Journal of Endocrinology最新文献

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Microbiome dysbiosis by antibiotics protects cartilage degradation in OAOP mice. 抗生素造成的微生物群失调保护了 OAOP 小鼠的软骨退化。
IF 4 3区 医学
Journal of Endocrinology Pub Date : 2024-03-13 Print Date: 2024-05-01 DOI: 10.1530/JOE-23-0330
Qin Yin, Jun Gu, Pengju Ren, Zhiqiang Guan, Yongxiang Wang, Ruijun Bai, Yu Liu
{"title":"Microbiome dysbiosis by antibiotics protects cartilage degradation in OAOP mice.","authors":"Qin Yin, Jun Gu, Pengju Ren, Zhiqiang Guan, Yongxiang Wang, Ruijun Bai, Yu Liu","doi":"10.1530/JOE-23-0330","DOIUrl":"10.1530/JOE-23-0330","url":null,"abstract":"<p><p>The role of this study was to evaluate the impact of gut microbiota depletion on the progression of osteoarthritis (OA) and osteoporosis (OP). We conducted an experimental mouse model of OA and OP over an 8-week period. The model involved destabilization of the medial meniscus and bilateral ovariectomy (OVX). To deplete the gut microbiota, we administered a course of antibiotics for 8 weeks. The severity of OA was assessed through micro-CT scanning, X-rays, and immunohistochemical staining. Microbiome analysis was performed using PCR of 16S DNA on fecal samples, and the levels of serum lipopolysaccharide, interleukin 6, tumor necrosis factor-α (TNF-α), osteocalcin, and estrogen were measured using enzyme-linked immunosorbent assay. We found that in comparison to the OVX+OA group, the OVX+OA+ABT group exhibited increased bone mineral density (P < 0.0001), bone volume fraction (P = 0.0051), and trabecular number (P = 0.0023) in the metaphyseal bone. Additionally, cartilage injury and levels of matrix metalloproteinase 13 were reduced in the OVX+OA+ABT group compared to the OVX+OA group. Moreover, the OVX+OA+ABT group demonstrated decreased relative abundance of Bacteroidetes, serum lipopolysaccharide (P = 0.0005), TNF-α (P < 0.0001), CTX-1 (P = 0.0002), and increased expression of bone formation markers. These findings were further supported by correlation network analyses. Depletion of gut microbiota was shown to protect against bone loss and cartilage degradation by modulating the composition of the gut microbiota in osteoporosis and osteoarthritis.</p>","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":" ","pages":""},"PeriodicalIF":4.0,"publicationDate":"2024-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139542364","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
Insulin induces bioenergetic changes and alters mitochondrial dynamics in podocytes 胰岛素诱导生物能变化并改变荚膜细胞中线粒体的动态变化
IF 4 3区 医学
Journal of Endocrinology Pub Date : 2024-03-01 DOI: 10.1530/joe-23-0357
Irena Audzeyenka, Patrycja Rachubik, Dorota Rogacka, Moin A Saleem, Agnieszka Piwkowska
{"title":"Insulin induces bioenergetic changes and alters mitochondrial dynamics in podocytes","authors":"Irena Audzeyenka, Patrycja Rachubik, Dorota Rogacka, Moin A Saleem, Agnieszka Piwkowska","doi":"10.1530/joe-23-0357","DOIUrl":"https://doi.org/10.1530/joe-23-0357","url":null,"abstract":"<p>Diabetic nephropathy (DN) is one of the most frequent complications of diabetes. Early stages of DN are associated with hyperinsulinemia and progressive insulin resistance in insulin-sensitive cells, including podocytes. The diabetic environment induces pathological changes, especially in podocyte bioenergetics, which is tightly linked with mitochondrial dynamics. The regulatory role of insulin in mitochondrial morphology in podocytes has not been fully elucidated. Therefore, the main goal of the present study was to investigate effects of insulin on the regulation of mitochondrial dynamics and bioenergetics in human podocytes. Biochemical analyses were performed to assess oxidative phosphorylation efficiency by measuring the oxygen consumption rate (OCR) and glycolysis by measuring the extracellular acidification rate (ECAR). mRNA and protein expression were determined by real-time polymerase chain reaction and Western blot. The intracellular mitochondrial network was visualized by MitoTracker staining. All calculations were conducted using CellProfiler software. Short-term insulin exposure exerted inhibitory effects on various parameters of oxidative respiration and adenosine triphosphate production, and glycolysis flux was elevated. After a longer time of treating cells with insulin, an increase in mitochondrial size was observed, accompanied by a reduction of expression of the mitochondrial fission markers DRP1 and FIS1 and an increase in mitophagy. Overall, we identified a previously unknown role for insulin in the regulation of oxidative respiration and glycolysis and elucidated mitochondrial dynamics in human podocytes. The present results emphasize the importance of the duration of insulin stimulation for its metabolic and molecular effects, which should be considered in clinical and experimental studies of DN.</p>","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":"9 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140324745","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
Role of CD20+ T cells in cancer, autoimmunity and obesity. CD20+ T 细胞在癌症、自身免疫和肥胖症中的作用。
IF 4 3区 医学
Journal of Endocrinology Pub Date : 2024-02-12 Print Date: 2024-03-01 DOI: 10.1530/JOE-23-0242
Aryane Cruz Oliveira Pinho, Paula Laranjeira, Eugenia Carvalho
{"title":"Role of CD20+ T cells in cancer, autoimmunity and obesity.","authors":"Aryane Cruz Oliveira Pinho, Paula Laranjeira, Eugenia Carvalho","doi":"10.1530/JOE-23-0242","DOIUrl":"10.1530/JOE-23-0242","url":null,"abstract":"<p><p>Despite the known link between obesity and insulin resistance (IR) to chronic low-grade inflammation, new markers capable of early IR detection are needed. Immune cells are components of adipose tissue's (AT) stromal vascular fraction (SVF) that regulate AT homeostasis. The altered phenotype and function of AT-infiltrating immune cells may contribute to the development and maintenance of local AT inflammation observed under obesity-induced IR conditions. Impaired AT-specific immunometabolic function may influence the whole organism. Therefore, AT-infiltrating immune cells may be important players in the development of obesity-related metabolic complications, such as type 2 diabetes mellitus (T2DM). B and T cells, particularly CD20+ T cells, play important roles in human pathology, such as autoimmune disease and cancer. However, the question remains as to whether CD20+ T cells have an important contribution to the development of obesity-related IR. While circulating CD20+ T cells are mostly of the central memory phenotype (i.e. antigen-experienced T cells with the ability to home to secondary lymphoid organs), tissues-infiltrated CD20+ T cells are predominantly of the effector memory phenotype (i.e. antigen-experienced T cells that preferentially infiltrate peripheral tissues). The latter produce pro-inflammatory cytokines, such as IFN-γ and IL-17, which play a role in obesity-related IR development. This review describes the CD20 molecule and its presence in both B and T cells, shedding light on its ontogeny and function, in health and disease, with emphasis on AT. The link between CD20+ T cell dysregulation, obesity, and IR development supports the role of CD20+ T cells as markers of adipose tissue dysmetabolism.</p>","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":" ","pages":""},"PeriodicalIF":4.0,"publicationDate":"2024-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139490184","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
Osteocalcin protects islet identity in LDL receptor knockout mice on high fat diet 骨钙素保护高脂饮食低密度脂蛋白受体基因敲除小鼠的胰岛特性
IF 4 3区 医学
Journal of Endocrinology Pub Date : 2024-02-01 DOI: 10.1530/joe-23-0352
Christine A Beamish, Yoon K. Lee, A. Osama Gaber, Priyanka Chanana, Edward A Graviss, Malgorzata Kloc, M. Waleed Gaber, Willa A Hsueh, Omaima M. Sabek
{"title":"Osteocalcin protects islet identity in LDL receptor knockout mice on high fat diet","authors":"Christine A Beamish, Yoon K. Lee, A. Osama Gaber, Priyanka Chanana, Edward A Graviss, Malgorzata Kloc, M. Waleed Gaber, Willa A Hsueh, Omaima M. Sabek","doi":"10.1530/joe-23-0352","DOIUrl":"https://doi.org/10.1530/joe-23-0352","url":null,"abstract":"<p>Metabolic syndrome (MetS) is an increasing global health threat and strong risk factor for type 2 diabetes (T2D). MetS causes both hyperinsulinemia and islet size overexpansion, and pancreatic beta (β)-cell failure impacts insulin and proinsulin secretion, mitochondrial density, and cellular identity loss. The low-density lipoprotein receptor knockout (LDLr-/-) model combined with high fat diet (HFD) has been used to study alterations in multiple organs, but little is known about changes to β-cell identity resulting from MetS. Osteocalcin (OC), an insulin-sensitizing protein secreted by bone, shows promising impact on β-cell identity and function. LDLr-/- mice at 12mo were fed chow or HFD for 3 months ± 4.5 ng/h osteocalcin. Islets were examined by immunofluorescence for alterations in nuclear Nkx6.1 and PDX1 presence, insulin-glucagon colocalization, islet size and %β-cell and islet area by insulin and synaptophysin, and mitochondria fluorescence intensity by Tomm20. Bone mineral density (BMD) and %fat changes were examined by Piximus Dexa scanning. HFD-fed mice showed fasting hyperglycemia by 15mo, increased weight gain, %fat, and fasting serum insulin and proinsulin; concurrent OC treatment mitigated weight increase and showed lower proinsulin/insulin ratio, and higher BMD. HFD increased %β and %islet area, while simultaneous osteocalcin-treatment with HFD was comparable to chow-fed mice. Significant reductions in nuclear PDX1 and Nkx6.1 expression, increased insulin-glucagon colocalization, and reduction in β-cell mitochondria fluorescence intensity were noted with HFD, but largely prevented with OC administration. Osteocalcin supplementation here suggests a benefit to β-cell identity in LDLr-/- mice and offers intriguing clinical implications for countering metabolic syndrome.</p>","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":"151 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139668392","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
Intestinal FFA2 promotes obesity by altering food intake in Western diet-fed mice. 肠道FFA2通过改变西方饮食喂养的小鼠的食物摄入来促进肥胖。
IF 4 3区 医学
Journal of Endocrinology Pub Date : 2024-01-11 Print Date: 2024-02-01 DOI: 10.1530/JOE-23-0184
Kristen R Lednovich, Sophie Gough, Medha Priyadarshini, Nupur Pandya, Chioma Nnyamah, Kai Xu, Barton Wicksteed, Sidharth Mishra, Shalini Jain, Joseph L Zapater, Jose Cordoba-Chacon, Hariom Yadav, Brian T Layden
{"title":"Intestinal FFA2 promotes obesity by altering food intake in Western diet-fed mice.","authors":"Kristen R Lednovich, Sophie Gough, Medha Priyadarshini, Nupur Pandya, Chioma Nnyamah, Kai Xu, Barton Wicksteed, Sidharth Mishra, Shalini Jain, Joseph L Zapater, Jose Cordoba-Chacon, Hariom Yadav, Brian T Layden","doi":"10.1530/JOE-23-0184","DOIUrl":"10.1530/JOE-23-0184","url":null,"abstract":"<p><p>Short-chain fatty acids (SCFAs) are key nutrients that play a diverse set of roles in physiological function, including regulating metabolic homeostasis. Generated through the fermentation of dietary fibers in the distal colon by the gut microbiome, SCFAs and their effects are partially mediated by their cognate receptors, including free fatty acid receptor 2 (FFA2). FFA2 is highly expressed in the intestinal epithelial cells, where its putative functions are controversial, with numerous in vivo studies relying on global knockout mouse models to characterize intestine-specific roles of the receptor. Here, we used the Villin-Cre mouse line to generate a novel, intestine-specific knockout mouse model for FFA2 (Vil-FFA2) to investigate receptor function within the intestine. Because dietary changes are known to affect the composition of the gut microbiome, and can thereby alter SCFA production, we performed an obesogenic challenge on male Vil-FFA2 mice and their littermate controls (FFA2-floxed, FFA2fl/fl) to identify physiological changes on a high-fat, high-sugar 'Western diet' (WD) compared to a low-fat control diet (CD). We found that the WD-fed Vil-FFA2 mice were transiently protected from the obesogenic effects of the WD and had lower fat mass and improved glucose homeostasis compared to the WD-fed FFA2fl/fl control group during the first half of the study. Additionally, major differences in respiratory exchange ratio and energy expenditure were observed in the WD-fed Vil-FFA2 mice, and food intake was found to be significantly reduced at multiple points in the study. Taken together, this study uncovers a novel role of intestinal FFA2 in mediating the development of obesity.</p>","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":" ","pages":""},"PeriodicalIF":4.0,"publicationDate":"2024-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10831573/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138460254","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
Prenatal cortisol exposure impairs adrenal function but not glucose metabolism in adult sheep 产前皮质醇暴露会损害成年绵羊的肾上腺功能,但不会影响葡萄糖代谢
IF 4 3区 医学
Journal of Endocrinology Pub Date : 2023-12-01 DOI: 10.1530/joe-23-0326
K L Davies, J Miles, E. J Camm, D.j. Smith, P Barker, K Taylor, A. J Forhead, A. L Fowden
{"title":"Prenatal cortisol exposure impairs adrenal function but not glucose metabolism in adult sheep","authors":"K L Davies, J Miles, E. J Camm, D.j. Smith, P Barker, K Taylor, A. J Forhead, A. L Fowden","doi":"10.1530/joe-23-0326","DOIUrl":"https://doi.org/10.1530/joe-23-0326","url":null,"abstract":"<p>Adverse environmental conditions before birth are known to program adult metabolic and endocrine phenotype in several species. However, whether increments in fetal cortisol concentrations of the magnitude commonly seen in these conditions can cause developmental programming remains unknown. Thus, this study investigated the outcome of physiological increases in fetal cortisol concentrations on glucose-insulin dynamics and pituitary-adrenal function in adult sheep. Compared to saline treatment, intravenous fetal cortisol infusion for 5 days in late gestation did not affect birthweight but increased lamb body weight at 1-2 weeks after birth. Adult glucose dynamics, insulin sensitivity and insulin secretion were unaffected by prenatal cortisol overexposure, assessed by glucose tolerance tests, hyperinsulinaemic-euglycaemic clamps and acute insulin administration. In contrast, prenatal cortisol infusion induced adrenal hypo-responsiveness in adulthood with significantly reduced cortisol responses to insulin-induced hypoglycaemia and exogenous adrenocorticotropic hormone (ACTH) administration relative to saline treatment. The area of adrenal cortex expressed as a percentage of the total cross-sectional area of the adult adrenal gland was also lower after prenatal cortisol than saline infusion. In adulthood, basal circulating ACTH but not cortisol concentrations were significantly higher in the cortisol than saline treated group. The results show that cortisol overexposure before birth programs pituitary-adrenal development with consequences for adult stress responses. Physiological variations in cortisol concentrations before birth may, therefore, have an important role in determining adult phenotypical diversity and adaptability to environmental challenges. </p>","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":"38 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138743520","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
Neuronal insulin signaling and resistance: a balancing act of kinases and phosphatases. 神经元胰岛素信号传导与抵抗:激酶和磷酸酶的平衡作用。
IF 3.4 3区 医学
Journal of Endocrinology Pub Date : 2023-12-01 Print Date: 2024-01-01 DOI: 10.1530/JOE-23-0151
Medha Sharma, Yamini Yadav, Chinmoy Sankar Dey
{"title":"Neuronal insulin signaling and resistance: a balancing act of kinases and phosphatases.","authors":"Medha Sharma, Yamini Yadav, Chinmoy Sankar Dey","doi":"10.1530/JOE-23-0151","DOIUrl":"10.1530/JOE-23-0151","url":null,"abstract":"<p><p>Insulin signaling cascade in peripheral insulin-sensitive tissues regulates whole-body glucose metabolism. Any deregulation in this pathway leads to insulin resistance, ultimately leading to metabolic diseases like type 1 diabetes, type 2 diabetes, and obesity. Insulin signaling in the brain has also been studied for many decades and associated with many primary functions like maintenance of synaptic plasticity, regulation of cognition, and circadian rhythm. Importantly, neuronal insulin signaling has also been associated with the regulation of neuronal glucose uptake. Any impairment in neuronal insulin signaling affecting neuronal glucose uptake has been associated with neurodegenerative disorders like Alzheimer's disease, the process now being termed as type 3 diabetes. Since the criticality lies in proper signaling cascade, determining important points of deregulation is important. In this review, we have discussed some critical points of such deregulation, dividing them into two classes of enzymes: kinases and phosphatases. We have highlighted their individual roles in neuronal insulin signaling, along with their possible implications in neuronal insulin resistance. Future strategies targeting these nodes in neuronal insulin signaling might be helpful in exploring potential therapeutic opportunities to overcome neuronal insulin resistance and related neurodegenerative diseases.</p>","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71482160","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
L. amylovorus KU4 induces adipose browning in obese mice by regulating PP4C L. amylovorus KU4通过调节PP4C诱导肥胖小鼠脂肪棕色化
IF 4 3区 医学
Journal of Endocrinology Pub Date : 2023-12-01 DOI: 10.1530/joe-23-0185
Garam Yang, Eunjeong Hong, Sejong Oh, Eungseok Kim
{"title":"L. amylovorus KU4 induces adipose browning in obese mice by regulating PP4C","authors":"Garam Yang, Eunjeong Hong, Sejong Oh, Eungseok Kim","doi":"10.1530/joe-23-0185","DOIUrl":"https://doi.org/10.1530/joe-23-0185","url":null,"abstract":"<p>We previously reported that Lactobacillus amylovorus KU4 (LKU4) promotes adipocyte browning in mice fed a high-fat diet (HFD mice) in part by remodeling the PPARγ transcription complex. However, the mechanism through which LKU4 enables PPARγ to drive adipocyte browning remains elusive. Here, we report that LKU4 inhibits the expression of PP4C in inguinal white adipose tissue of HFD mice and in insulin-resistant 3T3-L1 adipocytes, which promotes SIRT1-dependent PPARγ deacetylation by activating AMPK, leading to the browning of adipocytes. Consistently, the silencing of PP4C further enhanced this pathway. Furthermore, we observed that lactate, a key LKU4 metabolite, reduces insulin-induced PP4C expression and suppresses PP4C inhibition of PPARγ deacetylation and transcriptional activity via AMPK-SIRT1, thereby facilitating the browning of adipocytes. Together, these data demonstrate that LKU4 promotes the AMPK–SIRT1–PPARγ pathway by inhibiting PP4C, thereby facilitating adipocyte browning in mice fed a HFD.</p>","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":"33 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138743581","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
Continuing the success of Journal of Endocrinology and Journal of Molecular Endocrinology. 延续《内分泌学杂志》和《分子内分泌学杂志》的成功。
IF 3.4 3区 医学
Journal of Endocrinology Pub Date : 2023-11-29 Print Date: 2024-01-01 DOI: 10.1530/JOE-23-0333
Colin Farquharson, Ruth Andrew
{"title":"Continuing the success of Journal of Endocrinology and Journal of Molecular Endocrinology.","authors":"Colin Farquharson, Ruth Andrew","doi":"10.1530/JOE-23-0333","DOIUrl":"10.1530/JOE-23-0333","url":null,"abstract":"","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":"260 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2023-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11376209/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138451641","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
A bright future for glucagon and alpha cell biology. 胰高血糖素和α细胞生物学的光明前景。
IF 3.4 3区 医学
Journal of Endocrinology Pub Date : 2023-11-27 Print Date: 2024-01-01 DOI: 10.1530/JOE-22-0315
Julia K Panzer, Alejandro Caicedo
{"title":"A bright future for glucagon and alpha cell biology.","authors":"Julia K Panzer, Alejandro Caicedo","doi":"10.1530/JOE-22-0315","DOIUrl":"10.1530/JOE-22-0315","url":null,"abstract":"<p><p>Long lagging behind insulin, glucagon research has caught up in large part, thanks to technological breakthroughs. Here we review how the field was propelled by the development of novel techniques and approaches. The glucagon radioimmunoassay and islet isolation are methods that now seem trivial, but for decades they were crucial in defining the biology of the pancreatic alpha cell and the role of glucagon in glucose homeostasis. More recently, mouse models have become the main workhorse of this research effort, if not of biomedical research in general. The mouse model allowed detailed mechanistic studies that are revealing alpha cell functions beyond its canonical glucoregulatory role. A recent profusion of gene expression and transcription regulation studies is providing new vistas into what constitutes alpha cell identity. In particular, the combination of transcriptomic techniques with functional recordings promises to move molecular guesswork into real-time physiology. The challenge right now is not to get enamored with these powerful techniques and to make sure that the research continues to be transformative and paradigm shifting. We should imagine a future in which the biology of the alpha cell will be studied at single-cell resolution, non-invasively, and in real time in the human body.</p>","PeriodicalId":15740,"journal":{"name":"Journal of Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2023-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"54229311","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
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