Diabetes & Metabolism Journal

Reviews

Basic Research
Heterogeneity of Islet Cells during Embryogenesis and Differentiation: Shugo Sasaki, Takeshi Miyatsuka; Diabetes Metab J. 2023;47(2):173-184. Published online January 12, 2023; DOI: https://doi.org/10.4093/dmj.2022.0324

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Diabetes is caused by insufficient insulin secretion due to β-cell dysfunction and/or β-cell loss. Therefore, the restoration of functional β-cells by the induction of β-cell differentiation from embryonic stem (ES) and induced-pluripotent stem (iPS) cells, or from somatic non-β-cells, may be a promising curative therapy. To establish an efficient and feasible method for generating functional insulin-producing cells, comprehensive knowledge of pancreas development and β-cell differentiation, including the mechanisms driving cell fate decisions and endocrine cell maturation is crucial. Recent advances in single-cell RNA sequencing (scRNA-seq) technologies have opened a new era in pancreas development and diabetes research, leading to clarification of the detailed transcriptomes of individual insulin-producing cells. Such extensive high-resolution data enables the inference of developmental trajectories during cell transitions and gene regulatory networks. Additionally, advancements in stem cell research have not only enabled their immediate clinical application, but also has made it possible to observe the genetic dynamics of human cell development and maturation in a dish. In this review, we provide an overview of the heterogeneity of islet cells during embryogenesis and differentiation as demonstrated by scRNA-seq studies on the developing and adult pancreata, with implications for the future application of regenerative medicine for diabetes.

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Newly discovered knowledge pertaining to glucagon and its clinical applications
Dan Kawamori, Shugo Sasaki
Journal of Diabetes Investigation.2023; 14(7): 829. CrossRef

Altered Transendothelial Transport of Hormones as a Contributor to Diabetes: Nanyoung Yoon, Thanh Q. Dang, Helen Chasiotis, Scott P. Kelly, Gary Sweeney; Diabetes Metab J. 2014;38(2):92-99. Published online April 18, 2014; DOI: https://doi.org/10.4093/dmj.2014.38.2.92

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The vascular endothelium is a dynamic structure responsible for the separation and regulated movement of biological material between circulation and interstitial fluid. Hormones and nutrients can move across the endothelium either via a transcellular or paracellular route. Transcellular endothelial transport is well understood and broadly acknowledged to play an important role in the normal and abnormal physiology of endothelial function. However, less is known about the role of the paracellular route. Although the concept of endothelial dysfunction in diabetes is now widely accepted, we suggest that alterations in paracellular transport should be studied in greater detail and incorporated into this model. In this review we provide an overview of endothelial paracellular permeability and discuss its potential importance in contributing to the development of diabetes and associated complications. Accordingly, we also contend that if better understood, altered endothelial paracellular permeability could be considered as a potential therapeutic target for diabetes.

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Use of 2-dimensional cell monolayers and 3-dimensional microvascular networks on microfluidic devices shows that iron increases transendothelial adiponectin flux via inducing ROS production
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Tracking adiponectin biodistribution via fluorescence molecular tomography indicates increased vascular permeability after streptozotocin-induced diabetes
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Transendothelial movement of adiponectin is restricted by glucocorticoids
Thanh Q Dang, Nanyoung Yoon, Helen Chasiotis, Emily C Dunford, Qilong Feng, Pingnian He, Michael C Riddell, Scott P Kelly, Gary Sweeney
Journal of Endocrinology.2017; 234(2): 101. CrossRef
Insulin access to skeletal muscle is impaired during the early stages of diet‐induced obesity
Josiane L. Broussard, Ana V.B. Castro, Malini Iyer, Rebecca L. Paszkiewicz, Isaac Asare Bediako, Lidia S. Szczepaniak, Edward W. Szczepaniak, Richard N. Bergman, Cathryn M. Kolka
Obesity.2016; 24(9): 1922. CrossRef
Temporal and Molecular Analyses of Cardiac Extracellular Matrix Remodeling following Pressure Overload in Adiponectin Deficient Mice
Keith Dadson, Subat Turdi, Stellar Boo, Boris Hinz, Gary Sweeney, Nikolaos Frangogiannis
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The Hijacking of Cellular Signaling and the Diabetes Epidemic: Mechanisms of Environmental Disruption of Insulin Action and Glucose Homeostasis: Robert M. Sargis; Diabetes Metab J. 2014;38(1):13-24. Published online February 19, 2014; DOI: https://doi.org/10.4093/dmj.2014.38.1.13

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The burgeoning epidemic of metabolic disease causes significant societal and individual morbidity and threatens the stability of health care systems around the globe. Efforts to understand the factors that contribute to metabolic derangements are critical for reversing these troubling trends. While excess caloric consumption and physical inactivity superimposed on a susceptible genetic background are central drivers of this crisis, these factors alone fail to fully account for the magnitude and rapidity with which metabolic diseases have increased in prevalence worldwide. Recent epidemiological evidence implicates endocrine disrupting chemicals in the pathogenesis of metabolic diseases. These compounds represent a diverse array of chemicals to which humans are exposed via multiple routes in adulthood and during development. Furthermore, a growing ensemble of animal- and cell-based studies provides preclinical evidence supporting the hypothesis that environmental contaminants contribute to the development of metabolic diseases, including diabetes. Herein are reviewed studies linking specific endocrine disruptors to impairments in glucose homeostasis as well as tying these compounds to disturbances in insulin secretion and impairments in insulin signal transduction. While the data remains somewhat incomplete, the current body of evidence supports the hypothesis that our chemically polluted environment may play a contributing role in the current metabolic crisis.

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Arsenic metabolism, diabetes prevalence, and insulin resistance among Mexican Americans: A mendelian randomization approach
Margaret C. Weiss, Yu-Hsuan Shih, Molly Scannell Bryan, Brian P. Jackson, David Aguilar, Eric L. Brown, Goo Jun, Craig L. Hanis, Maria Argos, Robert M. Sargis
Environmental Advances.2023; 12: 100361. CrossRef
Transportation-related Environmental Mixtures and Diabetes Prevalence and Control in Urban/Metropolitan Counties in the United States
Margaret C Weiss, Sneha Adusumilli, Jyotsna S Jagai, Robert M Sargis
Journal of the Endocrine Society.2023;[Epub] CrossRef
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Saeed Karami Mehrian, Nasser Karimi, Fatemeh Rahmani
Scientific Reports.2023;[Epub] CrossRef
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Perfluorooctanoic acid promotes pancreatic β cell dysfunction and apoptosis through ER stress and the ATF4/CHOP/TRIB3 pathway
Xiaowei He, Dan Wu, Yanan Xu, Yaqin Zhang, Yue Sun, Xiaoai Chang, Yunxia Zhu, Wei Tang
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Increased gut serotonin production in response to bisphenol A structural analogs may contribute to their obesogenic effects
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American Journal of Physiology-Endocrinology and Metabolism.2022; 323(1): E80. CrossRef
Combinatorial pathway disruption is a powerful approach to delineate metabolic impacts of endocrine disruptors
Kévin Bernal, Charbel Touma, Chedi Erradhouani, Talía Boronat‐Belda, Lucas Gaillard, Sara Al Kassir, Hélène Le Mentec, Corinne Martin‐Chouly, Normand Podechard, Dominique Lagadic‐Gossmann, Sophie Langouet, François Brion, Anja Knoll‐Gellida, Patrick J. Ba
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Original Article

Transdifferentiation of Enteroendocrine K-cells into Insulin-expressing Cells.: Esder Lee, Jun Mo Yu, Min Kyung Lee, Gyeong Ryul Ryu, Seung Hyun Ko, Yu Bae Ahn, Sung Dae Moon, Ki Ho Song; Korean Diabetes J. 2009;33(6):475-484. Published online December 1, 2009; DOI: https://doi.org/10.4093/kdj.2009.33.6.475

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Abstract PDF

BACKGROUND
Despite a recent breakthough in human islet transplantation for treating type 1 diabetes mellitus, the limited availability of donor pancreases remains a major obstacle. Endocrine cells within the gut epithelium (enteroendocrine cells) and pancreatic beta cells share similar pathways of differentiation during embryonic development. In particular, K-cells that secrete glucose-dependent insulinotropic polypeptide (GIP) have been shown to express many of the key proteins found in beta cells. Therefore, we hypothesize that K-cells can be transdifferentiated into beta cells because both cells have remarkable similarities in their embryonic development and cellular phenotypes. METHODS: K-cells were purified from heterogeneous STC-1 cells originating from an endocrine tumor of a mouse intestine. In addition, a K-cell subclone expressing stable Nkx6.1, called "Kn4-cells," was successfully obtained. In vitro differentiation of K-cells or Kn4-cells into beta cells was completed after exendin-4 treatment and serum deprivation. The expressions of insulin mRNA and protein were examined by RT-PCR and immunocytochemistry. The interacellular insulin content was also measured. RESULTS: K-cells were found to express glucokinase and GIP as assessed by RT-PCR and Western blot analysis. RT-PCR showed that K-cells also expressed Pdx-1, NeuroD1/Beta2, and MafA, but not Nkx6.1. After exendin-4 treatment and serum deprivation, insulin mRNA and insulin or C-peptide were clearly detected in Kn4-cells. The intracellular insulin content was also increased significantly in these cells. CONCLUSION: K-cells are an attractive potential source of insulin-producing cells for treatment of type 1 diabetes mellitus. However, more experiments are necessary to optimize a strategy for converting K-cells into beta cells.

Citations

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Reprogramming of enteroendocrine K cells to pancreatic β-cells through the combined expression of Nkx6.1 and Neurogenin3, and reaggregation in suspension culture
Esder Lee, Gyeong Ryul Ryu, Sung-Dae Moon, Seung-Hyun Ko, Yu-Bae Ahn, Ki-Ho Song
Biochemical and Biophysical Research Communications.2014; 443(3): 1021. CrossRef

Review

Stimulation of Glucagon Like Peptide-1 Secretion in Enteroendocrine L cells.: Byung Joon Kim; Korean Diabetes J. 2009;33(6):458-463. Published online December 1, 2009; DOI: https://doi.org/10.4093/kdj.2009.33.6.458

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Abstract PDF

GLP-1 (glucagon like peptide-1) is new anti-diabetic drug with a number of beneficial effects. It stimulates glucose dependant insulin secretion and restoration of beta cell mass through enhancement of islet mass. However, it is easily inactivated after being secreted from enteroendocrine L cells. Recent trial to increased GLP-1 is to directly stimulate L cells through its receptor located in the surface of L cell. Taste receptor in the apical surface of L cell is activated by various tastants contained in the food. Tongue perceives taste sense through the heterotrimeric G-protein (alpha-gustducin) and its downstream signaling cascades. Same taste receptors are also expressed in enteroendocrine cells. In duodenal L cell, alpha-gustducin was detected by immunofluorescence stainig at the luminal projections of enteroendocrine cells. And several other taste signaling elements were also found in L cells. Ingestion of sweet or bitter compounds revealed stimulation of GLP-1 secretion and the regulation of plasma insulin and glucose. In this review, I will briefly introduce the possibilities to stimulate GLP-1 secretion though the membrane receptor in enteroendocrine cell. And it will be the good candidate to develop the treatment modality for obesity, diabetes and abnormal gut motility.

Citations

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Repression of sterol regulatory element-binding protein 1-c is involved in the protective effects of exendin-4 in pancreatic β-cell line
Seok-Woo Hong, Jinmi Lee, Se Eun Park, Eun-Jung Rhee, Cheol-Young Park, Ki-Won Oh, Sung-Woo Park, Won-Young Lee
Molecular and Cellular Endocrinology.2012; 362(1-2): 242. CrossRef
Exendin-4 Protects Oxidative Stress-Induced β-Cell Apoptosis through Reduced JNK and GSK3β Activity
Ju-Young Kim, Dong-Mee Lim, Chan Il Moon, Kyung-Jin Jo, Seong-Kyu Lee, Haing-Woon Baik, Ki-Ho Lee, Kang-Woo Lee, Keun-Young Park, Byung-Joon Kim
Journal of Korean Medical Science.2010; 25(11): 1626. CrossRef

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