Review
Biochemistry & Molecular Biology
Yanjiao Zhang, Xinyi Fang, Jiahua Wei, Runyu Miao, Haoran Wu, Kaile Ma, Jiaxing Tian
Summary: PDX-1 plays a crucial role in pancreatic development and the pathogenesis of diabetes. Overexpression of PDX-1 regulates pancreatic development and promotes beta-cell differentiation and insulin secretion. The absence of PDX-1 increases susceptibility to diabetes.
Review
Endocrinology & Metabolism
Zijing Chen, Leah Truskinovsky, Emmanuel S. Tzanakakis
Summary: This review discusses the application of optical methods, including optogenetics, optochemical, and photopharmacological strategies, in pancreatic cells and tissues. It highlights the potential of these methods in regulating insulin secretion and controlling blood sugar levels. Optical methods offer greater precision and controllability compared to traditional drugs, providing new possibilities for addressing pancreatic pathologies.
MOLECULAR METABOLISM
(2022)
Review
Biochemistry & Molecular Biology
Nour Ebrahim, Ksenia Shakirova, Erdem Dashinimaev
Summary: This article reviews the basic functions of PDX1 and its regulation by genetic and epigenetic factors. It also summarizes different variations of differentiation protocols used to obtain beta-cells from alternative cell sources, highlighting the unique position of PDX1 as a potential target in the genetic and cellular treatment of diabetes.
FRONTIERS IN MOLECULAR BIOSCIENCES
(2022)
Article
Biochemistry & Molecular Biology
Fred Levine
Summary: The reduction of beta-cell number and/or function is a common feature in diabetes. The formation of new beta-cells has been a major focus in diabetes research. Various mechanisms, including replication of preexisting beta-cells, neogenesis from ducts, redifferentiation of dedifferentiated beta-cells, and transdifferentiation from other cell types, have been proposed. However, there is still a lack of definitive evidence, especially in humans.
Article
Multidisciplinary Sciences
Romana Bohuslavova, Valeria Fabriciova, Ondrej Smolik, Laura Lebron-Mora, Pavel Abaffy, Sarka Benesova, Daniel Zucha, Lukas Valihrach, Zuzana Berkova, Frantisek Saudek, Gabriela Pavlinkova
Summary: NEUROD1 is a transcription factor that plays an important role in pancreatic development and is crucial for the differentiation of endocrine cells. Its deficiency disrupts endocrine cell identity acquisition and compromises their differentiation and functional properties.
NATURE COMMUNICATIONS
(2023)
Review
Biochemistry & Molecular Biology
Mariana V. Karimova, Inessa G. Gvazava, Ekaterina A. Vorotelyak
Summary: Researchers are developing methods to generate insulin-producing cells from stem cells, providing an unlimited source for diabetes treatment. While current methods can produce beta-like cells, they do not fully mature functionally compared to native beta cells. This paper reviews the development of various protocols, considers advantages, and proposes ways to improve them.
Article
Endocrinology & Metabolism
Nur Shabrina Amirruddin, Wei Xuan Tan, Yaw Sing Tan, Daphne Su-Lyn Gardner, Yong Mong Bee, Chandra Shekhar Verma, Shawn Hoon, Kok Onn Lee, Adrian Kee Keong Teo
Summary: This study examined the effects of heterozygous human INS gene mutations on insulin secretion and ER stress, revealing that mutant INS induces ER stress and defects in insulin processing, leading to decreased insulin secretion. Overexpression of mutant INS resulted in dominant-negative effects on insulin secretory capacity of beta cells after 9 weeks, with compensatory upregulation of genes involved in insulin secretion observed in patient-derived beta-like cells.
Article
Multidisciplinary Sciences
Leon van Gurp, Leon Fodoulian, Daniel Oropeza, Kenichiro Furuyama, Eva Bru-Tari, Anh Nguyet Vu, John S. Kaddis, Ivan Rodriguez, Fabrizio Thorel, Pedro L. Herrera
Summary: The authors used single-cell transcriptomics meta-analysis to construct gene sets that accurately describe the identity of various human islet cells. These gene sets have proven effective in analyzing cell identity changes and their underlying genetic mechanisms, providing reliable tools for cell therapy and diabetes treatment.
NATURE COMMUNICATIONS
(2022)
Article
Endocrinology & Metabolism
Iestyn M. Shapey, Angela Summers, James O'Sullivan, Catherine Fullwood, Neil A. Hanley, John Casey, Shareen Forbes, Miranda Rosenthal, Paul R. V. Johnson, Pratik Choudhary, James Bushnell, James A. M. Shaw, Daniel Neiman, Ruth Shemer, Benjamin Glaser, Yuval Dor, Titus Augustine, Martin K. Rutter, David van Dellen
Summary: In pancreas donors after brain death, the need for insulin treatment is strongly associated with beta-cell death, providing an explanation for the relationship between donor insulin treatment and post-transplant beta-cell dysfunction in recipients.
DIABETES OBESITY & METABOLISM
(2023)
Article
Endocrinology & Metabolism
Einas H. Alkhatib, Jody B. Grundman, Anna M. Adamusiak, Melena D. Bellin, Joel P. Brooks, Kevin S. Buckley, Erin M. Janssen, Maleewan Kitcharoensakkul, Kyle P. Mcnerney, Thea L. Pfeifer, Brooke I. Polk, Brynn E. Marks
Summary: Insulin hypersensitivity reactions are rare but serious complications of T1D treatment, negatively affecting glycemic control and quality of life.
FRONTIERS IN ENDOCRINOLOGY
(2023)
Article
Biology
Claudio Andres Carril Pardo, Laura Massoz, Marie A. Dupont, David Bergemann, Jordane Bourdouxhe, Arnaud Lavergne, Estefania Tarifeno-Saldivia, Christian S. M. Helker, Didier Y. R. Stainier, Bernard Peers, Marianne M. Voz, Isabelle Manfroid
Summary: Studying zebrafish, which have a high regenerative capacity, researchers found that most new insulin cells formed after beta-cell destruction differ from the original beta-cells as they coexpress Somatostatin and Insulin. These abundant and functional bihormonal cells were able to normalize glycemia and contribute to diabetes recovery.
Article
Endocrinology & Metabolism
Satoshi Kawata, Junji Kozawa, Sho Yoneda, Yukari Fujita, Risa Kashiwagi-Takayama, Takekazu Kimura, Yoshiya Hosokawa, Megu Y. Baden, Sae Uno, Rikako Uenaka, Kazuyuki Namai, Yoko Koh, Yoshito Tomimaru, Haruhiko Hirata, Motohide Uemura, Satoshi Nojima, Eiichi Morii, Hidetoshi Eguchi, Akihisa Imagawa, Iichiro Shimomura
Summary: Immune checkpoint inhibitors (ICIs) can cause type 1 diabetes (T1D). The study found that ICI therapy itself could reduce PD-L1 expression on islets, which may be related to beta-cell vulnerability. In addition, the absence of PD-L1 expression on beta-cells, genetic susceptibility, and infiltration of macrophages and T lymphocytes around islets might be responsible for T1D onset.
Review
Medicine, Research & Experimental
Alvin C. Powers
Summary: Type 1 diabetes is a result of autoimmune response requiring lifelong insulin therapy. Although there is considerable heterogeneity in genetics, pathology, and clinical course of T1D, there are still knowledge gaps and opportunities for improving understanding of its pathogenesis. Emerging therapies are being developed to treat or prevent T1D.
JOURNAL OF CLINICAL INVESTIGATION
(2021)
Article
Cell Biology
Han Zhu, Gaowei Wang, Kim-Vy Nguyen-Ngoc, Dongsu Kim, Michael Miller, Georgina Goss, Jenna Kovsky, Austin R. Harrington, Diane C. Saunders, Alexander L. Hopkirk, Rebecca Melton, Alvin C. Powers, Sebastian Preissl, Francesca M. Spagnoli, Kyle J. Gaulton, Maike Sander
Summary: By analyzing the single-cell transcriptomes and accessible chromatin profiles, we compared the differentiation process of pancreatic islet cells derived from human pluripotent stem cells with those from childhood and adult donors. We identified major cell types, defined their regulomes, and described the spatiotemporal gene regulatory relationships between transcription factors. Our study revealed CDX2 as a regulator of enterochromaffin-like cells and provided evidence against the proposed non-pancreatic origin. Additionally, we observed insufficient activation of signal-dependent transcriptional programs during in vitro beta cell maturation and identified sex hormones as drivers of beta cell proliferation in childhood.
DEVELOPMENTAL CELL
(2023)
Article
Biotechnology & Applied Microbiology
Takashi Taguchi, Wei Duan, Wendy Wolfson, Brandy Duhon, Emily G. Halphen, Mandi J. Lopez
Summary: This study explores the generation of functional insulin producing cell clusters from feline adipose-derived multipotent stromal cells, offering a new approach for treating feline diabetes mellitus. Results show that cluster functionality is enhanced through dynamic culture.
FRONTIERS IN BIOENGINEERING AND BIOTECHNOLOGY
(2022)
Article
Cell Biology
Karina A. Pena, Sofya Savransky, Breanna Lewis
Summary: Compartmentalization of GPCR signaling is an emerging topic that emphasizes the importance of spatial bias in signaling for physiological relevance. PTH1R was the first GPCR discovered to signal via cAMP from endosomes, challenging the conventional model of GPCR signaling. The location of cAMP generation determines the physiological outcomes of GPCR signaling.
MOLECULAR AND CELLULAR ENDOCRINOLOGY
(2024)
Article
Cell Biology
Cheng-Xu Ma, Xiao-Ni Ma, Jin-Jin Liu, Cong-Hui Guan, Ying-Dong Li, Nan Zhao, Didac Mauricio, Song-Bo Fu
Summary: The downregulation of primary cilia (PCs) due to BRAFV600E mutation contributes to the aggressiveness and lymph node metastasis of Papillary Thyroid Cancer (PTC).
MOLECULAR AND CELLULAR ENDOCRINOLOGY
(2024)
Article
Cell Biology
Kejun Wu, Cuihua Huang, Wenrong Zheng, Yubin Wu, Qintao Huang, Menghua Lin, Ruonan Gao, Liqin Qi, Guanlian He, Xiaoying Liu, Xiaohong Liu, Linxi Wang, Zhou Chen, Libin Liu
Summary: Recurrent non-severe hypoglycemia in patients with diabetes is associated with cognitive impairment. This study found that this condition is associated with reduced mitophagy in the hippocampus, leading to mitochondrial dysfunction and neurological impairment.
MOLECULAR AND CELLULAR ENDOCRINOLOGY
(2024)
Article
Cell Biology
Yifei Lv, Yizhou Huang, Huiyu Fan, Yunxiu Zhao, Linjuan Ma, Yibing Lan, Chunming Li, Peiqiong Chen, Zheng Lou, Jianhong Zhou
Summary: Before menopause, females have a lower incidence of cardiovascular disease than age-matched males, possibly due to the protective effects of sex hormones. 17 beta-E2 inhibits THBS1 expression, preventing cell senescence and apoptosis, and counteracts oxidative stress by suppressing the TGF-beta/Smad signaling pathway.
MOLECULAR AND CELLULAR ENDOCRINOLOGY
(2024)
Article
Cell Biology
Ana C. L. Camargo, Flavia B. Constantino, Sergio A. A. Santos, Ketlin T. Colombelli, Luiz M. F. Portela, Matheus N. Fioretto, Luisa A. Barata, Guilherme T. Valente, Carlos S. Moreno, Luis A. Justulin
Summary: This study examined the effects of maternal malnutrition on the transcriptomic landscape of the ventral prostate in rats. It found that changes in molecular pathways related to cellular development and tissue morphogenesis were associated with maternal malnutrition. The Abcg1 gene was found to be deregulated in both malnourished rats and prostate cancer models and patients.
MOLECULAR AND CELLULAR ENDOCRINOLOGY
(2024)
Article
Cell Biology
Sandra Romero-Cordoba, Mayel Chirinos, Nancy Noyola-Martinez, Nayeli Torres-Ramirez, Mitzi Garcia-Olivares, Juan Pablo Aragon-Hernandez, Ixchel Ramirez-Camacho, Rosa Zuniga, Fernando Larrea, Ali Halhali, David Barrera
Summary: This study analyzed the effects of calcitriol, TGF-131, and their combination on human trophoblast cells. The results showed that the combination treatment modified the transcriptional landscape and mainly affected the storage, activity, and metabolism of lipids, which may have an impact on placental development.
MOLECULAR AND CELLULAR ENDOCRINOLOGY
(2024)
Article
Cell Biology
Traver J. Wright, Richard B. Pyles, Melinda Sheffield-Moore, Rachel R. Deer, Kathleen M. Randolph, Kristen A. Mcgovern, Christopher P. Danesi, Charles R. Gilkison, Weston W. Ward, Jayson A. Vargas, Peyton A. Armstrong, Sarah E. Lindsay, Mohammed F. Zaidan, Justin Seashore, Tamara L. Wexler, Brent E. Masel, Randall J. Urban
Summary: This study investigates the persistent neurologic symptoms in COVID-19 patients after recovery and explores the association between these symptoms and disrupted growth hormone secretion and gastrointestinal discomfort.
MOLECULAR AND CELLULAR ENDOCRINOLOGY
(2024)
Article
Cell Biology
Li-Li Chen, Ya-Qin Li, Zhi-Hui Kang, Xuan Zhang, Su-Yan Gu, Na Wang, Xue-Yan Shen
Summary: Defects in trophoblastic EMT caused by dysregulation of circTNRC18's interaction with LIN28A play a vital role in the development of preeclampsia. LIN28A overexpression suppresses circTNRC18-mediated inhibition of trophoblast migration, invasion, and EMT, while LIN28A knockdown promotes them. Furthermore, circTNRC18 regulates the intracellular distribution of LIN28A and the expression of insulin-like growth factor II, affecting cell migration and invasion. Targeting the circTNRC18-LIN28A regulatory axis may provide a novel treatment approach for preeclampsia.
MOLECULAR AND CELLULAR ENDOCRINOLOGY
(2024)
