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Article ; Online: Islet inflammation in type 2 diabetes.

Marchetti, Piero

2016 Volume 59, Issue 4, Page(s) 668–672

MeSH term(s)	Animals ; Chemokines/metabolism ; Cytokines/metabolism ; Diabetes Mellitus, Type 2/immunology ; Diabetes Mellitus, Type 2/metabolism ; Humans ; Inflammation/metabolism ; Islets of Langerhans/immunology ; Islets of Langerhans/metabolism ; Macrophages/metabolism
Chemical Substances	Chemokines ; Cytokines
Language	English
Publishing date	2016-04
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1694-9
ISSN	1432-0428 ; 0012-186X
ISSN (online)	1432-0428
ISSN	0012-186X
DOI	10.1007/s00125-016-3875-x
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Article ; Online: Accuracy of intermittently scanned continuous glucose monitoring during caesarean delivery in pregnant women with insulin-treated diabetes.

Citro, Fabrizia / Bianchi, Cristina / Aragona, Michele / Belcari, Tommaso / Battini, Lorella / Marchetti, Piero / Bertolotto, Alessandra

Diabetes research and clinical practice

2024 Volume 210, Page(s) 111611

Abstract: Aim: Continuous Glucose Monitoring (CGM) systems are not currently recommended to guide intrapartum glucose and insulin infusion, due to insufficient data. In this study, intrapartum accuracy of intermittently scanned CGM (isCGM), compared to ... ...

Abstract	Aim: Continuous Glucose Monitoring (CGM) systems are not currently recommended to guide intrapartum glucose and insulin infusion, due to insufficient data. In this study, intrapartum accuracy of intermittently scanned CGM (isCGM), compared to simultaneously measured capillary glucose (CG), was evaluated. Methods: Paired isCGM (Freestyle Libre 2) - CG data during caesarean delivery in pregnant women with insulin-treated diabetes were prospectively collected. The isCGM accuracy was assessed by MARD and Clarke Error Grid analysis. Moreover, the impact on intrapartum management was evaluated. Results: Sixty-eight paired isCGM-CG data of 19 women were evaluated. The overallMARD was 9.28 %. All values were in A and B zones of Clarke Error Grid. Forty-six (68 %) isCGM-CG pairs were in the same glycemic range, meaning the same intrapartum management. All discordant data were identified by checking CG in case of isCGM above 110 mg/dL or less than 70 mg/dL [chi-square 21.76, p < 0.001]. At ROC curve, isCGM above 110 mg/dL was associated with 100 % sensitivity to discordant result at CG (AUC 0.859, p < 0.001). Conclusion: The accuracy of isCGM during caesarean delivery was good, particularly for glucose values between 70 and 110 mg/dL, when CG confirmation could be safely avoided.
MeSH term(s)	Pregnancy ; Female ; Humans ; Insulin/therapeutic use ; Continuous Glucose Monitoring ; Pregnant Women ; Blood Glucose Self-Monitoring ; Blood Glucose ; Insulin, Regular, Human ; Diabetes Mellitus ; Cesarean Section ; Glucose ; Diabetes Mellitus, Type 1 ; Hypoglycemic Agents/therapeutic use
Chemical Substances	Insulin ; Blood Glucose ; Insulin, Regular, Human ; Glucose (IY9XDZ35W2) ; Hypoglycemic Agents
Language	English
Publishing date	2024-03-11
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	632523-3
ISSN	1872-8227 ; 0168-8227
ISSN (online)	1872-8227
ISSN	0168-8227
DOI	10.1016/j.diabres.2024.111611
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Article ; Online: Human alpha cell transcriptomic signatures of types 1 and 2 diabetes highlight disease-specific dysfunction pathways.

Bosi, Emanuele / Marchetti, Piero / Rutter, Guy Allen / Eizirik, Decio Laks

iScience

2022 Volume 25, Issue 10, Page(s) 105056

Abstract: Although glucagon secretion is perturbed in both T1D and T2D, the pathophysiological changes in individual pancreatic alpha cells are still obscure. Using recently curated single-cell RNASeq data from T1D or T2D donors and their controls, we identified ... ...

Abstract	Although glucagon secretion is perturbed in both T1D and T2D, the pathophysiological changes in individual pancreatic alpha cells are still obscure. Using recently curated single-cell RNASeq data from T1D or T2D donors and their controls, we identified alpha cell transcriptomic alterations consistent with both common and discrete pathways. Although alterations in alpha cell identity gene (ARX, MAFB) expression were conserved, cytokine-regulated genes and genes involved in glucagon biosynthesis and processing were up-regulated in T1D. Conversely, mitochondrial genes associated with ROS (COX7B, NQO2) were dysregulated in T2D. Additionally, T1D alpha cells displayed altered expression of autoimmune-induced ER stress genes (ERLEC1, HSP90), whilst those from T2D subjects showed modified glycolytic and citrate cycle gene (LDHA?, PDHB, PDK4) expression. Thus, despite conserved alterations related to loss of function, alpha cells display disease-specific gene signatures which may be secondary to the main pathogenic events in each disease, namely immune- or metabolism-mediated-stress, in T1D and T2D, respectively.
Language	English
Publishing date	2022-09-03
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2022.105056
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Article: Aging with a Liver Graft: Analysis of Very Long-Term Survivors after Liver Transplantation.

De Simone, Paolo / Bronzoni, Jessica / Martinelli, Caterina / Ducci, Juri / Campani, Daniela / Gitto, Stefano / Marchetti, Piero / Biancofiore, Giandomenico

Journal of clinical medicine

2024 Volume 13, Issue 4

Abstract: Background: In Italy, data on long-term survivors after liver transplantation are lacking.: Materials and methods: We conducted a hybrid design study on a cohort of 359 adult recipients who received transplants between 1996 and 2002 to identify ... ...

Abstract	Background: In Italy, data on long-term survivors after liver transplantation are lacking. Materials and methods: We conducted a hybrid design study on a cohort of 359 adult recipients who received transplants between 1996 and 2002 to identify predictors of survival and the prevalence of co-morbidities among long-term survivors. Results: The actuarial (95% CI) patient survival was 96% (94.6-98.3%), 69% (64.2-73.6%), 55% (49.8-59.9%), 42.8% (37.6-47.8%), and 34% (29.2-38.9%) at 1, 5, 10, 15, and 20 years, respectively. The leading causes of death were hepatitis C virus recurrence (24.6%), extrahepatic malignancies (16.9%), infection (14.4%), and hepatocellular carcinoma recurrence (14.4%). The factors associated with the survival probability were younger donor and recipient ages ( Conclusions: Aging with a liver graft is associated with an increased risk of complications and requires ongoing care to reduce the long-term attrition rate resulting from chronic immunosuppression.
Language	English
Publishing date	2024-02-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662592-1
ISSN	2077-0383
ISSN	2077-0383
DOI	10.3390/jcm13041087
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Article: Proinflammatory Cytokines Suppress Nonsense-Mediated RNA Decay to Impair Regulated Transcript Isoform Processing in Pancreatic β-Cells.

Ghiasi, Seyed M / Marchetti, Piero / Piemonti, Lorenzo / Nielsen, Jens H / Porse, Bo T / Mandrup-Poulsen, Thomas / Rutter, Guy A

bioRxiv : the preprint server for biology

2024

Abstract: Proinflammatory cytokines are implicated in pancreatic β-cell failure in type 1 and type 2 diabetes and are known to stimulate alternative RNA splicing and the expression of Nonsense-Mediated RNA Decay (NMD) components. Here, we investigate whether ... ...

Abstract	Proinflammatory cytokines are implicated in pancreatic β-cell failure in type 1 and type 2 diabetes and are known to stimulate alternative RNA splicing and the expression of Nonsense-Mediated RNA Decay (NMD) components. Here, we investigate whether cytokines regulate NMD activity and identify transcript isoforms targeted in β-cells. A luciferase-based NMD reporter transiently expressed in rat INS1(832/13), human-derived EndoC-βH3 or dispersed human islet cells is used to examine the effect of proinflammatory cytokines (Cyt) on NMD activity. Gain- or loss-of function of two key NMD components UPF3B and UPF2 is used to reveal the effect of cytokines on cell viability and function. RNA-sequencing and siRNA-mediated silencing are deployed using standard techniques. Cyt attenuate NMD activity in insulin-producing cell lines and primary human β-cells. These effects are found to involve ER stress and are associated with downregulation of UPF3B. Increases or decreases in NMD activity achieved by UPF3B overexpression (OE) or UPF2 silencing, raises or lowers Cyt-induced cell death, respectively, in EndoC-βH3 cells, and are associated with decreased or increased insulin content, respectively. No effects of these manipulations are observed on glucose-stimulated insulin secretion. Transcriptomic analysis reveals that Cyt increase alternative splicing (AS)-induced exon skipping in the transcript isoforms, and this is potentiated by UPF2 silencing. Gene enrichment analysis identifies transcripts regulated by UPF2 silencing whose proteins are localized and/or functional in extracellular matrix (ECM) including the serine protease inhibitor SERPINA1/α-1-antitrypsin, whose silencing sensitises β-cells to Cyt cytotoxicity. Cytokines suppress NMD activity via UPR signalling, potentially serving as a protective response against Cyt-induced NMD component expression. Our findings highlight the central importance of RNA turnover in β-cell responses to inflammatory stress.
Language	English
Publishing date	2024-02-28
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.12.20.572623
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Article: Proinflammatory cytokines suppress nonsense-mediated RNA decay to impair regulated transcript isoform processing in pancreatic β cells.

Ghiasi, Seyed M / Marchetti, Piero / Piemonti, Lorenzo / Nielsen, Jens H / Porse, Bo T / Mandrup-Poulsen, Thomas / Rutter, Guy A

Frontiers in endocrinology

2024 Volume 15, Page(s) 1359147

Abstract: Introduction: Proinflammatory cytokines are implicated in pancreatic ß cell failure in type 1 and type 2 diabetes and are known to stimulate alternative RNA splicing and the expression of nonsense-mediated RNA decay (NMD) components. Here, we ... ...

Abstract	Introduction: Proinflammatory cytokines are implicated in pancreatic ß cell failure in type 1 and type 2 diabetes and are known to stimulate alternative RNA splicing and the expression of nonsense-mediated RNA decay (NMD) components. Here, we investigate whether cytokines regulate NMD activity and identify transcript isoforms targeted in ß cells. Methods: A luciferase-based NMD reporter transiently expressed in rat INS1(832/13), human-derived EndoC-ßH3, or dispersed human islet cells is used to examine the effect of proinflammatory cytokines (Cyt) on NMD activity. The gain- or loss-of-function of two key NMD components, UPF3B and UPF2, is used to reveal the effect of cytokines on cell viability and function. RNA-sequencing and siRNA-mediated silencing are deployed using standard techniques. Results: Cyt attenuate NMD activity in insulin-producing cell lines and primary human ß cells. These effects are found to involve ER stress and are associated with the downregulation of UPF3B. Increases or decreases in NMD activity achieved by UPF3B overexpression (OE) or UPF2 silencing raise or lower Cyt-induced cell death, respectively, in EndoC-ßH3 cells and are associated with decreased or increased insulin content, respectively. No effects of these manipulations are observed on glucose-stimulated insulin secretion. Transcriptomic analysis reveals that Cyt increases alternative splicing (AS)-induced exon skipping in the transcript isoforms, and this is potentiated by UPF2 silencing. Gene enrichment analysis identifies transcripts regulated by UPF2 silencing whose proteins are localized and/or functional in the extracellular matrix (ECM), including the serine protease inhibitor SERPINA1/α-1-antitrypsin, whose silencing sensitizes ß-cells to Cyt cytotoxicity. Cytokines suppress NMD activity via UPR signaling, potentially serving as a protective response against Cyt-induced NMD component expression. Conclusion: Our findings highlight the central importance of RNA turnover in ß cell responses to inflammatory stress.
MeSH term(s)	Humans ; Rats ; Animals ; RNA/metabolism ; Insulin-Secreting Cells/metabolism ; Cytokines/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Nonsense Mediated mRNA Decay ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; Insulins/metabolism ; RNA-Binding Proteins/genetics
Chemical Substances	RNA (63231-63-0) ; Cytokines ; Protein Isoforms ; Insulins ; UPF3B protein, human ; RNA-Binding Proteins
Language	English
Publishing date	2024-03-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2024.1359147
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Article: Everolimus Mitigates the Risk of Hepatocellular Carcinoma Recurrence after Liver Transplantation.

De Simone, Paolo / Precisi, Arianna / Lai, Quirino / Ducci, Juri / Campani, Daniela / Marchetti, Piero / Gitto, Stefano

Cancers

2024 Volume 16, Issue 7

Abstract: To obtain long-term data on the use of everolimus in patients who underwent liver transplantation for hepatocellular carcinoma, we conducted a retrospective, single-center analysis of adult recipients transplanted between 2013 and 2021. Patients on ... ...

Abstract	To obtain long-term data on the use of everolimus in patients who underwent liver transplantation for hepatocellular carcinoma, we conducted a retrospective, single-center analysis of adult recipients transplanted between 2013 and 2021. Patients on everolimus-incorporating immunosuppression were matched with those on tacrolimus using an inverse probability of treatment weighting methodology. Two propensity-matched groups of patients were thus compared: 233 (45.6%) receiving everolimus versus 278 (54.4%) on tacrolimus. At a median (interquartile range) follow-up of 4.4 (3.8) years after transplantation, everolimus patients showed a reduced risk of recurrence versus tacrolimus (7.7% versus 16.9%; RR = 0.45;
Language	English
Publishing date	2024-03-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers16071243
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Article: Insulin Autoimmune Syndrome (Hirata Disease): A Comprehensive Review Fifty Years After Its First Description.

Cappellani, Daniele / Macchia, Enrico / Falorni, Alberto / Marchetti, Piero

Diabetes, metabolic syndrome and obesity : targets and therapy

2020 Volume 13, Page(s) 963–978

Abstract: Insulin autoimmune syndrome (IAS), also named Hirata's disease, is a rare condition characterized by hypoglycemic episodes due to the presence of high titers of insulin autoantibodies (IAA). IAS is a form of immune-mediated hypoglycemia, which develops ... ...

Abstract	Insulin autoimmune syndrome (IAS), also named Hirata's disease, is a rare condition characterized by hypoglycemic episodes due to the presence of high titers of insulin autoantibodies (IAA). IAS is a form of immune-mediated hypoglycemia, which develops when a triggering factor (ie, a medication or a viral infection) acts on an underlying predisposing genetic background. IAS pathogenesis involves the formation of insulin-IAA complexes that induce glycemic alterations with a double-phase mechanism: IAA prevent insulin to bind its receptor in the postprandial phase, possibly resulting in mild hyperglycemia; thereafter, insulin is released from the complexes irrespective of blood glucose concentrations, thus inducing hypoglycemia. The diagnosis of IAS is challenging, requiring a careful workup aimed at excluding other causes of hyperinsulinemic hypoglycemia. The gold standard for the definitive diagnosis is the finding of IAA in a blood sample. Because IAS is frequently a self-remitting disease, its management mostly consists of supportive measures, such as dietary modifications, aimed at preventing the development of hypoglycemia. Pharmacological therapies may occasionally be necessary for patients presenting with severe manifestations of IAS. Available therapies may include drugs that reduce pancreatic insulin secretion (somatostatin analogues and diazoxide, for instance) and immunosuppressive agents (glucocorticoids, azathioprine and rituximab). The purpose of this review is to provide a comprehensive analysis of the disease, by describing the burden of knowledge that has been obtained in the 50 years following its first description, took in 1970, and by highlighting the points that are still unclear in its pathogenesis and management.
Language	English
Publishing date	2020-04-01
Publishing country	New Zealand
Document type	Journal Article ; Review
ZDB-ID	2494854-8
ISSN	1178-7007
ISSN	1178-7007
DOI	10.2147/DMSO.S219438
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Article ; Online: Nanoencapsulated human pancreatic islets for β-cell replacement in Type 1 diabetes.

Krol, Silke / Baronti, Walter / Marchetti, Piero

Nanomedicine (London, England)

2020 Volume 15, Issue 18, Page(s) 1735–1738

MeSH term(s)	Diabetes Mellitus, Type 1/therapy ; Humans ; Insulin ; Insulin-Secreting Cells ; Islets of Langerhans
Chemical Substances	Insulin
Language	English
Publishing date	2020-07-16
Publishing country	England
Document type	Editorial ; Research Support, Non-U.S. Gov't
ZDB-ID	2277839-1
ISSN	1748-6963 ; 1743-5889
ISSN (online)	1748-6963
ISSN	1743-5889
DOI	10.2217/nnm-2020-0166
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Article ; Online: β-Cell Pathophysiology: A Review of Advanced Optical Microscopy Applications.

Ferri, Gianmarco / Pesce, Luca / Tesi, Marta / Marchetti, Piero / Cardarelli, Francesco

International journal of molecular sciences

2021 Volume 22, Issue 23

Abstract: β-cells convert glucose (input) resulting in the controlled release of insulin (output), which in turn has the role to maintain glucose homeostasis. β-cell function is regulated by a complex interplay between the metabolic processing of the input, its ... ...

Abstract	β-cells convert glucose (input) resulting in the controlled release of insulin (output), which in turn has the role to maintain glucose homeostasis. β-cell function is regulated by a complex interplay between the metabolic processing of the input, its transformation into second-messenger signals, and final mobilization of insulin-containing granules towards secretion of the output. Failure at any level in this process marks β-cell dysfunction in diabetes, thus making β-cells obvious potential targets for therapeutic purposes. Addressing quantitatively β-cell (dys)function at the molecular level in living samples requires probing simultaneously the spatial and temporal dimensions at the proper resolution. To this aim, an increasing amount of research efforts are exploiting the potentiality of biophysical techniques. In particular, using excitation light in the visible/infrared range, a number of optical-microscopy-based approaches have been tailored to the study of β-cell-(dys)function at the molecular level, either in label-free mode (i.e., exploiting intrinsic autofluorescence of cells) or by the use of organic/genetically-encoded fluorescent probes. Here, relevant examples from the literature are reviewed and discussed. Based on this, new potential lines of development in the field are drawn.
MeSH term(s)	Animals ; Fluorescent Dyes/chemistry ; Glucose/metabolism ; Homeostasis ; Humans ; Insulin-Secreting Cells/metabolism ; Insulin-Secreting Cells/pathology ; Microscopy, Fluorescence/methods
Chemical Substances	Fluorescent Dyes ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2021-11-26
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms222312820
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