forms of diabetes can be enhanced by concurrent GLP-1 receptor (GLP-1R) activation. This narrative review discusses various approaches of pharmacological GIPR antagonism including small molecule, peptide, monoclonal antibody and peptide-antibody conjugates, indicating stage of development and significance to the field. Taken together, there is little doubt that interesting times lie ahead for GIPR agonism and antagonism, either alone or when combined with GLP-1R agonists, as a therapeutic intervention for the management of obesity and associated metabolic disease.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11301427/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141306091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Liraglutide alleviates experimental diabetic cardiomyopathy in a PDH-dependent manner. 利拉鲁肽以 PDH 依赖性方式缓解实验性糖尿病心肌病。

IF 3.4 3区医学

Journal of Endocrinology Pub Date : 2024-07-08 Print Date: 2024-08-01 DOI: 10.1530/JOE-24-0032

Jordan S F Chan, Amanda A Greenwell, Christina T Saed, Magnus J Stenlund, Indiresh A Mangra-Bala, Seyed Amirhossein Tabatabaei Dakhili, Kunyan Yang, Sally R Ferrari, Farah Eaton, Keshav Gopal, John R Ussher

{"title":"Liraglutide alleviates experimental diabetic cardiomyopathy in a PDH-dependent manner.","authors":"Jordan S F Chan, Amanda A Greenwell, Christina T Saed, Magnus J Stenlund, Indiresh A Mangra-Bala, Seyed Amirhossein Tabatabaei Dakhili, Kunyan Yang, Sally R Ferrari, Farah Eaton, Keshav Gopal, John R Ussher","doi":"10.1530/JOE-24-0032","DOIUrl":"10.1530/JOE-24-0032","url":null,"abstract":"Liraglutide, a glucagon-like peptide-1 receptor (GLP-1R) agonist used for the treatment of T2D, has been shown to alleviate diabetic cardiomyopathy (DbCM) in experimental T2D, which was associated with increased myocardial glucose oxidation. To determine whether this increase in glucose oxidation is necessary for cardioprotection, we hypothesized that liraglutide's ability to alleviate DbCM would be abolished in mice with cardiomyocyte-specific deletion of pyruvate dehydrogenase (PDH; Pdha1CM-/- mice), the rate-limiting enzyme of glucose oxidation. Male Pdha1CM-/- mice and their α-myosin heavy chain Cre expressing littermates (αMHCCre mice) were subjected to experimental T2D via 10 weeks of high-fat diet supplementation, with a single low-dose injection of streptozotocin (75 mg/kg) provided at week 4. All mice were randomized to treatment with either vehicle control or liraglutide (30 µg/kg) twice daily during the final 2.5 weeks, with cardiac function assessed via ultrasound echocardiography. As expected, liraglutide treatment improved glucose homeostasis in both αMHCCre and Pdha1CM-/- mice with T2D, in the presence of mild weight loss. Parameters of systolic function were unaffected by liraglutide treatment in both αMHCCre and Pdha1CM-/- mice with T2D. However, liraglutide treatment alleviated diastolic dysfunction in αMHCCre mice, as indicated by an increase and decrease in the e'/a' and E/e' ratios, respectively. Conversely, liraglutide failed to rescue these indices of diastolic dysfunction in Pdha1CM-/- mice. Our findings suggest that increases in glucose oxidation are necessary for GLP-1R agonist mediated alleviation of DbCM. As such, strategies aimed at increasing PDH activity may represent a novel approach for the treatment of DbCM.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141300723","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

RISING STARS: Evidence for established and emerging forms of β-cell death. 已有的和新出现的β细胞死亡形式的证据。

IF 3.4 3区医学

Journal of Endocrinology Pub Date : 2024-07-04 Print Date: 2024-08-01 DOI: 10.1530/JOE-23-0378

Kaitlyn A Colglazier, Noyonika Mukherjee, Christopher J Contreras, Andrew T Templin

{"title":"RISING STARS: Evidence for established and emerging forms of β-cell death.","authors":"Kaitlyn A Colglazier, Noyonika Mukherjee, Christopher J Contreras, Andrew T Templin","doi":"10.1530/JOE-23-0378","DOIUrl":"10.1530/JOE-23-0378","url":null,"abstract":"β-Cell death contributes to β-cell loss and insulin insufficiency in type 1 diabetes (T1D), and this β-cell demise has been attributed to apoptosis and necrosis. Apoptosis has been viewed as the lone form of programmed β-cell death, and evidence indicates that β-cells also undergo necrosis, regarded as an unregulated or accidental form of cell demise. More recently, studies in non-islet cell types have identified and characterized novel forms of cell death that are biochemically and morphologically distinct from apoptosis and necrosis. Several of these mechanisms of cell death have been categorized as forms of regulated necrosis and linked to inflammation and disease pathogenesis. In this review, we revisit discoveries of β-cell death in humans with diabetes and describe studies characterizing β-cell apoptosis and necrosis. We explore literature on mechanisms of regulated necrosis including necroptosis, ferroptosis and pyroptosis, review emerging literature on the significance of these mechanisms in β-cells, and discuss experimental approaches to differentiate between various mechanisms of β-cell death. Our review of the literature leads us to conclude that more detailed experimental characterization of the mechanisms of β-cell death is warranted, along with studies to better understand the impact of various forms of β-cell demise on islet inflammation and β-cell autoimmunity in pathophysiologically relevant models. Such studies will provide insight into the mechanisms of β-cell loss in T1D and may shed light on new therapeutic approaches to protect β-cells in this disease.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11285760/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141261777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Differential regulation of STARD1, STARD4 and STARD6 in the human ovary. 人类卵巢中 STARD1、STARD4 和 STARD6 的差异调控。

IF 3.4 3区医学

Journal of Endocrinology Pub Date : 2024-07-03 Print Date: 2024-08-01 DOI: 10.1530/JOE-23-0385

Nawal A Yahya, Steven R King, Bo Shi, Aisha Shaaban, Nicole E Whitfield, Chunmei Yan, Richard J Kordus, Gail F Whitman-Elia, Holly A LaVoie

{"title":"Differential regulation of STARD1, STARD4 and STARD6 in the human ovary.","authors":"Nawal A Yahya, Steven R King, Bo Shi, Aisha Shaaban, Nicole E Whitfield, Chunmei Yan, Richard J Kordus, Gail F Whitman-Elia, Holly A LaVoie","doi":"10.1530/JOE-23-0385","DOIUrl":"10.1530/JOE-23-0385","url":null,"abstract":"Cells actively engaged in de novo steroidogenesis rely on an expansive intracellular network to efficiently transport cholesterol. The final link in the transport chain is STARD1, which transfers cholesterol to the enzyme complex that initiates steroidogenesis. However, the regulation of ovarian STARD1 is not fully characterized, and even less is known about the upstream cytosolic cholesterol transporters STARD4 and STARD6. Here, we identified both STARD4 and STARD6 mRNAs in the human ovary but only detected STARD4 protein since the primary STARD6 transcript turned out to be a splice variant. Corpora lutea contained the highest levels of STARD4 and STARD1 mRNA and STARD1 protein, while STARD4 protein was uniformly distributed across ovarian tissues. Cyclic AMP analog (8Br-cAMP) and phorbol ester (PMA) individually increased STARD1 and STARD4 mRNA along with STARD1 protein and its phosphoform in cultured primary human luteinized granulosa cells (hGCs). STARD6 transcripts and STARD4 protein were unresponsive to these stimuli. Combining lower doses of PMA and 8Br-cAMP blunted the 8Br-cAMP stimulation of STARD1 protein. Increasing cholesterol levels by blocking its conversion to steroid with aminoglutethimide or by adding LDL reduced the STARD4 mRNA response to stimuli. Sterol depletion reduced the STARD1 mRNA and protein response to PMA. These data support a possible role for STARD4, but not STARD6, in supplying cholesterol for steroidogenesis in the ovary. We demonstrate for the first time how cAMP, PMA and sterol pathways separately and in combination differentially regulate STARD4, STARD6 and STARD1 mRNA levels, as well as STARD1 and STARD4 protein in human primary ovarian cells.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11267794/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141199445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Reduced serum CLCF1 levels in hyperthyroidism patients and T3-treated mice. 甲状腺功能亢进症患者和 T3 治疗小鼠的血清 CLCF1 水平降低。

IF 3.4 3区医学

Journal of Endocrinology Pub Date : 2024-07-03 Print Date: 2024-08-01 DOI: 10.1530/JOE-23-0412

Xuan Zhou, Yanan Zhang, Youwen Yuan, Fei Teng, Jiayang Lin, Xueru Ye, Yaojin Pan, Huijie Zhang

{"title":"Reduced serum CLCF1 levels in hyperthyroidism patients and T3-treated mice.","authors":"Xuan Zhou, Yanan Zhang, Youwen Yuan, Fei Teng, Jiayang Lin, Xueru Ye, Yaojin Pan, Huijie Zhang","doi":"10.1530/JOE-23-0412","DOIUrl":"10.1530/JOE-23-0412","url":null,"abstract":"Characteristic symptoms of hyperthyroidism include weight loss, heart palpitation, and sweating. Thyroid hormones (TH) can stimulate thermogenesis through central and peripheral mechanisms. Previous studies have shown an association between dysfunction of cardiotrophin-like cytokine factor 1 (CLCF1) and cold-induced sweating syndrome, with recent research also indicating a link between CLCF1 and brown adipose tissue thermogenesis. However, it remains unclear whether CLCF1 and TH have synergistic or antagonistic effects on thermogenesis. This study aims to investigate the influence of thyroid hormone on circulating CLCF1 levels in humans and explore the potential possibilities of thyroid hormone in regulating energy metabolism by modulating Clcf1 in mice. By recruiting hyperthyroid patients and healthy subjects, we observed significantly lower serum CLCF1 levels in hyperthyroid patients compared to healthy subjects, with serum CLCF1 levels independently associated with hyperthyroidism after adjusting for potential confounders. Tissue analysis from mice treated with T3 revealed a decrease in CLCF1 expression in BAT and iWAT of C57BL/6 mice. These findings suggest that TH may play a role in regulating CLCF1 expression in adipose tissue.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141261760","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

ATP-binding cassette family C member 1 constrains metabolic responses to high-fat diet in male mice. ATP 结合盒 C 家族成员 1 限制了对高脂肪饮食的代谢反应。

IF 3.4 3区医学

Journal of Endocrinology Pub Date : 2024-07-03 Print Date: 2024-08-01 DOI: 10.1530/JOE-24-0024

Elisa Villalobos, Allende Miguelez-Crespo, Ruth A Morgan, Lisa Ivatt, Mhairi Paul, Joanna P Simpson, Natalie Z M Homer, Dominic Kurian, Judit Aguilar, Rachel A Kline, Thomas M Wishart, Nicholas M Morton, Roland H Stimson, Ruth Andrew, Brian R Walker, Mark Nixon

{"title":"ATP-binding cassette family C member 1 constrains metabolic responses to high-fat diet in male mice.","authors":"Elisa Villalobos, Allende Miguelez-Crespo, Ruth A Morgan, Lisa Ivatt, Mhairi Paul, Joanna P Simpson, Natalie Z M Homer, Dominic Kurian, Judit Aguilar, Rachel A Kline, Thomas M Wishart, Nicholas M Morton, Roland H Stimson, Ruth Andrew, Brian R Walker, Mark Nixon","doi":"10.1530/JOE-24-0024","DOIUrl":"10.1530/JOE-24-0024","url":null,"abstract":"Glucocorticoids modulate glucose homeostasis, acting on metabolically active tissues such as liver, skeletal muscle, and adipose tissue. Intracellular regulation of glucocorticoid action in adipose tissue impacts metabolic responses to obesity. ATP-binding cassette family C member 1 (ABCC1) is a transmembrane glucocorticoid transporter known to limit the accumulation of exogenously administered corticosterone in adipose tissue. However, the role of ABCC1 in the regulation of endogenous glucocorticoid action and its impact on fuel metabolism has not been studied. Here, we investigate the impact of Abcc1 deficiency on glucocorticoid action and high-fat-diet (HFD)-induced obesity. In lean male mice, deficiency of Abcc1 increased endogenous corticosterone levels in skeletal muscle and adipose tissue but did not impact insulin sensitivity. In contrast, Abcc1-deficient male mice on HFD displayed impaired glucose and insulin tolerance, and fasting hyperinsulinaemia, without alterations in tissue corticosterone levels. Proteomics and bulk RNA sequencing revealed that Abcc1 deficiency amplified the transcriptional response to an obesogenic diet in adipose tissue but not in skeletal muscle. Moreover, Abcc1 deficiency impairs key signalling pathways related to glucose metabolism in both skeletal muscle and adipose tissue, in particular those related to OXPHOS machinery and Glut4. Together, our results highlight a role for ABCC1 in regulating glucose homeostasis, demonstrating diet-dependent effects that are not associated with altered tissue glucocorticoid concentrations.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11301423/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141199436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Glucagon infusion alters the circulating metabolome and urine amino acid excretion in dogs. 输注胰高血糖素会改变狗的循环代谢组和尿液氨基酸排泄。

IF 3.4 3区医学

Journal of Endocrinology Pub Date : 2024-06-27 Print Date: 2024-08-01 DOI: 10.1530/JOE-24-0051

Michael Merkhassine, Reilly W Coch, Carol E Frederick, Lucinda L Bennett, Seth A Peng, Benjamin Morse, Bethany P Cummings, John P Loftus

{"title":"Glucagon infusion alters the circulating metabolome and urine amino acid excretion in dogs.","authors":"Michael Merkhassine, Reilly W Coch, Carol E Frederick, Lucinda L Bennett, Seth A Peng, Benjamin Morse, Bethany P Cummings, John P Loftus","doi":"10.1530/JOE-24-0051","DOIUrl":"10.1530/JOE-24-0051","url":null,"abstract":"Glucagon plays a central role in amino acid (AA) homeostasis. The dog is an established model of glucagon biology, and recently, metabolomic changes in people associated with glucagon infusions have been reported. Glucagon also has effects on the kidney; however, changes in urinary AA concentrations associated with glucagon remain under investigation. Therefore, we aimed to fill these gaps in the canine model by determining the effects of glucagon on the canine plasma metabolome and measuring urine AA concentrations. Employing two constant rate glucagon infusions (CRI) - low-dose (CRI-LO: 3 ng/kg/min) and high-dose (CRI-HI: 50 ng/kg/min) on five research beagles, we monitored interstitial glucose and conducted untargeted liquid chromatography-tandem mass spectrometry (LC-MS/MS) on plasma samples and urine AA concentrations collected pre- and post-infusion. The CRI-HI induced a transient glucose peak (90-120 min), returning near baseline by infusion end, while only the CRI-LO resulted in 372 significantly altered plasma metabolites, primarily reductions (333). Similarly, CRI-HI affected 414 metabolites, with 369 reductions, evidenced by distinct clustering post-infusion via data reduction (PCA and sPLS-DA). CRI-HI notably decreased circulating AA levels, impacting various AA-related and energy-generating metabolic pathways. Urine analysis revealed increased 3-methyl-l-histidine and glutamine, and decreased alanine concentrations post-infusion. These findings demonstrate glucagon's glucose-independent modulation of the canine plasma metabolome and highlight the dog's relevance as a translational model for glucagon biology. Understanding these effects contributes to managing dysregulated glucagon conditions and informs treatments impacting glucagon homeostasis.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11301426/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141174641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Maternal androgen exposure induces intergenerational effects via paternal inheritance. 母体雄激素暴露通过父系遗传诱导代际效应。

IF 3.4 3区医学

Journal of Endocrinology Pub Date : 2024-06-24 Print Date: 2024-08-01 DOI: 10.1530/JOE-23-0368

Yu Zhou, Chao Lian, Yingfei Lu, Tianming Wang, Chengcheng Zhao, Cuilan Zhang, Min Gong, Jianquan Chen, Rong Ju

{"title":"Maternal androgen exposure induces intergenerational effects via paternal inheritance.","authors":"Yu Zhou, Chao Lian, Yingfei Lu, Tianming Wang, Chengcheng Zhao, Cuilan Zhang, Min Gong, Jianquan Chen, Rong Ju","doi":"10.1530/JOE-23-0368","DOIUrl":"10.1530/JOE-23-0368","url":null,"abstract":"Polycystic ovary syndrome (PCOS) is a condition resulting from the interaction between environmental factors and hereditary components, profoundly affecting offspring development. Although the etiology of this disease remains unclear, aberrant in utero androgen exposure is considered one of the pivotal pathogenic factors. Herein, we demonstrate the intergenerational inheritance of PCOS-like phenotypes in F2 female offspring through F1 males caused by maternal testosterone exposure in F0 mice. We found impaired serum hormone expression and reproductive system development in prenatal testosterone-treated F1 male and F2 female mice (PTF1 and PTF2). In addition, downregulated N6-methyladenosine (m6A) methyltransferase and binding proteins induced mRNA hypomethylation in the PTF1 testis, including frizzled-6 (Fzd6). In the PTF2 ovary, decreased FZD6 protein expression inhibited the mammalian target of rapamycin (mTOR) signaling pathway and activated Forkhead box O3 (FoxO3) phosphorylation, which led to impaired follicular development. These data indicate that epigenetic modification of the mTOR signaling pathway could be involved in the intergenerational inheritance of maternal testosterone exposure-induced impairments in the PTF2 ovary through male PTF1 mice.","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161817","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

ERRATUM: GH modulates hepatic epidermal growth factor signaling in the mouse. ERRATUM：GH 可调节小鼠肝脏表皮生长因子信号传导。

IF 3.4 3区医学

Journal of Endocrinology Pub Date : 2024-06-24 DOI: 10.1530/JOE-09-0372e

Lorena González, Ma Eugenia Díaz, Johanna G Miquet, Ana I Sotelo, Diego Fernández, Fernando P Dominici, Andrzej Bartke, Daniel Turyn

引用次数: 0