Статті в журналах: "Beta cell preservation"

1

Sperling, Mark A. "Preservation of beta cell function." Pediatric Diabetes 11, no. 3 (August 25, 2009): 152–53. http://dx.doi.org/10.1111/j.1399-5448.2010.00675.x.

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2

Bach, Jean-François, Christian Boitard, and Claude Carnaud. "Preservation of beta cell mass." Journal of Autoimmunity 3, no. 1 (February 1990): 45. http://dx.doi.org/10.1016/0896-8411(90)90010-p.

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3

Korbutt, Gregory S., and Daniel G. Pipeleers. "Cold-Preservation of Pancreatic Beta Cells." Cell Transplantation 3, no. 4 (July 1994): 291–97. http://dx.doi.org/10.1177/096368979400300405.

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Clinical islet transplantation requires graft preservation conditions with a minimal loss in viable beta cells. The present study examines whether rat pancreatic beta cells survive a 96 h storage period at 4°C. In a single cell viability assay, less than 20% viable cells were counted after 48 h storage in physiological HAM's F10 medium; cell survival was better in the high potassium solutions UW or Collins and further improved by supplementing Collins with albumin and benzamidine (CAB - 77% viability after 96 h). Suspended beta cell aggregates were also well preserved during 4 days in CAB-4°C as judged from DNA recovery and electron microscopy. After cold-storage in CAB, beta cells exhibited a higher insulin content than after culture in HAM's F10 at 20° or 37°C, but their capacity for subsequent insulin synthesis and release was comparable. When isolated islets were stored in CAB-4°C for 96 h, they yielded slightly higher numbers of dissociated cells than after culture in HAM's F10 at 20°C. Implantation of cold stored islets from 2 donor pancreata corrected hyperglycemia in streptozotocin-diabetic rats. It is concluded that rat beta cells can be stored in a supplemented Collins solution for at least 4 days at 4°C, with preservation of initial cell number, hormone content and glucose responsiveness. During short-term periods, this new storage condition is at least equivalent to cultures at 20° or 37°C. Further studies are needed to assess any advantage for long-term storage of islet cell grafts.

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4

Mazza, Angela D., Richard E. Pratley, and Steven R. Smith. "Beta-Cell Preservation…Is Weight Loss the Answer?" Review of Diabetic Studies 8, no. 4 (2011): 446–53. http://dx.doi.org/10.1900/rds.2011.8.446.

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5

Boughton, Charlotte K., Neil Munro, and Martin Whyte. "Targeting beta-cell preservation in the management of type 2 diabetes." British Journal of Diabetes 17, no. 4 (December 15, 2017): 134–44. http://dx.doi.org/10.15277/bjd.2017.148.

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Type 2 diabetes (T2D) is widely considered a chronic and progressive disease without cure. As beta-cell function progressively declines over time, blood glucose rises. Current management of T2D involves incremental introduction of dietary and drug therapies to achieve normoglycaemia. However, recent studies have demonstrated remission of T2D following bariatric surgery, very low calorie diet or intensive insulin therapy, raising the possibility that the declining beta-cell function in T2D may be arrested or even reversed. The point at which such interventions are introduced in the course of T2D is key for clinical benefit. Future treatment strategies should be revised to target early beta-cell preservation and thus disease remission. This article reviews the pathogenesis of beta-cell dysfunction and evidence for the clinical benefit of preserving beta-cell function in T2D, and discusses the evidence for beta-cell preservation of current glucose-lowering therapies with particular reference to their effect when initiated at the time of diagnosis of T2D.

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6

Savari, O., K. Golab, L. Schenck, R. Grose, M. Tibudan, S. Ramachandran, Z. Tekin, et al. "Preservation of Beta Cell Function Following Pancreatic Islet Autotransplantation." Transplantation 98 (July 2014): 685–86. http://dx.doi.org/10.1097/00007890-201407151-02331.

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7

Nyalakonda, Kavita, Tarang Sharma, and Faramarz Ismail-Beigi. "Preservation of Beta-Cell Function in Type 2 Diabetes." Endocrine Practice 16, no. 6 (November 2010): 1038–55. http://dx.doi.org/10.4158/ep10112.ra.

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8

Lam, Tony K. T., and David Z. I. Cherney. "Beta cell preservation in patients with type 1 diabetes." Nature Medicine 24, no. 8 (August 2018): 1089–90. http://dx.doi.org/10.1038/s41591-018-0144-1.

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9

Couri, Carlos Eduardo Barra, and Júlio César Voltarelli. "Potencial role of stem cell therapy in type 1 diabetes mellitus." Arquivos Brasileiros de Endocrinologia & Metabologia 52, no. 2 (March 2008): 407–15. http://dx.doi.org/10.1590/s0004-27302008000200029.

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Type 1 diabetes mellitus is the result of the autoimmune response against pancreatic beta-cell(s). At the time of clinical diagnosis near 70% of beta-cell mass is been destroyed as a consequence of the auto-destruction that begins months or even years before the clinical diagnosis. Although marked reduction of chronic complications was seen after development and progression of insulin therapy over the years for type 1 diabetic population, associated risks of chronic end-organ damage and hypoglycemia still remain. Besides tight glucose control, beta-cell mass preservation and/or increase are known to be other important targets in management of type 1 diabetes as long as it reduces chronic microvascular complications in the eyes, kidneys and nerves. Moreover, the larger the beta-cell mass, the lower the incidence of hypoglycemic events. In this article, we discuss some insights about beta-cell regeneration, the importance of regulation of the autoimmune process and what is being employed in human type 1 diabetes in regard to stem cell repertoire to promote regeneration and/or preservation of beta-cell mass.

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10

Pescovitz, Mark D., Carla J. Greenbaum, Heidi Krause-Steinrauf, Dorothy J. Becker, Stephen E. Gitelman, Robin Goland, Peter A. Gottlieb, et al. "Rituximab, B-Lymphocyte Depletion, and Preservation of Beta-Cell Function." New England Journal of Medicine 361, no. 22 (November 26, 2009): 2143–52. http://dx.doi.org/10.1056/nejmoa0904452.

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11

Nagaoka, Hideo, Ryuichi Innami, Masazumi Watanabe, Motoaki Satoh, Fumio Murayama, and Naoya Funakoshi. "Preservation of pancreatic beta cell function with pulsatile cardiopulmonary bypass." Annals of Thoracic Surgery 48, no. 6 (December 1989): 798–802. http://dx.doi.org/10.1016/0003-4975(89)90673-5.

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12

Buchanan, Thomas A. "Pancreatic beta-cell loss and preservation in type 2 diabetes." Clinical Therapeutics 25 (January 2003): B32—B46. http://dx.doi.org/10.1016/s0149-2918(03)80241-2.

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13

Stockman, J. A. "Rituximab, B-Lymphocyte Depletion, and Preservation of Beta-Cell Function." Yearbook of Pediatrics 2011 (January 2011): 128–30. http://dx.doi.org/10.1016/s0084-3954(10)79725-6.

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14

Inaishi, Jun, and Yoshifumi Saisho. "Beta-Cell Mass in Obesity and Type 2 Diabetes, and Its Relation to Pancreas Fat: A Mini-Review." Nutrients 12, no. 12 (December 16, 2020): 3846. http://dx.doi.org/10.3390/nu12123846.

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Type 2 diabetes (T2DM) is characterized by insulin resistance and beta-cell dysfunction. Although insulin resistance is assumed to be a main pathophysiological feature of the development of T2DM, recent studies have revealed that a deficit of functional beta-cell mass is an essential factor for the pathophysiology of T2DM. Pancreatic fat contents increase with obesity and are suggested to cause beta-cell dysfunction. Since the beta-cell dysfunction induced by obesity or progressive decline with disease duration results in a worsening glycemic control, and treatment failure, preserving beta-cell mass is an important treatment strategy for T2DM. In this mini-review, we summarize the current knowledge on beta-cell mass, beta-cell function, and pancreas fat in obesity and T2DM, and we discuss treatment strategies for T2DM in relation to beta-cell preservation.

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15

Ritzel, Robert, A. "Therapeutic approaches based on beta-cell mass preservation and/or regeneration." Frontiers in Bioscience Volume, no. 14 (2009): 1835. http://dx.doi.org/10.2741/3345.

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16

Retnakaran, Ravi. "JOE DOUPE LECTURE: Emerging Strategies for the Preservation of Pancreatic Beta-cell Function in early Type 2 Diabetes." Clinical & Investigative Medicine 37, no. 6 (December 1, 2014): 414. http://dx.doi.org/10.25011/cim.v37i6.22247.

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A fundamental problem in the clinical management of type 2 diabetes is the inability to prevent the ongoing deterioration of pancreatic beta-cell function over time that underlies the chronic progressive nature of this condition. Importantly, beta-cell dysfunction has both reversible and irreversible components. Furthermore, the amelioration of reversible beta-cell dysfunction through the early institution of short-term insulin-based therapy has emerged as a strategy that can yield temporary remission of type 2 diabetes. In this context, we have forwarded a novel therapeutic paradigm consisting of initial induction therapy to improve beta-cell function early in the course of diabetes followed by maintenance therapy aimed at preserving this beneficial beta-cell effect. Ultimately, this approach may yield an optimized therapeutic strategy for the durable preservation of beta-cell function and consequent modification of the natural history of type 2 diabetes.

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17

Pozzilli, Paolo. "Immuno-intervention and preservation of beta-cell function in type 1 diabetes." Diabetes/Metabolism Research and Reviews 23, no. 4 (2007): 255–56. http://dx.doi.org/10.1002/dmrr.746.

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18

Kalinowska, Agnieszka, Barbara Orlińska, Mateusz Panasiuk, Milena Jamiołkowska, Aneta Zasim, Bożena Florys, Katarzyna Wojtkielewicz, Włodzimierz Łuczyński, Barbara Głowińska-Olszewska, and Artur Bossowski. "Assessment of preservation of beta-cell function in children with long-standing type 1 diabetes with „ultrasensitive c-peptide” method." Pediatric Endocrinology Diabetes and Metabolism 23, no. 3 (2017): 130–38. http://dx.doi.org/10.18544/pedm-23.03.0084.

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19

Oh, Yoon Sin, and Hee-Sook Jun. "Role of Bioactive Food Components in Diabetes Prevention: Effects on Beta-Cell Function and Preservation." Nutrition and Metabolic Insights 7 (January 2014): NMI.S13589. http://dx.doi.org/10.4137/nmi.s13589.

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Bioactive compounds found in fruits and vegetables can have anti-oxidant, anti-inflammatory, and anti-carcinogenic effects and can be protective against various diseases and metabolic disorders. These beneficial effects make them good candidates for the development of new functional foods with potential protective and preventive properties for type 1 and type 2 diabetes. This review summarizes the most relevant results concerning the effects of various bioactive compounds such as flavonoids, vitamins, and carotenoids on several aspects of beta-cell functionality. Studies using animal models with induced diabetes and diabetic patients support the hypothesis that bioactive compounds could ameliorate diabetic phenotypes. Published data suggest that there might be direct effects of bioactive compounds on enhancing insulin secretion and preventing beta-cell apoptosis, and some compounds might modulate beta-cell proliferation. Further research is needed to establish any clinical effects of these compounds.

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20

Carlsson, P., D. Espes, L. Davies, and M. Svahn. "Dose-dependent Preservation of beta-cell function in type i diabetes by mesenchymal stromal cells." Cytotherapy 22, no. 5 (May 2020): S192—S193. http://dx.doi.org/10.1016/j.jcyt.2020.04.053.

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21

De Paep, Diedert L., Freya Van Hulle, Zhidong Ling, Marian Vanhoeij, Robert Hilbrands, Wim Distelmans, Pieter Gillard, Bart Keymeulen, Daniel Pipeleers, and Daniel Jacobs-Tulleneers-Thevissen. "Utility of Islet Cell Preparations From Donor Pancreases After Euthanasia." Cell Transplantation 31 (January 2022): 096368972210961. http://dx.doi.org/10.1177/09636897221096160.

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Patients fulfilling criteria for euthanasia can choose to donate their organs after circulatory death [donors after euthanasia (DCD V)]. This study assesses the outcome of islet cell isolation from DCD V pancreases. A procedure for DCD V procurement provided 13 pancreases preserved in Institut Georges Lopez-1 preservation solution and following acirculatory warm ischemia time under 10 minutes. Islet cell isolation outcomes are compared with those from reference donors after brain death (DBD, n = 234) and a cohort of donors after controlled circulatory death (DCD III, n = 29) procured under the same conditions. Islet cell isolation from DCD V organs resulted in better in vitro outcome than for selected DCD III or reference DBD organs. A 50% higher average beta cell number before and after culture and a higher average beta cell purity (35% vs 24% and 25%) was observed, which led to more frequent selection for our clinical protocol (77% of isolates vs 50%). The functional capacity of a DCD V islet cell preparation was illustrated by its in vivo effect following intraportal transplantation in a type 1 diabetes patient: injection of 2 million beta cells/kg body weight (1,900 IEQ/kg body weight) at 39% insulin purity resulted in an implant with functional beta cell mass that represented 30% of that in non-diabetic controls. In conclusion, this study describes procurement and preservation conditions for donor organs after euthanasia, which allow preparation of cultured islet cells, that more frequently meet criteria for clinical use than those from DBD or DCD III organs.

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22

Saisho, Yoshifumi. "Changing the Concept of Type 2 Diabetes: Beta Cell Workload Hypothesis Revisited." Endocrine, Metabolic & Immune Disorders - Drug Targets 19, no. 2 (February 7, 2019): 121–27. http://dx.doi.org/10.2174/1871530318666180821161825.

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Background: Despite a number of innovations in anti-diabetic drugs and substantial improvement in diabetes care, the number of people with diabetes continues to increase, suggesting further need to explore novel approaches to prevent diabetes. Type 2 diabetes (T2DM) is characterized by beta cell dysfunction and insulin resistance. However, insulin resistance, usually a consequence of obesity, is often emphasized and the role of beta cell dysfunction in T2DM is less appreciated. </P><P> Objective and Results: This paper summarizes recent evidence showing the importance of beta cell dysfunction in T2DM and refines the “beta cell workload hypothesis”, emphasizing the importance of beta cell preservation for the prevention and management of T2DM. Conclusion: It is hoped that this novel concept will foster a better understanding of the pathophysiology of T2DM by not only medical staff and patients with diabetes, but also the general population, and encourage more people to adhere to a healthy lifestyle, eventually resulting in “stopping diabetes”.

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23

De Paep, Diedert L., Freya Van Hulle, Zhidong Ling, Marian Vanhoeij, Jacques Pirenne, Bart Keymeulen, Daniel Pipeleers, and Daniel Jacobs-Tulleneers-Thevissen. "Lower beta cell yield from donor pancreases after controlled circulatory death prevented by shortening acirculatory warm ischemia time and by using IGL-1 cold preservation solution." PLOS ONE 16, no. 5 (May 3, 2021): e0251055. http://dx.doi.org/10.1371/journal.pone.0251055.

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Organs from donors after controlled circulatory death (DCD III) exhibit a higher risk for graft dysfunction due to an initial period of warm ischemia. This procurement condition can also affect the yield of beta cells in islet isolates from donor pancreases, and hence their use for transplantation. The present study uses data collected and generated by our Beta Cell Bank to compare the number of beta cells in isolates from DCD III (n = 141) with that from donors after brain death (DBD, n = 609), before and after culture, and examines the influence of donor and procurement variables. Beta cell number per DCD III-organ was significantly lower (58 x 106 versus 84 x 106 beta cells per DBD-organ; p < 0.001) but their purity (24% insulin positive cells) and insulin content (17 μg / 106 beta cells in DCD III-organs versus 19 μg / 106 beta cells in DBD-organs) were similar. Beta cell number correlated negatively with duration of acirculatory warm ischemia time above 10 min; for shorter acirculatory warm ischemia time, DCD III-organs did not exhibit a lower beta cell yield (74 x 106 beta cells). Use of Institut Georges Lopez-1 cold preservation solution instead of University of Wisconsin solution or histidine-tryptophan-ketoglutarate also protected against the loss in beta cell yield from DCD III-organs (86 x 106 for IGL-1 versus 54 x 106 and 65 x 106 beta cells respectively, p = 0.042). Multivariate analysis indicates that both limitation of acirculatory warm ischemia time and use of IGL-1 prevent the reduced beta cell yield in islet cell isolates from DCD III-organs.

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24

de Groot, Pieter, Tanja Nikolic, Silvia Pellegrini, Valeria Sordi, Sultan Imangaliyev, Elena Rampanelli, Nordin Hanssen, et al. "Faecal microbiota transplantation halts progression of human new-onset type 1 diabetes in a randomised controlled trial." Gut 70, no. 1 (October 26, 2020): 92–105. http://dx.doi.org/10.1136/gutjnl-2020-322630.

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ObjectiveType 1 diabetes (T1D) is characterised by islet autoimmunity and beta cell destruction. A gut microbiota–immunological interplay is involved in the pathophysiology of T1D. We studied microbiota-mediated effects on disease progression in patients with type 1 diabetes using faecal microbiota transplantation (FMT).DesignPatients with recent-onset (<6 weeks) T1D (18–30 years of age) were randomised into two groups to receive three autologous or allogenic (healthy donor) FMTs over a period of 4 months. Our primary endpoint was preservation of stimulated C peptide release assessed by mixed-meal tests during 12 months. Secondary outcome parameters were changes in glycaemic control, fasting plasma metabolites, T cell autoimmunity, small intestinal gene expression profile and intestinal microbiota composition.ResultsStimulated C peptide levels were significantly preserved in the autologous FMT group (n=10 subjects) compared with healthy donor FMT group (n=10 subjects) at 12 months. Small intestinal Prevotella was inversely related to residual beta cell function (r=−0.55, p=0.02), whereas plasma metabolites 1-arachidonoyl-GPC and 1-myristoyl-2-arachidonoyl-GPC levels linearly correlated with residual beta cell preservation (rho=0.56, p=0.01 and rho=0.46, p=0.042, respectively). Finally, baseline CD4 +CXCR3+T cell counts, levels of small intestinal Desulfovibrio piger and CCL22 and CCL5 gene expression in duodenal biopsies predicted preserved beta cell function following FMT irrespective of donor characteristics.ConclusionFMT halts decline in endogenous insulin production in recently diagnosed patients with T1D in 12 months after disease onset. Several microbiota-derived plasma metabolites and bacterial strains were linked to preserved residual beta cell function. This study provides insight into the role of the intestinal gut microbiome in T1D.Trial registration numberNTR3697.

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25

Ali, Mohammad Alhadj, and Colin M. Dayan. "Review: The importance of residual endogenous beta-cell preservation in type 1 diabetes." British Journal of Diabetes & Vascular Disease 9, no. 6 (November 2009): 248–53. http://dx.doi.org/10.1177/1474651409351881.

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26

Jacobsen, Laura M., Brian N. Bundy, Madison N. Greco, Desmond A. Schatz, Mark A. Atkinson, Todd M. Brusko, Clayton E. Mathews, et al. "Comparing Beta Cell Preservation Across Clinical Trials in Recent-Onset Type 1 Diabetes." Diabetes Technology & Therapeutics 22, no. 12 (December 1, 2020): 948–53. http://dx.doi.org/10.1089/dia.2020.0305.

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27

Poudel, Ananta, Omid Savari, Deborah A. Striegel, Vipul Periwal, Jerome Taxy, J. Michael Millis, Piotr Witkowski, Mark A. Atkinson, and Manami Hara. "Beta-cell destruction and preservation in childhood and adult onset type 1 diabetes." Endocrine 49, no. 3 (January 22, 2015): 693–702. http://dx.doi.org/10.1007/s12020-015-0534-9.

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28

Savari, Omid, Karolina Golab, Ling-Jia Wang, Lindsay Schenck, Randall Grose, Martin Tibudan, Sabarinathan Ramachandran, et al. "Preservation of Beta Cell Function after Pancreatic Islet Autotransplantation: University of Chicago Experience." American Surgeon 81, no. 4 (April 2015): 421–27. http://dx.doi.org/10.1177/000313481508100435.

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The aim of the study was to assess the rate of insulin independence in patients after total pancreatectomy (TP) and islet autotransplantation in our center. TP followed by islet auto-transplantation was performed in 10 patients. Severe unrelenting pain associated with chronic pancreatitis was the major indication for surgery. Islets were isolated using the modified Ricordi method and infused through the portal vein. Exogenous insulin therapy was implemented for at least two months posttransplant to support islet engraftment and was subsequently weaned off, if possible. Median follow-up was 26 months (range, 2 to 60 months). Median islet yield was 158,860 islet equivalents (IEQ) (range, 40,203 to 330,472 IEQ) with an average islet yield of 2,478 IEQ/g (range, 685 to 6,002 IEQ/g) of processed pancreas. One patient developed transient partial portal vein thrombosis, which resolved without sequela. Five (50%) patients are currently off insulin with excellent glucose control and HbA1c below 6. Patients who achieved and maintained insulin independence were transplanted with significantly more islets (median, 202,291 IEQ; range, 145,000 to 330,474 IEQ) than patients who required insulin support (64,348 IEQ; range, 40,203 to 260,476 IEQ; P < 0.05). Patient body mass index and time of chronic pancreatitis prior transplant procedure did not correlate with the outcome. The remaining five patients, who require insulin support, had present C-peptide in blood and experience good glucose control without incidence of severe hypoglycemic episodes. Islet autotransplantation efficiently preserved beta cell function in selected patients with chronic pancreatitis and the outcome correlated with transplanted islet mass.

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29

Pekareva, E. V. "The advantages of the treatment of the patients with type 2 diabetes mellitus with gliclazide MR." Problems of Endocrinology 58, no. 2 (April 15, 2012): 58–61. http://dx.doi.org/10.14341/probl201258258-61.

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Type 2 diabetes mellitus (DM2) is a chronic condition characterized by progressive hyperglycemia resulting from beta-cell dysfunction and impaired insulin secretion. The maintenance of the target blood glucose level not only promotes preservation of the beta-cell pool but also reduces the risk of the development and progression of vascular complications of diabetes. This paper is designed to report the results of comparative investigations of the application of sulphonylurea derivatives for the treatment of the patients with type 2 diabetes mellitus.

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30

Singh, Kailash, Orian Bricard, Jeason Haughton, Mikaela Björkqvist, Moa Thorstensson, Zhengkang Luo, Loriana Mascali, et al. "Gene Delivery of Manf to Beta-Cells of the Pancreatic Islets Protects NOD Mice from Type 1 Diabetes Development." Biomolecules 12, no. 10 (October 16, 2022): 1493. http://dx.doi.org/10.3390/biom12101493.

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In type 1 diabetes, dysfunctional glucose regulation occurs due to the death of insulin-producing beta-cells in the pancreatic islets. Initiation of this process is caused by the inheritance of an adaptive immune system that is predisposed to responding to beta-cell antigens, most notably to insulin itself, coupled with unknown environmental insults priming the autoimmune reaction. While autoimmunity is a primary driver in beta-cell death, there is growing evidence that cellular stress participates in the loss of beta-cells. In the beta-cell fragility model, partial loss of islet mass requires compensatory upregulation of insulin production in the remaining islets, driving a cellular stress capable of triggering apoptosis in the remaining cells. The Glis3-Manf axis has been identified as being pivotal to the relative fragility or robustness of stressed islets, potentially operating in both type 1 and type 2 diabetes. Here, we have used an AAV-based gene delivery system to enhance the expression of the anti-apoptotic protein Manf in the beta-cells of NOD mice. Gene delivery substantially lowered the rate of diabetes development in treated mice. Manf-treated mice demonstrated minimal insulitis and superior preservation of insulin production. Our results demonstrating the therapeutic potential of Manf delivery to enhance beta-cell robustness and avert clinical diabetes.

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31

Chen, Yunan, Xueyan Li, Lei Su, Qianrong Hu, Wenli Li, Jialin He, and Lina Zhao. "Cyanidin-3-O-Glucoside Ameliorates Palmitic-Acid-Induced Pancreatic Beta Cell Dysfunction by Modulating CHOP-Mediated Endoplasmic Reticulum Stress Pathways." Nutrients 14, no. 9 (April 28, 2022): 1835. http://dx.doi.org/10.3390/nu14091835.

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Cyanidin-3-O-glucoside (C3G) is a natural colorant with anti-diabetic properties, while its underlying mechanisms remain far from clear. Here, we investigated the protective role of C3G on palmitic acid (PA)-induced pancreatic beta cell dysfunction and further decipher its possible molecular mechanisms. Both primary isolated mouse islets and the INS-1E cell were used, and treated with a mixture of PA (0.5 mM) and C3G (12.5 µM, 25 µM, 50 µM) for different durations (12, 24, 48 h). We found that C3G could dose-dependently ameliorate beta cell secretory function and further alleviate cell apoptosis. Mechanistically, the primary role of the PKR-like ER kinase (PERK) endoplasmic reticulum (ER) stress pathway was detected by RNA sequencing, and the PERK-pathway-related protein expression, especially the pro-apoptotic marker C/EBP homologous protein (CHOP) expression, was significantly downregulated by C3G treatment. The critical role of CHOP in mediating the protective effect of C3G was further validated by small interfering RNA. Conclusively, C3G could ameliorate PA-induced pancreatic beta cell dysfunction targeting the CHOP-related ER stress pathway, which might be used as a nutritional intervention for the preservation of beta cell dysfunction in type 2 diabetes mellitus.

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32

Cabello-Olmo, Miriam, Miriam Araña, Ilian Radichev, Paul Smith, Eduardo Huarte, and Miguel Barajas. "New Insights into Immunotherapy Strategies for Treating Autoimmune Diabetes." International Journal of Molecular Sciences 20, no. 19 (September 26, 2019): 4789. http://dx.doi.org/10.3390/ijms20194789.

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Type 1 diabetes mellitus (T1D) is an autoimmune illness that affects millions of patients worldwide. The main characteristic of this disease is the destruction of pancreatic insulin-producing beta cells that occurs due to the aberrant activation of different immune effector cells. Currently, T1D is treated by lifelong administration of novel versions of insulin that have been developed recently; however, new approaches that could address the underlying mechanisms responsible for beta cell destruction have been extensively investigated. The strategies based on immunotherapies have recently been incorporated into a panel of existing treatments for T1D, in order to block T-cell responses against beta cell antigens that are very common during the onset and development of T1D. However, a complete preservation of beta cell mass as well as insulin independency is still elusive. As a result, there is no existing T1D targeted immunotherapy able to replace standard insulin administration. Presently, a number of novel therapy strategies are pursuing the goals of beta cell protection and normoglycemia. In the present review we explore the current state of immunotherapy in T1D by highlighting the most important studies in this field, and envision novel strategies that could be used to treat T1D in the future.

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33

Li, Xia, Yan Chen, Yuting Xie, Yufei Xiang, Xiang Yan, Gan Huang, and Zhiguang Zhou. "Decline Pattern of Beta-cell Function in Adult-onset Latent Autoimmune Diabetes: an 8-year Prospective Study." Journal of Clinical Endocrinology & Metabolism 105, no. 7 (April 20, 2020): 2331–40. http://dx.doi.org/10.1210/clinem/dgaa205.

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Abstract Objective To explore the decline pattern and possible determinants of beta-cell function progression in patients with latent-onset autoimmune diabetes in adults (LADA). Research Design and Methods In this 8-year prospective study, 106 LADA individuals underwent annual follow-up and their pattern of beta-cell function progression was assessed. Beta-cell function failure was defined by fasting C-peptide (FCP) < 75 pmol/L. Other clinical characteristics, including age of onset, body mass index (BMI), and glutamic acid decarboxylase autoantibody (GADA) titer, were analyzed to find out possible determinants of beta-cell function progression. Results The dropout rate was 4.7%. During the 8-year follow-up period, 29 (28.7%) of the 101 subjects developed beta-cell function failure. The decline pattern of C-peptide in LADA was biphasic, showing an initial rapid linear progression and then followed by a stable mode. The declination speed of FCP was 55.19 pmol/L/year (95% CI, −62.54 to −47.84, P < 0.001) during the first 5 years and 4.62 pmol/L/year (95% CI, −69.83 to 60.60, P = 0.790) thereafter. Further analysis showed that GADA titer was the most valuable discriminatory parameter related to a higher risk of development of beta-cell function failure (GADA titer of 173.5 WHO units/mL; area under the curve [AUC], 0.824). Beta-cell function failure occurred in 71.3% of high-GADA titer patients while only 6.2% of low-titer patients. Conclusions The decline pattern of C-peptide was a fast-followed-by-slow biphasic mode, with about a quarter of LADA patients developing beta-cell function failure during the first 8 years. GADA titer less than 173.5 WHO units /mL was propitious for the preservation of beta-cell function.

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34

Freed, Michael A., and Peter Sterling. "Microcircuitry of the cat retina: Connections between arrays of neurons." Proceedings, annual meeting, Electron Microscopy Society of America 45 (August 1987): 706–11. http://dx.doi.org/10.1017/s0424820100127864.

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One of the most basic of structure-function relationships in the mammalian visual system is the relationship between the size of a ganglion cell's receptive field and the number of rod photoreceptors which are connected to it. There is also the flip side of the coin: how many ganglion cells does a single photoreceptor connect to? We have estimated the number of rods which converge upon an on-beta type of retinal ganglion cell; we have also estimated the number of on-beta ganglion cells which a single rod diverges to. Our method is to extract a three-dimensional circuit from a series of two-dimensional electron microscope sections. The results have implications for the preservation of the signal/noise ratio in the ganglion cell.There are two well-documented routes from the rods to the on-beta ganglion cell.

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Howe, C. L., L. M. Sacramone, M. S. Mooseker, and J. S. Morrow. "Mechanisms of cytoskeletal regulation: modulation of membrane affinity in avian brush border and erythrocyte spectrins." Journal of Cell Biology 101, no. 4 (October 1, 1985): 1379–85. http://dx.doi.org/10.1083/jcb.101.4.1379.

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The spectrins isolated from chicken erythrocytes and chicken intestinal brush border, TW260/240, share a common alpha subunit and a tissue-specific beta subunit. The ability of these related proteins to bind human erythrocyte inside out vesicles (IOVs) and human erythrocyte ankyrin in vitro have been quantitatively compared with human erythrocyte spectrin. Chicken erythrocyte spectrin binds human IOVs and human ankyrin with affinities nearly identical to that for human erythrocyte spectrin. TW260/240 does not significantly bind to either IOVs or ankyrin. These results demonstrate a remarkable tissue preservation of ankyrin-binding capacity, even between diverse species, and confirm the role of the avian beta-spectrins in modulating this functionality. Avian brush border spectrin may represent a unique spectrin which serves primarily as a filament cross-linker and which does not interact strongly with membrane-associated proteins.

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36

Leiter, L. A. "beta-cell preservation: a potential role for thiazolidinediones to improve clinical care in Type 2 diabetes." Diabetic Medicine 22, no. 8 (August 2005): 963–72. http://dx.doi.org/10.1111/j.1464-5491.2005.01605.x.

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37

Keymeulen, B. "NEW THERAPIES AIMED AT THE PRESERVATION OR RESTORATION OF BETA CELL FUNCTION IN TYPE 1 DIABETES." Acta Clinica Belgica 61, no. 5 (October 2006): 275–85. http://dx.doi.org/10.1179/acb.2006.047.

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38

Silins, S. L., S. M. Cross, S. L. Elliott, S. J. Pye, S. R. Burrows, J. M. Burrows, D. J. Moss, V. P. Argaet, and I. S. Misko. "Development of Epstein-Barr virus-specific memory T cell receptor clonotypes in acute infectious mononucleosis." Journal of Experimental Medicine 184, no. 5 (November 1, 1996): 1815–24. http://dx.doi.org/10.1084/jem.184.5.1815.

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The importance of cytotoxic T lymphocytes (CTLs) in the immunosurveillance of Epstein-Barr virus (EBV)-infected B cells is firmly established, and the viral antigens of CTL recognition in latent infection are well defined. The epitopes targeted by CTLs during primary infection have not been identified, however, and there is only limited information about T cell receptor (TCR) selection. In the present report, we have monitored the development of memory TCR-beta clonotypes selected in response to natural EBV infection in a longitudinal study of an HLA-B8+ individual with acute infectious mononucleosis (IM). By stimulating peripheral blood lymphocytes with HLA-B8+ EBV-transformed B lymphoblastoid cells, the primary virus-specific CTL response was shown to include specificities for two HLA-B8-restricted antigenic determinants, FLRGRAYGL and QAKWRLQTL, which are encoded within the latent EBV nuclear antigen EBNA-3. TCR-beta sequence analysis of CTL clones specific for each epitope showed polyclonal TCR-beta repertoire selection, with structural restrictions on recognition that indicated antigen-driven selection. Furthermore, longitudinal repertoire analysis revealed long-term preservation of a multiclonal effector response throughout convalescence, with the reemergence of distinct memory T cell clonotypes sharing similar structural restrictions. Tracking the progression of specific TCR-beta clonotypes and antigen-specific TCR-V beta family gene expression in the peripheral repertoire ex vivo using semiquantitative PCR strongly suggested that selective TCR-beta expansions were present at the clonotype level, but not at the TCR-V beta family level. Overall, in this first analysis of antigen-specific TCR development in IM, a picture of polyclonal TCR stimulation is apparent. This diversity may be especially important in the establishment of an effective CTL control during acute EBV infection and in recovery from disease.

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39

Akinrinde, Akinleye, Trevor Koekemoer, Maryna Van De Venter, and Graeme Bradley. "In Vitro Investigation of Potential Anti-Diabetic Activity of the Corm Extract of Hypoxis Argentea Harv. Ex Baker." Acta Pharmaceutica 68, no. 4 (December 1, 2018): 389–407. http://dx.doi.org/10.2478/acph-2018-0023.

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Abstract The corms of Hypoxis argentea are widely used as a traditional remedy for diabetes mellitus in South Africa. In this study, we investigated the effects of non-toxic concentrations (12.5-100 μg mL-1) of the aqueous extract of H. argentea (HAA) corms on glucose uptake, pancreatic beta cell proliferation, and adipocyte differentiation. HAA stimulated glucose uptake in HepG2 cells up to 19.6 % and 17.0 % in L6 myotubes. Live-cell imaging microscopy revealed significant increases (p < 0.001) in total INS-1 cell numbers exposed to HAA, although no effect was observed on adipogenesis in 3T3-L1 pre-adipocytes. HAA produced weak to moderate inhibition of porcine pancreatic α-amylase, α-glucosidase, porcine pancreatic lipase, dipeptidyl peptidase IV (DPP IV) activities, as well as protein glycation. Our results suggest that the acclaimed anti-diabetic effects of H. argentea could be mediated by its promotion of glucose utilization and preservation of pancreatic beta cell populations while preventing fat accumulation in adipocytes.

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40

Cabrera-Rode, Eduardo, Ileana Cubas-Dueñas, Janet Rodríguez-Acosta, Yudith García-García, Yelena Torres-López, Claudia Prieto-Noa, Bárbara M. Vázquez-Izada, et al. "An Exploratory Study of Itolizumab on the Preservation of Beta Cell Function in Adults with Recent-Onset Type 1 Diabetes." Journal of Clinical Medicine 11, no. 7 (March 24, 2022): 1789. http://dx.doi.org/10.3390/jcm11071789.

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We conducted a phase I-IIa, randomized, monocentric, double-blind, placebo-controlled clinical trial to evaluate the safety and impact of the combination treatment of Itolizumab and insulin on preserving beta cell function in adults with recent-onset type 1 diabetes. Twelve patients were randomly assigned to three treatment groups, each receiving a different Itolizumab dose (0.4/0.8/1.6 mg/kg body weight, respectively) and a placebo group. All patients received concomitant intensive multiple-dose insulin therapy. Endogenous insulin secretion was assessed by the measurement of C-peptide during the mixed-meal tolerance test. No serious adverse events were reported. No changes in the total daily insulin doses, glycated hemoglobin levels, and stimulated C-peptide were observed between the Itolizumab and placebo groups at 52 weeks. A significant decrease in stimulated C-peptide was observed during the follow-up period (p = 0.012). One subject treated with 1.6 mg of Itolizumab showed a marked increase in the levels of stimulated C-peptide three years after completion of the trial. Taken together, this is the first study to demonstrate that combination treatment with Itolizumab and insulin is safe in humans and does not affect the residual function of beta cells up to 52 weeks. The findings from our study show preliminary evidence that high doses of Itolizumab could potentially arrest the loss of beta cell function in the long term. Further studies with a longer follow-up and larger numbers of patients are envisaged to assess the effect with high dose Itolizumab.

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Winkler, Gábor. "The use of gliclazide in the mirror of the individualized sulfonylurea therapy." Orvosi Hetilap 155, no. 14 (April 2014): 541–48. http://dx.doi.org/10.1556/oh.2014.29850.

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In addition to the common blood glucose lowering effect, sulfonylurea compounds are different in many aspects from each other. Based on earlier findings the second generation gliclazide has special advantages within this group. Although the number of experimental and clinical observations on gliclazide is continuously increasing, these novel findings are not in the focus anymore due to the appearance of new antidiabetics. The article overviews recent experimental (receptorial effect, the absence of Epac2 activation, antioxidant properties, possible incentive of factors participating in beta-cell differentiation) and pharmacogenomic data, and compares them with clinical observations obtained from gliclazide treatment (hypoglycaemias, parameters of cardiovascular outcome). The data underline the advantages of gliclazide, the highly pancreas-selective nature, preservation of the ischemic precondition, favourable hemodynamic properties and potential reduction of the beta-cell loss as compared to other compounds of the group. However, gliclazide is not free from disadvantages characteristic to sulfonylureas in general (blood glucose independent insulin stimulation, beta-cell depletion). Comparing gliclazide with other derivatives of the group, the above data indicate individual benefits for the application when sulfonylurea compound is the drug of choice. Orv. Hetil., 2014, 155(14), 541–548.

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42

Franklin, Zara J., Anastasia Tsakmaki, Patricia Fonseca Pedro, Aileen J. King, Guo Cai Huang, Sakeena Amjad, Shanta J. Persaud, and Gavin A. Bewick. "Islet neuropeptide Y receptors are functionally conserved and novel targets for the preservation of beta-cell mass." Diabetes, Obesity and Metabolism 20, no. 3 (November 6, 2017): 599–609. http://dx.doi.org/10.1111/dom.13119.

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43

Kolb, H., and E. A. M. Gale. "Does partial preservation of residual beta-cell function justify immune intervention in recent onset Type I diabetes?" Diabetologia 44, no. 10 (October 1, 2001): 1349–53. http://dx.doi.org/10.1007/s001250100636.

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44

Retnakaran, Ravi, Caroline K. Kramer, Haysook Choi, Balakumar Swaminathan, and Bernard Zinman. "Liraglutide and the Preservation of Pancreatic Beta-Cell Function in Early Type 2 Diabetes: The LIBRA Trial." Canadian Journal of Diabetes 38, no. 5 (October 2014): S4—S5. http://dx.doi.org/10.1016/j.jcjd.2014.07.012.

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45

Anagnou, NP, T. Papayannopoulou, G. Stamatoyannopoulos, and AW Nienhuis. "Structurally diverse molecular deletions in the beta-globin gene cluster exhibit an identical phenotype on interaction with the beta S- gene." Blood 65, no. 5 (May 1, 1985): 1245–51. http://dx.doi.org/10.1182/blood.v65.5.1245.bloodjournal6551245.

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We have characterized a new deletion that increases hemoglobin F synthesis in an American black woman who is doubly heterozygous for this mutation and the beta S-gene. The 5 ' endpoint is 2.4 +/- 0.1 kilobases (kb) upstream from the delta-globin gene, and the 3′ endpoint is 0.2 +/- 0.1 kb downstream from the beta-globin gene; the deletion is 12 kb long. Both members of the Alu moderately repetitive DNA sequence family, normally present upstream from the delta-globin gene, are preserved. The patient is asymptomatic with a mild anemia and 24.8% HbF. The patient's husband and daughter have a similar clinical syndrome, with HbF levels of 22.4% and 25.4%, respectively. Both husband and daughter are doubly heterozygous for the beta S-gene and the Ghana type of hereditary persistence of fetal hemoglobin (HPFH) deletion (HPFH-2). The 5′ end of this deletion is in the psi beta-gene, and its total length is more than 70 kb. All three members of the family have normocytic red cells, of which 95% or more are F cells as detected by immunofluorescence. Previous studies have shown that culture of the erythroid progenitors (BFU-E) from both types of these compound heterozygotes in the presence of fetal sheep serum, rich in 'switching factor,” resulted in complete suppression of HbF synthesis. Although the newly described deletion resembles the Sicilian type of delta beta-thalassemia by its size and preservation of the Alu sequences, the clinical and biological phenotype produced by its interaction with the beta S-gene is very similar to that of the HPFH- type deletion.

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46

Nguyen, Hai T., Mathew T. Dufort, Cate Speake, Carla Greenbaum, Peter S. Linsley, and Eddie A. James. "High dimensional single cell characterization of autoreactive CD8 T-cells reveals heterogeneous phenotypes that play a role in disease progression in Type 1 Diabetes." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 224.20. http://dx.doi.org/10.4049/jimmunol.204.supp.224.20.

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Abstract Type 1 Diabetes (T1D) is caused by beta cell destruction, eventually resulting in loss of glycemic control. Following onset, subjects with T1D exhibit diverse amounts of residual c-peptide, indicating varying levels of beta cell function. Persistence of c-peptide is correlated with reduced risk of complications and its preservation has been used as an endpoint in clinical trials. However, the immunologic factors that differentiate subjects who retain measurable c-peptide from those who do not are not well characterized. We investigated the number and phenotype of beta cell specific CD8+ T-cells in peripheral blood samples from a cohort of T1D subjects, stratified into slow progressors (c-peptide > 0.1ng/ml) and rapid progressors (undetectable c-peptide), including longitudinal samples. Using tetramers corresponding to HLA-A2 epitopes, we enumerated epitope specific T-cells and sorted single cells for RNA-Seq. Differential gene expression between slow and rapid progressors indicated differences in effector, exhaustion, and regulatory pathways which were consistent with a recently published high dimensional CyTOF data set. Assembly of autoantigen specific TCRs revealed differences in clonal expansion for specific cell clusters. Pseudotime trajectory analysis of the scRNAseq data revealed that CD8+ T cells expressing the same TCR resided in different phenotypic end states. Furthermore, flow cytometric analyses demonstrated differential expression of lineage-specific cell surface markers, which correlated well with the transcriptional profiles within each cluster. Cumulatively, we discovered specific aspects of T cell function and repertoire that differ between slow- and rapid-progressing T1D subjects.

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47

Kolb, Hubert, Stephan Martin, and Kerstin Kempf. "Coffee and Lower Risk of Type 2 Diabetes: Arguments for a Causal Relationship." Nutrients 13, no. 4 (March 31, 2021): 1144. http://dx.doi.org/10.3390/nu13041144.

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Prospective epidemiological studies concur in an association between habitual coffee consumption and a lower risk of type 2 diabetes. Several aspects of these studies support a cause–effect relationship. There is a dependency on daily coffee dose. Study outcomes are similar in different regions of the world, show no differences between sexes, between obese versus lean, young versus old, smokers versus nonsmokers, regardless of the number of confounders adjusted for. Randomized controlled intervention trials did not find a consistent impact of drinking coffee on acute metabolic control, except for effects of caffeine. Therefore, lowering of diabetes risk by coffee consumption does not involve an acute effect on the post-meal course of blood glucose, insulin or insulin resistance. Several studies in animals and humans find that the ingestion of coffee phytochemicals induces an adaptive cellular response characterized by upregulation and de novo synthesis of enzymes involved in cell defense and repair. A key regulator is the nuclear factor erythroid 2-related factor 2 (Nrf2) in association with the aryl hydrocarbon receptor, AMP-activated kinase and sirtuins. One major site of coffee actions appears to be the liver, causing improved fat oxidation and lower risk of steatosis. Another major effect of coffee intake is preservation of functional beta cell mass via enhanced mitochondrial function, lower endoplasmic reticulum stress and prevention or clearance of aggregates of misfolded proinsulin or amylin. Long-term preservation of proper liver and beta cell function may account for the association of habitual coffee drinking with a lower risk of type 2 diabetes, rather than acute improvement of metabolic control.

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48

Anagnou, NP, T. Papayannopoulou, G. Stamatoyannopoulos, and AW Nienhuis. "Structurally diverse molecular deletions in the beta-globin gene cluster exhibit an identical phenotype on interaction with the beta S- gene." Blood 65, no. 5 (May 1, 1985): 1245–51. http://dx.doi.org/10.1182/blood.v65.5.1245.1245.

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Abstract We have characterized a new deletion that increases hemoglobin F synthesis in an American black woman who is doubly heterozygous for this mutation and the beta S-gene. The 5 ' endpoint is 2.4 +/- 0.1 kilobases (kb) upstream from the delta-globin gene, and the 3′ endpoint is 0.2 +/- 0.1 kb downstream from the beta-globin gene; the deletion is 12 kb long. Both members of the Alu moderately repetitive DNA sequence family, normally present upstream from the delta-globin gene, are preserved. The patient is asymptomatic with a mild anemia and 24.8% HbF. The patient's husband and daughter have a similar clinical syndrome, with HbF levels of 22.4% and 25.4%, respectively. Both husband and daughter are doubly heterozygous for the beta S-gene and the Ghana type of hereditary persistence of fetal hemoglobin (HPFH) deletion (HPFH-2). The 5′ end of this deletion is in the psi beta-gene, and its total length is more than 70 kb. All three members of the family have normocytic red cells, of which 95% or more are F cells as detected by immunofluorescence. Previous studies have shown that culture of the erythroid progenitors (BFU-E) from both types of these compound heterozygotes in the presence of fetal sheep serum, rich in 'switching factor,” resulted in complete suppression of HbF synthesis. Although the newly described deletion resembles the Sicilian type of delta beta-thalassemia by its size and preservation of the Alu sequences, the clinical and biological phenotype produced by its interaction with the beta S-gene is very similar to that of the HPFH- type deletion.

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49

Ezanno, Hélène, Valérie Pawlowski, Saida Abdelli, Raphael Boutry, Valery Gmyr, Julie Kerr-Conte, Christophe Bonny, François Pattou, and Amar Abderrahmani. "JNK3 Is Required for the Cytoprotective Effect of Exendin 4." Journal of Diabetes Research 2014 (2014): 1–5. http://dx.doi.org/10.1155/2014/814854.

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Preservation of beta cell against apoptosis is one of the therapeutic benefits of the glucagon-like peptide-1 (GLP1) antidiabetic mimetics for preserving the functional beta cell mass exposed to diabetogenic condition including proinflammatory cytokines. The mitogen activated protein kinase 10 also called c-jun amino-terminal kinase 3 (JNK3) plays a protective role in insulin-secreting cells against death caused by cytokines. In this study, we investigated whether the JNK3 expression is associated with the protective effect elicited by the GLP1 mimetic exendin 4. We found an increase in the abundance of JNK3 in isolated human islets and INS-1E cells cultured with exendin 4. Induction of JNK3 by exendin 4 was associated with an increased survival of INS-1E cells. Silencing of JNK3 prevented the cytoprotective effect of exendin 4 against apoptosis elicited by culture condition and cytokines. These results emphasize the requirement of JNK3 in the antiapoptotic effects of exendin 4.

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50

Ludvigsson, Johnny. "Combination therapy for preservation of beta cell function in Type 1 diabetes: New attitudes and strategies are needed!" Immunology Letters 159, no. 1-2 (May 2014): 30–35. http://dx.doi.org/10.1016/j.imlet.2014.02.006.

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