Endocrinology最新文献

{"title":"Body Mass Index and Risk of All-Cause and Cardiovascular Disease Mortality in Patients With Type 2 Diabetes Mellitus.","authors":"Cui Wu, Yuandong Li, Na Li, Ka Kei Chan, Chunli Piao","doi":"10.1210/endocr/bqaf040","DOIUrl":"10.1210/endocr/bqaf040","url":null,"abstract":"<p><strong>Context: </strong>The correlations between body mass index (BMI) and risk of all-cause and cardiovascular disease (CVD) mortality in patients with type 2 diabetes mellitus (T2DM) are still controversial.</p><p><strong>Objective: </strong>To explore the correlation between BMI and the risk of all-cause and CVD mortality in patients with T2DM.</p><p><strong>Methods: </strong>The data sources China National Knowledge Infrastructure, Wanfang Data Knowledge Service Platform, PubMed, Web of Science, Embase, and The Cochrane Library were searched up until May 25, 2024. After adjusting for confounding factors, the original study on the association between BMI and all-cause and CVD mortality in patients with T2DM was analyzed. Number of all-cause and CVD mortality events, BMI, and basic characteristics were extracted.</p><p><strong>Results: </strong>Twenty-eight papers with a total of 728 321 participants were finally included. Compared to normal-weight patients with T2DM, the risk of all-cause (HR = 1.61; 95% CI [1.51, 1.72]; P = .000) and CVD (HR = 1.31; 95% CI [1.10, 1.54]; P = .002) mortality were increased in underweight patients; however, they were reduced (HR = 0.85; 95% CI [0.81, 0.89]; P = .000) and (HR = 0.86; 95% CI [0.78, 0.96]; P = .007), respectively in patients with overweight. Also, there were significant reductions in the risk of all-cause (HR = 0.85; 95% CI [0.78, 0.92]; P = .000) and CVD (HR = 0.81; 95% CI [0.74, 0.89]; P = .000] mortality in patients with mild obesity. The difference in the risk of all-cause mortality (HR = 0.98; 95% CI [0.80, 1.21]; P = .881) in patients with moderate obesity was not statistically significant.</p><p><strong>Conclusion: </strong>We found that there were correlations between BMI and the risk of all-cause and CVD mortality in patients with T2DM. The obesity paradox remains.</p>","PeriodicalId":11819,"journal":{"name":"Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143556242","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}

{"title":"Gut Microbiome Regulation of Gut Hormone Secretion.","authors":"Jessica Chao, Rosemary A Coleman, Damien J Keating, Alyce M Martin","doi":"10.1210/endocr/bqaf004","DOIUrl":"10.1210/endocr/bqaf004","url":null,"abstract":"<p><p>The gut microbiome, comprising bacteria, viruses, fungi, and bacteriophages, is one of the largest microbial ecosystems in the human body and plays a crucial role in various physiological processes. This review explores the interaction between the gut microbiome and enteroendocrine cells (EECs), specialized hormone-secreting cells within the intestinal epithelium. EECs, which constitute less than 1% of intestinal epithelial cells, are key regulators of gut-brain communication, energy metabolism, gut motility, and satiety. Recent evidence shows that gut microbiota directly influence EEC function, maturation, and hormone secretion. For instance, commensal bacteria regulate the production of hormones like glucagon-like peptide 1 and peptide YY by modulating gene expression and vesicle cycling in EE cells. Additionally, metabolites such as short-chain fatty acids, derived from microbial fermentation, play a central role in regulating EEC signaling pathways that affect metabolism, gut motility, and immune responses. Furthermore, the interplay between gut microbiota, EECs, and metabolic diseases, such as obesity and diabetes, is examined, emphasizing the microbiome's dual role in promoting health and contributing to disease states. This intricate relationship between the gut microbiome and EECs offers new insights into potential therapeutic strategies for metabolic and gut disorders.</p>","PeriodicalId":11819,"journal":{"name":"Endocrinology","volume":"166 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11879239/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143556171","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}

{"title":"Leukemic Cells Infiltrate the Ovaries Without Damaging Ovarian Reserve in an Acute Myeloid Leukemia Mouse Model.","authors":"Amirhossein Abazarikia, Yi Luan, Wonmi So, Michelle Becker, Sipra Panda, Samantha A Swenson, Elizabeth A Kosmacek, Rebecca E Oberley-Deegan, Shuo Xiao, Ricia Katherine Hyde, So-Youn Kim","doi":"10.1210/endocr/bqaf022","DOIUrl":"10.1210/endocr/bqaf022","url":null,"abstract":"<p><p>Leukemia is one of the most common cancers in prepubertal girls and adolescents, with advances improving survival rates. However, treatments like chemotherapy and radiation are highly gonadotoxic, often causing ovarian insufficiency, early menopause, infertility, and endocrine disorders. Fertility preservation for young female patients with cancer, especially prepubertal girls without mature germ cells, relies heavily on ovarian tissue cryopreservation. Yet, a major concern is the potential presence of leukemic cells within preserved tissue, posing a risk of reintroducing malignancy upon grafting. Additionally, the direct effects of leukemia on ovarian function remain unclear. In this study, we used an acute myeloid leukemia (AML) mouse model to explore the impact of leukemia on ovarian function. Leukemic cells infiltrated the ovaries, particularly the stromal regions and granulosa layers of antral follicles, while also being present in the spleen and liver. Despite this infiltration, ovarian structure, follicular counts, and primordial follicle reserves were largely preserved, with the notable absence of corpus luteum indicating impaired ovulation. Furthermore, leukemic infiltration induced inflammatory cytokines TNF-α and COX-2, potentially influencing ovarian health. These findings suggest opportunities for fertility preservation by selectively removing leukemic cells, though risks of malignancy remain. This model offers a platform for advancing fertility-preservation strategies during gonadotoxic cancer therapies.</p>","PeriodicalId":11819,"journal":{"name":"Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890401/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143064813","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}

{"title":"Vasoinhibin is Generated by the Renin-angiotensin System.","authors":"Francisco Freinet Núñez, Lourdes Siqueiros-Marquez, Elva Adán-Castro, Magdalena Zamora, Juan Pablo Robles, Xarubet Ruíz-Herrera, Thomas Bertsch, Jakob Triebel, Gonzalo Martínez de la Escalera, Carmen Clapp","doi":"10.1210/endocr/bqaf023","DOIUrl":"10.1210/endocr/bqaf023","url":null,"abstract":"<p><p>Vasoinhibin is a fragment of the hormone prolactin (PRL) that inhibits angiogenesis, vasopermeability, and vasodilation. Cathepsin D (CTSD) cleaves the N-terminal of PRL to generate vasoinhibin in the retina of neonate mice as revealed by the CTSD inhibitor, pepstatin A. However, pepstatin A also inhibits renin. Because renin is expressed in the retina and the renin-angiotensin system gives rise to peptides with positive and negative effects on blood vessel growth and function, we investigated whether renin cleaves PRL to vasoinhibin in the newborn mouse retina and in the circulation. Newborn mouse retinal extracts from wild-type and CTSD-null newborn mice cleaved PRL to a 14 kDa vasoinhibin and such cleavage was prevented by heat-inactivation, pepstatin A, and the selective renin inhibitor VTP-27999 suggesting the contribution of renin. In agreement, recombinant renin cleaved different species PRLs to the expected 14-kDa vasoinhibin, a mass consistent with a consensus renin cleavage site located at Leu124-Leu125 in rat and mouse PRLs and at Leu126-Leu127 in human, bovine, and ovine PRLs. Dehydration followed by rehydration (D/R) in rats increased the levels of renin and PRL in plasma. Further increase in PRL circulating levels by the dopamine D2 receptor blocker, sulpiride, enabled detection of 14 kDa vasoinhibin in D/R rats. Moreover, the incubation of PRL with plasma from D/R rats generated a 14-kDa vasoinhibin that was prevented by VTP-27999. These findings add renin to the list of PRL-cleaving proteases and introduce vasoinhibin as a putative renin-angiotensin system-mediated mechanism for regulating blood vessel growth and function.</p>","PeriodicalId":11819,"journal":{"name":"Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11833480/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143188652","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}

{"title":"Lack of PTEN in Osteocytes Increases Lipocalin-2 Level and Confers Resistance to High-Fat Diet-Induced Obesity in Mice.","authors":"Saori Kinoshita, Shinsuke Onuma, Natsuko Yamazaki, Yukinao Shibukawa, Keiichi Ozono, Toshimi Michigami, Masanobu Kawai","doi":"10.1210/endocr/bqaf026","DOIUrl":"10.1210/endocr/bqaf026","url":null,"abstract":"<p><p>Osteocytes have been shown to play critical roles in the regulation of a wide range of metabolic processes. However, their role in the regulation of glucose metabolism remains to be determined despite accumulating evidence of the integral role of osteoblasts in this regulation, in which osteoblast-derived lipocalin-2 (LCN2) has been shown to regulate glucose metabolism. Additionally, Lcn2 expression is induced by AKT activation. These results led us to hypothesize that AKT activation in osteocytes regulates glucose metabolism by modulating Lcn2 expression. Therefore, in this study, the Pten gene was deleted in osteocytes to activate AKT signaling by crossing Pten-flox mice with Dmp1-Cre mice (PtenOcy-/- mice). Deleting Pten expression in osteocytes resulted in osteocytic AKT activation, which was associated with decreased adipose tissue mass and enhanced insulin sensitivity. Expression of Pparg2 and lipogenesis-associated genes were decreased in the adipose tissue of PtenOcy-/- mice. Mechanistically, the lack of Phosphatase and Tensin Homolog Deleted from Chromosome 10 (PTEN) in osteocytes increased Lcn2 expression in the femur, which was associated with increased serum and urine LCN2 levels. The urinary LCN2 level was negatively associated with white adipose tissue mass. Additionally, the treatment of primary white adipocytes with recombinant LCN2 reduced the expression of Pparg2 and lipogenesis-related genes. These results suggest that the absence of PTEN in osteocytes increases the expression of Lcn2, which acts in the adipose tissue to suppress lipogenesis, resulting in enhanced insulin sensitivity in these mice. This study provides novel insights into the critical role of AKT activation in osteocytes in regulating glucose metabolism by increasing Lcn2 expression.</p>","PeriodicalId":11819,"journal":{"name":"Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143373590","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}

{"title":"Mice Lacking the Fructose Transporter Glut5 Exhibit Excessive Androgens and Reduced Sperm Motility.","authors":"Aikaterini Kallianioti, Guillaume Bourdon, Jeremy Grandhaye, Claire Chevaleyre, Soulaimane Aboulouard, Christine Péchoux, Sandy Ribes, Eli Sellem, Christelle Ramé, Ingrid Plotton, Isabelle Fournier, Michel Salzet, Joelle Dupont, Véronique Douard, Pascal Froment","doi":"10.1210/endocr/bqaf005","DOIUrl":"10.1210/endocr/bqaf005","url":null,"abstract":"<p><p>Overconsumption of fructose is linked to metabolic diseases, which are often associated with reduced fertility. GLUT5 is the most specific fructose transporter. To investigate its role in the testes, we analyzed the male reproductive phenotype of transgenic male mice deficient in GLUT5 (GLUT5-/- or GLUT5 knockout [KO] mice). Glut5 expression was shown in Leydig cells and germ cells, from primary spermatocytes to spermatozoa. We found reduced intratesticular fructose and pyruvate concentrations in GLUT5-/- mice. These mice exhibited 30% lower litter sizes compared with control mice. Histological analysis of the testes revealed some seminiferous tubules with a \"Sertoli cell-only\" phenotype, although spermatogenesis occurred normally in most tubules. Reduced fertility in GLUT5 KO mice was linked to lower sperm production and impaired sperm quality. Spermatozoa from these mice displayed reduced motility, head abnormalities, and a diminished acrosome reaction, which was associated with reduced cyclic adenosine monophosphate content and impaired phosphorylation of protein kinase A substrates in the acrosome. Unexpectedly, androgen production in GLUT5 KO mice was 3-fold higher than in controls, despite unchanged luteinizing hormone levels. Electron microscopy of Leydig cells revealed a highly developed smooth endoplasmic reticulum, increased lipid droplets, and abnormal mitochondrial structures, suggesting disrupted mitochondrial dynamics. Proteomic analysis identified 155 deregulated proteins in the testicular tissue of GLUT5 KO mice, nearly half of which were associated with sperm motility, germ cell morphology, glycolysis, mitochondrial dynamics, and oxidative stress. In conclusion, the absence of the specific fructose transporter GLUT5 reduced testicular fructose content and led to an asthenozoospermia phenotype accompanied by hyperandrogenism.</p>","PeriodicalId":11819,"journal":{"name":"Endocrinology","volume":"166 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143425203","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}

{"title":"The Hypothalamic Arcuate Nucleus Dopaminergic Neurons: More Than Just Prolactin Secretion.","authors":"Luis Wei Cheng Lim, Christopher Thomas Egnot, Panagiotis Papaioannou, Siew Hoong Yip","doi":"10.1210/endocr/bqaf025","DOIUrl":"10.1210/endocr/bqaf025","url":null,"abstract":"<p><p>The hypothalamic arcuate nucleus dopaminergic (A12) neurons are well known for their central role in regulating prolactin secretion through a sophisticated negative feedback loop. In this canonical pathway, prolactin stimulates A12 neurons to release dopamine, which suppresses further prolactin release from lactotrophs in the anterior pituitary. However, a collective of recent and past evidence strongly implies that the A12 neurons are far more dynamic and multifaceted than previously appreciated. This minireview discusses the developmental trajectory of A12 neurons, from prenatal origins to postnatal maturation, highlighting their diversity and heterogeneity. Beyond their well-characterized role in prolactin regulation, the A12 neurons contribute to a broader array of hypothalamic functions, including autoregulation, metabolism, and growth. By shedding light on these underexplored roles, this review outlines the expansive significance of A12 neurons as more than mere gatekeepers of prolactin secretion, positioning them as versatile players in endocrine and metabolic homeostasis.</p>","PeriodicalId":11819,"journal":{"name":"Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11837187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143370729","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}

{"title":"Interaction of B0AT1 Deficiency and Diet on Metabolic Function and Diabetes Incidence in Male Nonobese Diabetic Mice.","authors":"Matthew F Waters, Viviane Delghingaro-Augusto, Muhammad Shamoon, Kiran Javed, Gaetan Burgio, Jane E Dahlstrom, Stefan Bröer, Christopher J Nolan","doi":"10.1210/endocr/bqaf016","DOIUrl":"10.1210/endocr/bqaf016","url":null,"abstract":"<p><strong>Context: </strong>The obesity epidemic parallels an increasing type 1 diabetes incidence, such that westernized diets, containing high fat, sugar, and/or protein, through inducing nutrient-induced islet β-cell stress, have been proposed as contributing factors. The broad-spectrum neutral amino acid transporter (B0AT1), encoded by Slc6a19, is the major neutral amino acids transporter in intestine and kidney. B0AT1 deficiency in C567Bl/6J mice causes aminoaciduria, lowers insulinemia, and improves glucose tolerance.</p><p><strong>Objective: </strong>We investigated the effects of standard rodent chow (chow), high-fat high-sucrose (HFHS), and high-fat high-protein (HFHP) diets, in addition to B0AT1 deficiency, on the diabetes incidence of male nonobese diabetic (NOD/ShiLtJArc (NOD)) mice.</p><p><strong>Methods: </strong>Male NOD.Slc6a19+/+ and NOD.Slc6a19-/- mice were fed chow, HFHS and HFHP diets from 6 to 24 weeks of age. A separate cohort of male NOD mice were fed the three diets from 6-30 weeks of age. Body weight and fed-state blood glucose and plasma insulin were monitored, and urinary amino-acid profiles, intraperitoneal glucose tolerance, diabetes incidence, pancreatic islet number, insulitis scores and beta-cell mass were measured.</p><p><strong>Results: </strong>The incidence of diabetes and severe glucose intolerance was 3.8% in HFHS-fed, 25.0% in HFHP-fed, and 14.7% in chow-fed mice, with higher pancreatic islet number and lower insulitis scores in HFHS-fed mice. B0AT1 deficiency had no effect on diabetes incidence, but curtailed HFHS-induced excessive weight gain, adipose tissue expansion, and hyperinsulinemia. In HFHP-fed mice, B0AT1 deficiency significantly increased pancreatic β-cell clusters and small islets. Male NOD mice that did not develop autoimmune diabetes were resistant to diet-induced hyperglycemia.</p><p><strong>Conclusion: </strong>Dietary composition does, but B0AT1 deficiency does not, affect autoimmune diabetes incidence in male NOD mice. B0AT1 deficiency, however, reduces diet-induced metabolic dysfunction and in HFHP-fed mice increases pancreatic β-cell clusters and small islets.</p>","PeriodicalId":11819,"journal":{"name":"Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11815506/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143022622","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}

{"title":"Integral Roles of the TGFβ Signaling Pathway in Uterine Function and Disease.","authors":"Anna Catherine Unser, Diana Monsivais","doi":"10.1210/endocr/bqaf032","DOIUrl":"10.1210/endocr/bqaf032","url":null,"abstract":"<p><p>The uterus is a complex organ that requires precise signaling networks to mediate functions necessary for homeostasis and reproductive processes. The transforming growth factor β (TGFβ) superfamily regulates integral signaling pathways throughout many physiological processes, including cell proliferation, differentiation, and development. In this review, we summarize the current understanding of how the TGFβ signaling family controls key uterine functions, with a specific focus on the endometrium. These uterine functions include endometrial receptivity, implantation, decidualization, placentation, remodeling, and regeneration. Improving our understanding of the signaling networks that regulate these processes is integral to identifying, diagnosing, and treating uterine and reproductive diseases such as endometriosis, adenomyosis, recurrent pregnancy loss, and recurrent implantation failure.</p>","PeriodicalId":11819,"journal":{"name":"Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843549/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143413037","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}

{"title":"Integration of Glucagon-Like Peptide 1 Receptor Actions Through the Central Amygdala.","authors":"Miguel Duran, Jennifer R Willis, Nilay Dalvi, Zoe Fokakis, Sonja A Virkus, J Andrew Hardaway","doi":"10.1210/endocr/bqaf019","DOIUrl":"10.1210/endocr/bqaf019","url":null,"abstract":"<p><p>Understanding the detailed mechanism of action of glucagon-like peptide 1 receptor (GLP-1R) agonists on distinct topographic and genetically defined brain circuits is critical for improving the efficacy and mitigating adverse side effects of these compounds. In this mini-review, we propose that the central nucleus of the amygdala (CeA) is a critical mediator of GLP-1R agonist-driven hypophagia. Here, we review the extant literature demonstrating CeA activation via GLP-1R agonists across multiple species and through multiple routes of administration. The precise role of GLP-1Rs within the CeA is unclear but the site-specific GLP-1Rs may mediate distinct behavioral and physiological hallmarks of GLP-1R agonists on food intake. Thus, we propose important novel directions and methods to test the role of the CeA in mediating GLP-1R actions.</p>","PeriodicalId":11819,"journal":{"name":"Endocrinology","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11850305/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143064739","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}