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Development of a 3D subcutaneous construct containing insulin-producing beta cells using bioprinting

Bio-Design and Manufacturing 2022年第2期5卷 265-276页

作者： Chi B.Ahn Ji-Hyun Lee Joo H.Kim Tae H.Kim Hee-Sook Jun Kuk H.Son Jin W.Lee Department of Molecular Medicine College of MedicineGachon University155Gaetbeol-roYeonsu-kuIncheonRepublic of Korea Department of Health Sciences and Technology GAIHSTGachon University155Gaetbeol-roYeonsu-kuIncheonRepublic of Korea College of Pharmacy Gachon University191Hambangmoe-roYeonsu-kuIncheonRepublic of Korea Department Thoracic and Cardiovascular Surgery Gachon University Gil Medical CenterCollege of MedicineGachon University21Namdong-daero 774 beon-gilNamdong-guIncheonRepublic of Korea

Type 1 diabetes is caused by insulin deficiency due to the loss of beta cells in the islets of *** severe cases,islet transplantation into the portal vein is ***,due to the loss of transplanted islets and the failure of islet function,the 5-year insulin independence rate of these patients isbeta-cell(mouse insulinoma-6:MIN-6)-encapsulated alginate bioink and poly(caprolactone)biodegradable polymer.A glucose response assay revealed that the bioprinted constructs proliferated and released insulin normally during the 4-week in vitro *** MIN-6 generated clusters with a diameter of 100-200μm,similar to the original pancreatic islets in the *** an in vivo study using type 1 diabetes mice,animals implanted with bioprinted constructs showed three times higher insulin secretion and controlled glucose levels at 8 weeks after *** the implanted,bioprinted constructs had a positive effect on insulin secretion in the experimental animals,the survival rate of the implanted group(75%)was three times higher than that of the non-implanted group(25%).The results suggest that the proposed,3 D-bioprinted,subcutaneous construct can be a better alternative to portal vein islet transplantation.

关键词： 3D bioprinting Subcutaneous construct Type 1 diabetes Insulin beta cells

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Maternal obesity as a risk factor for developing diabetes in offspring:An epigenetic point of view

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World Journal of Diabetes 2021年第4期12卷 366-382页

作者： Simon Lecoutre Salwan Maqdasy Christophe Breton Department of Medicine(H7) Karolinska InstitutetStockholm 141-86Sweden University of Lille EA4489Maternal Malnutrition and Programming of Metabolic DiseasesLille 59000France Clermont-Ferrand CHU Department of EndocrinologyDiabetology and Metabolic DiseasesClermont-Ferrand 63003France

According to the developmental origin of health and disease concept,the risk of many age-related diseases is not only determined by genetic and adult lifestyle factors but also by factors acting during early *** particular,maternal obesity and neonatal accelerated growth predispose offspring to overweight and type 2 diabetes(T2 D) in *** concept mainly relies on the developmental plasticity of adipose tissue and pancreatic β-cell programming in response to suboptimal milieu during the perinatal *** changes result in unhealthy hypertrophic adipocytes with decreased capacity to store fat,lowgrade inflammation and loss of insulin-producing pancreatic β-*** the past years,many efforts have been made to understand how maternal obesity induces long-lasting adipose tissue and pancreatic β-cell dysfunction in offspring and what are the molecular basis of the transgenerational inheritance of T2 *** particular,rodent studies have shed light on the role of epigenetic mechanisms in linking maternal nutritional manipulations to the risk for T2 D in *** this review,we discuss epigenetic adipocyte and β-cell remodeling during development in the progeny of obese mothers and the persistence of these marks as a basis of obesity and T2 D predisposition.

关键词： Development Epigenome Obesity Type 2 diabetes Adipose tissue beta cells

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Role of nucleic acid sensing in the pathogenesis of type 1 diabetes

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World Journal of Diabetes 2021年第10期12卷 1655-1673页

作者： Darshan Badal Naresh Sachdeva Deep Maheshwari Preetam Basak Department of Pediatrics Post Graduate Institute of Medical Education and ResearchChandigarh 160012India Department of Endocrinology Post Graduate Institute of Medical Education and ResearchChandigarh 160012India

During infections,nucleic acids of pathogens are also engaged in recognition via several exogenous and cytosolic pattern recognition receptors,such as the toll-like receptors,retinoic acid inducible gene-I-like receptors,and nucleotide-binding and oligomerization domain-like *** binding of the pathogen-derived nucleic acids to their corresponding sensors initiates certain downstream signaling cascades culminating in the release of type-I interferons(IFNs),especially IFN-αand other cytokines to induce proinflammatory responses towards invading pathogens leading to their clearance from the *** these sensors are hardwired to recognize pathogen associated molecular patterns,like viral and bacterial nucleic acids,under unusual physiological conditions,such as excessive cellular stress and increased apoptosis,endogenous self-nucleic acids like DNA,RNA,and mitochondrial DNA are also *** presence of these self-nucleic acids in extranuclear compartments or extracellular spaces or their association with certain proteins sometimes leads to the failure of discriminating mechanisms of nucleic acid sensors leading to proinflammatory responses as seen in autoimmune disorders,like systemic lupus erythematosus,psoriasis and to some extent in type 1 diabetes(T1D).This review discusses the involvement of various nucleic acid sensors in autoimmunity and discusses how aberrant recognition of self-nucleic acids by their sensors activates the innate immune responses during the pathogenesis of T1D.

关键词： Nucleic acid sensing Type 1 diabetes Pattern recognition receptors Nucleic acid receptors Type 1 interferon beta cells

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Host Factors Alter Effects of Angiopoietin-Like Protein 8 on Glucose Homeostasis in Diabetic Mice

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Journal of Diabetes Mellitus 2016年第4期6卷 277-290页

作者： Sichen Liu Emily M. Smith Timothy H. King Lindsey Glenn Michelle Trevino So Hyun Park Yui Machida Ciriaco Villaflor Wojciech Grzesik Margaret A. Morris Yumi Imai Jerry L. Nadler Eastern Virginia Medical School Department of Internal Medicine Strelitz Diabetes Center Norfolk VA USA Department of Internal Medicine Fraternal Order of Eagles Diabetes Research Center The University of Iowa Carver College of Medicine Iowa City IA USA

Recovery of functional beta cell mass offers a biological cure for type 1 diabetes. However, beta cell mass is difficult to regain once lost since the proliferation rate of beta cells after youth is very low. Angiopoietin like-protein 8 (ANGPTL8), a peptide that has a role in the regulation of lipoprotein lipase activity, was reported to increase beta cell proliferation in mice in 2013. Subsequent studies of human ANGPTL8 for short term (3 to 8 days) in non-diabetic mice showed little or no increase in beta cell proliferation. Here, we examined the effect of ANGPTL8 on glucose homeostasis in models that have not been examined previously. We expressed mouse ANGPTL8 using adenovirus in 2 mouse models of diabetes (streptozotocin and Non-Obese Diabetic (NOD) mice) over 2 weeks. Also, we tested ANGPTL8 in NOD mice deficient in leukocyte 12-lipoxygenase (12LO), an enzyme that contributes to insulitis and loss of beta cell function in NOD, in an effort to determine whether 12LO deficiency alters the response to ANGPTL8. Adenovirus-mediated expression of ANGPTL8 lowered blood glucose levels in streptozotocin treated mice without an increase in beta cell proliferation or serum insulin concentration. While ANGPTL8 did not reverse hyperglycemia in overtly hyperglycemic NOD mice or alter glucose homeostasis of non-diabetic NOD mice, ANGPTL8 reduced blood glucose levels in 12LOKO NOD mice. However, the lower glucose levels in 12LOKO NOD were not associated with higher serum insulin levels or beta cell proliferation. In summary, while mouse ANGPTL8 does not increase beta cell proliferation in NOD mice or streptozotocin treated mice in agreement with studies in non-diabetic mice, it lowers blood glucose levels in multiple low-dose streptozotocin induced diabetes and 12LO deficiency indicating that host factors influence the impact of ANGPTL8 on glucose homeostasis.

关键词： Angiopoietin-Like Protein 8 Type 1 Diabetes NOD 12-Lipoxygenase beta cells Glucose Homeostasis

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