Diabetes最新文献_第6页

Targeting REDD1 in Podocytes: A Promising Strategy for Mitigating Diabetic Kidney Injury. 靶向足细胞中的REDD1：减轻糖尿病肾损伤的一个有希望的策略。

Diabetes Pub Date : 2025-03-01 DOI: 10.2337/dbi24-0042

Ruslan Bohovyk, Alexander Staruschenko

引用次数: 0

Stopping the Intergenerational Risk of Diabetes-From Mechanisms to Interventions: A Report on Research Supported by Pathway to Stop Diabetes. 阻止糖尿病的代际风险--从机制到干预措施。

Diabetes Pub Date : 2025-03-01 DOI: 10.2337/dbi24-0014

Soren Harnois-Leblanc, Marie-France Hivert

{"title":"Stopping the Intergenerational Risk of Diabetes-From Mechanisms to Interventions: A Report on Research Supported by Pathway to Stop Diabetes.","authors":"Soren Harnois-Leblanc, Marie-France Hivert","doi":"10.2337/dbi24-0014","DOIUrl":"10.2337/dbi24-0014","url":null,"abstract":"Embedded in the developmental origins of health and disease (DOHaD) hypothesis, maternal hyperglycemia in utero, from preexisting diabetes or gestational diabetes mellitus, predisposes the offspring to excess adiposity and heightened risk of prediabetes and type 2 diabetes development. This transmission creates a vicious cycle increasing the presence of diabetes from one generation to another, leading to the question: How can we interrupt this vicious cycle? In this article, we present the current state of knowledge on the intergenerational transmission of diabetes from epidemiological life course studies. Then, we discuss the potential mechanisms implicated in the intergenerational transmission of diabetes with a focus on epigenetics. We present novel findings stemming from epigenome-wide association studies of offspring DNA methylation in blood and placental tissues, which shed light on potential molecular mechanisms implicated in the mother-offspring transmission of diabetes. Lastly, with a perspective on how to break the cycle, we consider interventions to prevent offspring obesity and diabetes development before puberty, as a critical period of the intergenerational cycle. This article is part of a series of perspectives that report on research funded by the American Diabetes Association Pathway to Stop Diabetes program.","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":"255-264"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142668002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Imaging Human Pancreatic Endocrinogenesis During Early Prenatal Life. 产前早期人类胰腺内分泌生成成像。

Diabetes Pub Date : 2025-03-01 DOI: 10.2337/db24-0641

Adrian Villalba, Yorick Gitton, Virginie Aiello, Maryne Toupin, Séverine Mazaud-Guittot, Alain Chédotal, Raphaël Scharfmann

{"title":"Imaging Human Pancreatic Endocrinogenesis During Early Prenatal Life.","authors":"Adrian Villalba, Yorick Gitton, Virginie Aiello, Maryne Toupin, Séverine Mazaud-Guittot, Alain Chédotal, Raphaël Scharfmann","doi":"10.2337/db24-0641","DOIUrl":"10.2337/db24-0641","url":null,"abstract":"Murine pancreatic endocrinogenesis has been extensively studied, but human data remain scarce due to limited sample availability. Here, we first built a large collection of human embryonic and fetal pancreases covering the first trimester of pregnancy to explore human endocrinogenesis. Using an experimental pipeline combining in toto staining, tissue clearing, and light-sheet fluorescence microscopy, we show that insulin-, glucagon-, and somatostatin-positive cells appear simultaneously at Carnegie stage (CS) 16. This contrasts with rodents, in which glucagon-positive cells appear first, followed by insulin-positive and, finally, somatostatin-positive cells and highlights interspecies differences. We also detected bihormonal endocrine cells in 7 of 9 human pancreases between CS16 and CS18, which were no longer detected at later stages. We observed that cell distribution within human fetal islets resembles adult mouse islets, with a core of β-cells surrounded by α- and δ-cells, differing from a more complex arrangement in adult human islets. This, in connection with the small size of human fetal islets when compared with adult islets, suggests that adult human islets may form by fusion of preexisting islets, in contrast to the mouse fission model. Together, our study provides a detailed and comprehensive description of the spatiotemporal dynamics of human pancreatic endocrinogenesis.Article highlights: Data on human pancreas development are limited and derived from two-dimensional staining. We overcome this using in toto staining, tissue clearing, and light-sheet imaging. We sought to understand when and where endocrine cells first emerge and how they cluster. First, endocrine cell types appear simultaneously, and early pancreases contain bihormonal cells. There are morphometric differences between fetal and adult islets. We propose a mechanism of adult islet formation by fusion: a new base to reconstitute in vitro islet neogenesis.","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":"368-375"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11842602/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142741705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Response to Comment on Manduchi et al. No Evidence for Persistent Enteroviral B Infection of Pancreatic Islets in Patients With Type 1 Diabetes and Prediabetes From RNA Sequencing Data. Diabetes 2024;73:1697-1704. 对Manduchi等人评论的回应。从RNA测序数据来看，没有证据表明1型糖尿病和前驱糖尿病患者胰岛存在持续的肠病毒B感染。2024年糖尿病;73:1697 - 1704。

Diabetes Pub Date : 2025-03-01 DOI: 10.2337/dbi24-0043

Elisabetta Manduchi, Hélène C Descamps, Jonathan Schug, Tong Da, Deeksha Lahori, Hilana El-Mekkoussi, Michael R Betts, Klaus H Kaestner

引用次数: 0

Type 1 Diabetes Genetic Risk Contributes to Phenotypic Presentation in Monogenic Autoimmune Diabetes. 单基因自身免疫性糖尿病的表型表现与 1 型糖尿病遗传风险有关。

Diabetes Pub Date : 2025-02-01 DOI: 10.2337/db24-0485

Amber M Luckett, Gareth Hawkes, Harry D Green, Elisa De Franco, William A Hagopian, Bart O Roep, Michael N Weedon, Richard A Oram, Matthew B Johnson

引用次数: 0

Diabetes Associated With Maternally Inherited Diabetes and Deafness (MIDD): From Pathogenic Variant to Phenotype. 与母系遗传性糖尿病和耳聋有关的糖尿病（MIDD）：从致病变异到表型。

Diabetes Pub Date : 2025-02-01 DOI: 10.2337/db24-0515

Jean-Pierre Chanoine, David M Thompson, Anna Lehman

引用次数: 0

Identification of Metabolic Patterns in Korean Patients With Type 2 Diabetes and Their Association With Diabetes-Related Complications. 识别韩国 2 型糖尿病患者的代谢模式及其与糖尿病相关并发症的关系。

Diabetes Pub Date : 2025-02-01 DOI: 10.2337/db23-0798

Minji Kang, Kumhee Son, You-Cheol Hwang, Sihoon Lee, Hyunji Sang, Sunyoung Kim, Dong Keon Yon, Sang Youl Rhee, Hyunjung Lim

引用次数: 0

Increased COX6A2 Promotes Pancreatic β-Cell Apoptosis and Is Suppressed in Diabetic GK Rats After Roux-en-Y Gastric Bypass. COX6A2 增加会促进胰腺 β 细胞凋亡，并在糖尿病 GK 大鼠接受 Roux-en-Y 胃旁路术后受到抑制。

Diabetes Pub Date : 2025-02-01 DOI: 10.2337/db24-0301

Xiangchen Kong, Dan Yan, Lianqi Shao, Bingfeng Li, Simian Lv, Yifan Tu, Yingqi Zhang, Xingsheng Shu, Ying Ying, Xiaosong Ma

引用次数: 0

Genetics of C-Peptide and Age at Diagnosis in Type 1 Diabetes. 1 型糖尿病患者 C 肽的遗传与诊断年龄。

Diabetes Pub Date : 2025-02-01 DOI: 10.2337/db24-0340

Delnaz Roshandel, Athina Spiliopoulou, Stuart J McGurnaghan, Andrii Iakovliev, Debby Lipschutz, Caroline Hayward, Shelley B Bull, Barbara E K Klein, Kristine E Lee, Gregory L Kinney, Marian Rewers, Tina Costacou, Rachel G Miller, Paul M McKeigue, Andrew D Paterson, Helen M Colhoun

引用次数: 0

Nicotinic Signaling Stimulates Glucagon Secretion in Mouse and Human Pancreatic α-Cells. 烟碱信号刺激小鼠和人类胰腺α细胞分泌胰高血糖素。

Diabetes Pub Date : 2025-01-01 DOI: 10.2337/db23-0809

Alexander Hamilton, Quan Zhang, Rui Gao, Thomas G Hill, Albert Salehi, Jakob G Knudsen, Matthew B Draper, Paul R V Johnson, Patrik Rorsman, Andrei I Tarasov

{"title":"Nicotinic Signaling Stimulates Glucagon Secretion in Mouse and Human Pancreatic α-Cells.","authors":"Alexander Hamilton, Quan Zhang, Rui Gao, Thomas G Hill, Albert Salehi, Jakob G Knudsen, Matthew B Draper, Paul R V Johnson, Patrik Rorsman, Andrei I Tarasov","doi":"10.2337/db23-0809","DOIUrl":"10.2337/db23-0809","url":null,"abstract":"Smoking is widely regarded as a risk factor for type 2 diabetes because nicotine contributes to insulin resistance by desensitizing the insulin receptors in muscle, liver, or fat. Little is known, however, about the immediate regulation of islet hormonal output by nicotine, an agonist of ionotropic cholinergic receptors. We investigated this by imaging cytosolic Ca2+ dynamics in mouse and human islets using confocal microscopy and measuring glucagon secretion in response to the alkaloid from isolated mouse islets. Nicotine acutely stimulated cytosolic Ca2+ in glucagon-secreting α-cells but not in insulin-secreting β-cells. The 2.8- ± 0.5-fold (P < 0.05) increase in Ca2+, observed in >70% of α-cells, correlated well with a 2.5- ± 0.3-fold stimulation of glucagon secretion. Nicotine-induced elevation of cytosolic Ca2+ relied on influx from the extracellular compartment rather than release of the cation from intracellular depots. Metabotropic cholinergic signaling, monitored at the level of intracellular diacylglycerol, was limited to 69% of α-cells versus 94% of β-cells. We conclude that parasympathetic regulation of pancreatic islet hormone release uses different signaling pathways in β-cells (metabotropic) and α-cells (metabotropic and ionotropic), resulting in the fine-tuning of acetylcholine-induced glucagon exocytosis. Sustained nicotinic stimulation is, therefore, likely to attenuate insulin sensitivity by increasing glucagon release.Article highlights: ","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":"53-64"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11663815/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142549648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0