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6. Inflammation in obesity, diabetes, and related disorders

Author

Rohm, Theresa V, Meier, Daniel T, Olefsky, Jerrold M, and Donath, Marc Y

Subjects
Biomedical and Clinical Sciences, Immunology, Nutrition, Prevention, Diabetes, Obesity, 2.1 Biological and endogenous factors, Metabolic and endocrine, Inflammatory and immune system, Animals, Diabetes Complications, Diabetes Mellitus, Type 2, Humans, Immunomodulation, Inflammation, Insulin Resistance
Abstract

Obesity leads to chronic, systemic inflammation and can lead to insulin resistance (IR), β-cell dysfunction, and ultimately type 2 diabetes (T2D). This chronic inflammatory state contributes to long-term complications of diabetes, including non-alcoholic fatty liver disease (NAFLD), retinopathy, cardiovascular disease, and nephropathy, and may underlie the association of type 2 diabetes with other conditions such as Alzheimer's disease, polycystic ovarian syndrome, gout, and rheumatoid arthritis. Here, we review the current understanding of the mechanisms underlying inflammation in obesity, T2D, and related disorders. We discuss how chronic tissue inflammation results in IR, impaired insulin secretion, glucose intolerance, and T2D and review the effect of inflammation on diabetic complications and on the relationship between T2D and other pathologies. In this context, we discuss current therapeutic options for the treatment of metabolic disease, advances in the clinic and the potential of immune-modulatory approaches.

Published
2022

9. Canakinumab in patients with COVID-19 and type 2 diabetes – A multicentre, randomised, double-blind, placebo-controlled trial

Author

Hepprich, Matthias, Mudry, Jonathan M., Gregoriano, Claudia, Jornayvaz, Francois R., Carballo, Sebastian, Wojtusciszyn, Anne, Bart, Pierre-Alexandre, Chiche, Jean-Daniel, Fischli, Stefan, Baumgartner, Thomas, Cavelti-Weder, Claudia, Braun, Dominique L., Günthard, Huldrych F., Beuschlein, Felix, Conen, Anna, West, Emily, Isenring, Egon, Zechmann, Stefan, Bucklar, Gabriela, Aubry, Yoann, Dey, Ludovic, Müller, Beat, Hunziker, Patrick, Schütz, Philipp, Cattaneo, Marco, and Donath, Marc Y.

Published
2022
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10. The cephalic phase of insulin release is modulated by IL-1β

Author

Wiedemann, Sophia J., Trimigliozzi, Kelly, Dror, Erez, Meier, Daniel T., Molina-Tijeras, Jose Alberto, Rachid, Leila, Le Foll, Christelle, Magnan, Christophe, Schulze, Friederike, Stawiski, Marc, Häuselmann, Stéphanie P., Méreau, Hélène, Böni-Schnetzler, Marianne, and Donath, Marc Y.

Published
2022
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11. Type 1 diabetes: what is the role of autoimmunity in [beta] cell death?

Author

Donath, Marc Y.

Abstract

Current views on the pathogenesis of type 1 diabetes The current state of knowledge on the pathogenesis of type 1 diabetes proposes that insulin-producing [beta] cells become altered and destroyed [...], The current dogma of type 1 diabetes pathogenesis asserts that an autoimmune attack leads to the destruction of pancreatic [beta] cells, with subsequent hyperglycemia. This dogma is based on islet autoantibodies emerging prior to the onset of type 1 diabetes. In this issue of the JCI, Warncke et al. report on their investigation of the development of hyperglycemia below the diabetes threshold as an early proxy of [beta] cell demise. Surprisingly, they found that an elevation in blood glucose preceded the appearance of autoimmunity. This observation calls into question the importance of autoimmunity as the primary cause of [beta] cell destruction and has implications for prevention and treatment in diabetes.

Published
2022
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15. TNF-α inhibitors for type 1 diabetes: exploring the path to a pivotal clinical trial.

Author

Bazile, Cassandra, Abdel Malik, Magdy M., Ackeifi, Courtney, Anderson, Randy L., Beck, Roy W., Donath, Marc Y., Dutta, Sanjoy, Hedrick, Joseph A., Karpen, Stephen R., Kay, Thomas W. H., Marder, Thomas, Marinac, Marjana, McVean, Jennifer, Meyer, Robert, Pettus, Jeremy, Quattrin, Teresa, Verstegen, Ruud H. J., Vieth, Joshua A., and Latres, Esther

Subjects
TYPE 1 diabetes, TUMOR necrosis factors, YOUNG adults, TREND setters, INSULIN pumps
Abstract

Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of insulin-producing β-cells in the pancreas. This destruction leads to chronic hyperglycemia, necessitating lifelong insulin therapy to manage blood glucose levels. Typically diagnosed in children and young adults, T1D can, however, occur at any age. Ongoing research aims to uncover the precise mechanisms underlying T1D and to develop potential interventions. These include efforts to modulate the immune system, regenerate β-cells, and create advanced insulin delivery systems. Emerging therapies, such as closed-loop insulin pumps, stem cell-derived β-cell replacement and disease-modifying therapies (DMTs), offer hope for improving the quality of life for individuals with T1D and potentially moving towards a cure. Currently, there are no disease-modifying therapies approved for stage 3 T1D. Preserving β-cell function in stage 3 T1D is associated with better clinical outcomes, including lower HbA1c and decreased risk of hypoglycemia, neuropathy, and retinopathy. Tumor Necrosis Factor alpha (TNF-α) inhibitors have demonstrated efficacy at preserving β-cell function by measurement of C-peptide in two clinical trials in people with stage 3 T1D. However, TNF-α inhibitors have yet to be evaluated in a pivotal trial for T1D. To address the promising clinical findings of TNF-α inhibitors in T1D, Breakthrough T1D convened a panel of key opinion leaders (KOLs) in the field. The workshop aimed to outline an optimal clinical path for moving TNF-α inhibitors to a pivotal clinical trial in T1D. Here, we summarize the evidence for the beneficial use of TNF-α inhibitors in T1D and considerations for strategies collectively identified to advance TNF-α inhibitors beyond phase 2 clinical studies for stage 3 T1D. [ABSTRACT FROM AUTHOR]

Published
2024
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17. Continuing versus tapering glucocorticoids after achievement of low disease activity or remission in rheumatoid arthritis (SEMIRA): a double-blind, multicentre, randomised controlled trial

Author

Constantin, Arnaud, Gottenberg, Jacques Eric, Loiseau-Peres, Sylvie, Nguyen, Minh, Schaeverbeke, Thierry, Alten, Rieke H.-E., Amberger, Christopher, Biewer, Werner A., Boche, Konrad, Burmester, Gerd Ruediger, Engel, Andreas, Feuchtenberger, Martin, Fleck, Martin, Gauler, Georg, Heilig, Bernhard, Höhle, Maria, Iking-Konert, Christof, Kästner, Peter, Kofler, David, Krueger, Klaus, Kühne, Cornelia, Kurthen, Reiner, Schulze-Koops, Hendrik, Schwenke, Holger, Sieburg, Maren, Specker, Christof, Tony, Hans-Peter, Wassenberg, Siegfried, Wendler, Jörg, Caporali, Roberto, Epis, Oscar, Matucci-Cerinic, Marco, Salvarani, Carlo, Dubikov, Alexander, Kamalova, Rimma, Korolev, Maxim, I. Mazurov, Vadim, Puntus, Ekaterina, Damjanov, Nemanja, Ilic, Tatjana, Lazarevic, Milijanka, Milenkovic, Sasa, Petronijevic, Milan, Gabay, Cem, Bouajina, Elyes, Elleuch, Mohamed, Burmester, Gerd R, Buttgereit, Frank, Bernasconi, Corrado, Álvaro-Gracia, Jose M, Castro, Nidia, Dougados, Maxime, van Laar, Jacob M, Nebesky, Jan Michael, Pethoe-Schramm, Attila, Donath, Marc Y, and John, Markus R

Published
2020
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22. Effects of interleukin-1 receptor antagonism in women with polycystic ovary syndrome-- the FertIL trial.

Author

Wälchli-Popovic, Milica, Monnerat, Sophie, Taylor, Angela E., Gilligan, Lorna C., Schiffer, Lina, Arlt, Wiebke, Vogt, Deborah R., De Geyter, Christian, Hutter, Nina, Donath, Marc Y., Sartorius, Gideon, and Christ-Crain, Mirjam

Subjects
POLYCYSTIC ovary syndrome, TANDEM mass spectrometry, INTERLEUKIN-1 receptors, END of treatment, C-reactive protein
Abstract

Introduction: Chronic low-grade inflammation might contribute to hyperandrogenemia and metabolic complications in polycystic ovary syndrome (PCOS). The proinflammatory cytokine interleukin (IL)-1 stimulates androgen production from ovarian cells, whereas blockade of the IL-1 pathway improves cardiometabolic health. We aimed to investigate whether blocking the IL-1 pathway ameliorates hyperandrogenemia in patients with PCOS. Methods: This is a prospective, interventional, single-arm, proof-of-concept trial performed at a tertiary hospital in Switzerland (August 2018 to July 2020) in 18 premenopausal women with a diagnosis of PCOS according to the Rotterdam criteria, total testosterone levels ≥ 1.7 nmol/L, and C-reactive protein (CRP) ≥ 1.0 mg/L. Patients received 100 mg/day of the IL-1-receptor antagonist anakinra for 28 days and underwent weekly blood sampling until 1 week after the end of treatment. The primary endpoint was the change in serum androstenedione levels on day 7 of treatment, assessed with liquid chromatography--tandem mass spectrometry. Seven of these women participated in a subsequent observational sub-study (May 2021 to December 2021). Results: Median [interquartile range (IQR)] androstenedione increased by 0.5 [--0.1, 1.6] nmol/L (p = 0.048) with anakinra and by 1.3 [0.08, 2.4] nmol/L [p = 0.38] without anakinra between baseline and day 7. Anakinra reduced CRP levels on days 7, 21, and 28 (p < 0.001) but did not lead to an absolute reduction in androgens. However, four of six patients (67%) had smaller areas under the curves for androstenedione and/or testosterone during the 28-day intervention with anakinra as compared to 28 days without treatment. Discussion: Our findings suggest that anakinra suppresses IL-1-mediated chronic lowgrade inflammation in PCOS and might attenuate biochemical hyperandrogenemia. [ABSTRACT FROM AUTHOR]

Published
2024
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25. Interleukin-1 antagonism in type 1 diabetes of recent onset: two multicentre, randomised, double-blind, placebo-controlled trials

Author

Moran, Antoinette, Bundy, Brian, Becker, Dorothy J, DiMeglio, Linda A, Gitelman, Stephen E, Goland, Robin, Greenbaum, Carla J, Herold, Kevan C, Marks, Jennifer B, Raskin, Philip, Sanda, Srinath, Schatz, Desmond, Wherrett, Diane K, Wilson, Darrell M, Krischer, Jeffrey P, Skyler, Jay S, Group, for the Type 1 Diabetes TrialNet Canakinumab Study, Pickersgill, Linda, de Koning, Eelco, Ziegler, Anette-G, Böehm, Bernhard, Badenhoop, Klaus, Schloot, Nanette, Bak, Jens Friis, Pozzilli, Paolo, Mauricio, Didac, Donath, Marc Y, Castaño, Luis, Wägner, Ana, Lervang, Hans Henrik, Perrild, Hans, Mandrup-Poulsen, Thomas, and Group, for the AIDA Study

Subjects
Clinical Trials and Supportive Activities, Clinical Research, Diabetes, Autoimmune Disease, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Metabolic and endocrine, Adolescent, Adult, Analysis of Variance, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, C-Peptide, Child, Diabetes Mellitus, Type 1, Double-Blind Method, Female, Humans, Hypoglycemic Agents, Immunologic Factors, Insulin-Secreting Cells, Interleukin 1 Receptor Antagonist Protein, Interleukin-1, Male, Treatment Outcome, Young Adult, Type 1 Diabetes TrialNet Canakinumab Study Group, AIDA Study Group, Medical and Health Sciences, General & Internal Medicine
Abstract

BackgroundInnate immunity contributes to the pathogenesis of autoimmune diseases, such as type 1 diabetes, but until now no randomised, controlled trials of blockade of the key innate immune mediator interleukin-1 have been done. We aimed to assess whether canakinumab, a human monoclonal anti-interleukin-1 antibody, or anakinra, a human interleukin-1 receptor antagonist, improved β-cell function in recent-onset type 1 diabetes.MethodsWe did two randomised, placebo-controlled trials in two groups of patients with recent-onset type 1 diabetes and mixed-meal-tolerance-test-stimulated C peptide of at least 0·2 nM. Patients in the canakinumab trial were aged 6-45 years and those in the anakinra trial were aged 18-35 years. Patients in the canakinumab trial were enrolled at 12 sites in the USA and Canada and those in the anakinra trial were enrolled at 14 sites across Europe. Participants were randomly assigned by computer-generated blocked randomisation to subcutaneous injection of either 2 mg/kg (maximum 300 mg) canakinumab or placebo monthly for 12 months or 100 mg anakinra or placebo daily for 9 months. Participants and carers were masked to treatment assignment. The primary endpoint was baseline-adjusted 2-h area under curve C-peptide response to the mixed meal tolerance test at 12 months (canakinumab trial) and 9 months (anakinra trial). Analyses were by intention to treat. These studies are registered with ClinicalTrials.gov, numbers NCT00947427 and NCT00711503, and EudraCT number 2007-007146-34.FindingsPatients were enrolled in the canakinumab trial between Nov 12, 2010, and April 11, 2011, and in the anakinra trial between Jan 26, 2009, and May 25, 2011. 69 patients were randomly assigned to canakinumab (n=47) or placebo (n=22) monthly for 12 months and 69 were randomly assigned to anakinra (n=35) or placebo (n=34) daily for 9 months. No interim analyses were done. 45 canakinumab-treated and 21 placebo-treated patients in the canakinumab trial and 25 anakinra-treated and 26 placebo-treated patients in the anakinra trial were included in the primary analyses. The difference in C peptide area under curve between the canakinumab and placebo groups at 12 months was 0·01 nmol/L (95% CI -0·11 to 0·14; p=0·86), and between the anakinra and the placebo groups at 9 months was 0·02 nmol/L (-0·09 to 0·15; p=0·71). The number and severity of adverse events did not differ between groups in the canakinumab trial. In the anakinra trial, patients in the anakinra group had significantly higher grades of adverse events than the placebo group (p=0·018), which was mainly because of a higher number of injection site reactions in the anakinra group.InterpretationCanakinumab and anakinra were safe but were not effective as single immunomodulatory drugs in recent-onset type 1 diabetes. Interleukin-1 blockade might be more effective in combination with treatments that target adaptive immunity in organ-specific autoimmune disorders.FundingNational Institutes of Health and Juvenile Diabetes Research Foundation.

Published
2013

31. Interleukin-33-Activated Islet-Resident Innate Lymphoid Cells Promote Insulin Secretion through Myeloid Cell Retinoic Acid Production

Author

Dalmas, Elise, Lehmann, Frank M., Dror, Erez, Wueest, Stephan, Thienel, Constanze, Borsigova, Marcela, Stawiski, Marc, Traunecker, Emmanuel, Lucchini, Fabrizio C., Dapito, Dianne H., Kallert, Sandra M., Guigas, Bruno, Pattou, Francois, Kerr-Conte, Julie, Maechler, Pierre, Girard, Jean-Philippe, Konrad, Daniel, Wolfrum, Christian, Böni-Schnetzler, Marianne, Finke, Daniela, and Donath, Marc Y.

Published
2017
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39. Glucocorticoid withdrawal and glucocorticoid-induced adrenal insufficiency: Study protocol of the randomized controlled «TOASST' (Taper Or Abrupt Steroid STop) multicenter trial

Author

Komminoth, Mathis; https://orcid.org/0000-0002-0024-6284, Donath, Marc Y, Hepprich, Matthias; https://orcid.org/0000-0002-6905-6235, Schuetz, Philipp, Blum, Claudine A; https://orcid.org/0000-0003-0487-5587, Mueller, Beat, Reny, Jean-Luc, Gosselin, Pauline, Breville, Gautier; https://orcid.org/0000-0003-0890-1981, Brändle, Michael, Henzen, Christoph, Leuppi, Jörg D, Kistler, Andreas D; https://orcid.org/0000-0002-4114-9560, Thurnheer, Robert, Beuschlein, Felix, Rudofsky, Gottfried, Aeberli, Daniel, Villiger, Peter M, Böhm, Stephan, Chifu, Irina; https://orcid.org/0000-0002-6741-2689, Fassnacht, Martin, Meyer, Gesine, Bojunga, Jörg, Cattaneo, Marco; https://orcid.org/0000-0002-6610-8431, Sluka, Constantin; https://orcid.org/0000-0001-7672-4986, Schneider, Helga, Rutishauser, Jonas, «TOASST» study group, Komminoth, Mathis; https://orcid.org/0000-0002-0024-6284, Donath, Marc Y, Hepprich, Matthias; https://orcid.org/0000-0002-6905-6235, Schuetz, Philipp, Blum, Claudine A; https://orcid.org/0000-0003-0487-5587, Mueller, Beat, Reny, Jean-Luc, Gosselin, Pauline, Breville, Gautier; https://orcid.org/0000-0003-0890-1981, Brändle, Michael, Henzen, Christoph, Leuppi, Jörg D, Kistler, Andreas D; https://orcid.org/0000-0002-4114-9560, Thurnheer, Robert, Beuschlein, Felix, Rudofsky, Gottfried, Aeberli, Daniel, Villiger, Peter M, Böhm, Stephan, Chifu, Irina; https://orcid.org/0000-0002-6741-2689, Fassnacht, Martin, Meyer, Gesine, Bojunga, Jörg, Cattaneo, Marco; https://orcid.org/0000-0002-6610-8431, Sluka, Constantin; https://orcid.org/0000-0001-7672-4986, Schneider, Helga, Rutishauser, Jonas, and «TOASST» study group

Abstract

BACKGROUND Despite the widespread use of glucocorticoids in inflammatory and autoimmune disorders, there is uncertainty about the safe cessation of long-term systemic treatment, as data from prospective trials are largely missing. Due to potential disease relapse or glucocorticoid-induced hypocortisolism, the drug is often tapered to sub-physiological doses rather than stopped when the underlying disease is clinically stable, increasing the cumulative drug exposure. Conversely, the duration of exposure to glucocorticoids should be minimized to lower the risk of side effects. METHODS We designed a multicenter, randomized, triple-blinded, placebo-controlled trial to test the clinical noninferiority of abrupt glucocorticoid stop compared to tapering after ≥28 treatment days with ≥420 mg cumulative and ≥7.5 mg mean daily prednisone-equivalent dose. 573 adult patients treated systemically for various disorders will be included after their underlying disease has been stabilized. Prednisone in tapering doses or matching placebo is administered over 4 weeks. A 250 mg ACTH-test, the result of which will be revealed a posteriori, is performed at study inclusion; all patients are instructed on glucocorticoid stress cover dosing. Follow-up is for 6 months. The composite primary outcome measure is time to hospitalization, death, initiation of unplanned systemic glucocorticoid therapy, or adrenal crisis. Secondary outcomes include the individual components of the primary outcome, cumulative glucocorticoid doses, signs and symptoms of hypocortisolism, and the performance of the ACTH test in predicting the clinical outcome. Cox proportional hazard, linear, and logistic regression models will be used for statistical analysis. CONCLUSION This trial aims to demonstrate the clinical noninferiority and safety of abrupt treatment cessation after ≥28 days of systemic glucocorticoid therapy in patients with stabilized underlying disease. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NC

Published
2023

40. A human antibody against pathologic IAPP aggregates protects beta cells in type 2 diabetes models

Author

Wirth, Fabian; https://orcid.org/0000-0001-6458-1893, Heitz, Fabrice D, Seeger, Christine, Combaluzier, Ioana, Breu, Karin, Denroche, Heather C; https://orcid.org/0000-0002-0976-2656, Thevenet, Julien; https://orcid.org/0000-0001-6873-8640, Osto, Melania; https://orcid.org/0000-0002-7176-3684, Arosio, Paolo; https://orcid.org/0000-0002-2740-1205, Kerr-Conte, Julie; https://orcid.org/0000-0002-7590-1896, Verchere, C Bruce, Pattou, François; https://orcid.org/0000-0001-8388-3766, Lutz, Thomas A; https://orcid.org/0000-0002-5056-8548, Donath, Marc Y; https://orcid.org/0000-0002-3143-5045, Hock, Christoph, Nitsch, Roger M, Grimm, Jan; https://orcid.org/0000-0002-3898-3298, Wirth, Fabian; https://orcid.org/0000-0001-6458-1893, Heitz, Fabrice D, Seeger, Christine, Combaluzier, Ioana, Breu, Karin, Denroche, Heather C; https://orcid.org/0000-0002-0976-2656, Thevenet, Julien; https://orcid.org/0000-0001-6873-8640, Osto, Melania; https://orcid.org/0000-0002-7176-3684, Arosio, Paolo; https://orcid.org/0000-0002-2740-1205, Kerr-Conte, Julie; https://orcid.org/0000-0002-7590-1896, Verchere, C Bruce, Pattou, François; https://orcid.org/0000-0001-8388-3766, Lutz, Thomas A; https://orcid.org/0000-0002-5056-8548, Donath, Marc Y; https://orcid.org/0000-0002-3143-5045, Hock, Christoph, Nitsch, Roger M, and Grimm, Jan; https://orcid.org/0000-0002-3898-3298

Abstract

In patients with type 2 diabetes, pancreatic beta cells progressively degenerate and gradually lose their ability to produce insulin and regulate blood glucose. Beta cell dysfunction and loss is associated with an accumulation of aggregated forms of islet amyloid polypeptide (IAPP) consisting of soluble prefibrillar IAPP oligomers as well as insoluble IAPP fibrils in pancreatic islets. Here, we describe a human monoclonal antibody selectively targeting IAPP oligomers and neutralizing IAPP aggregate toxicity by preventing membrane disruption and apoptosis in vitro. Antibody treatment in male rats and mice transgenic for human IAPP, and human islet-engrafted mouse models of type 2 diabetes triggers clearance of IAPP oligomers resulting in beta cell protection and improved glucose control. These results provide new evidence for the pathological role of IAPP oligomers and suggest that antibody-mediated removal of IAPP oligomers could be a pharmaceutical strategy to support beta cell function in type 2 diabetes.

Published
2023

41. Randomized, Double-Blind, Placebo-Controlled Crossover Trial of Once Daily Empagliflozin 25 mg for the Treatment of Postprandial Hypoglycemia After Roux-en-Y Gastric Bypass

Author

Ferreira, Antonio, Schönenberger, Katja A; https://orcid.org/0000-0002-2122-4746, Potoczna, Natascha, Vogt, Andreas, Gerber, Philipp A, Zehetner, Jörg, Giachino, Daniel, Nett, Philipp, Gawinecka, Joanna, Cossu, Luca; https://orcid.org/0000-0002-8804-0722, Fuster, Daniel G, Dalla Man, Chiara, Facchinetti, Andrea, Melmer, Andreas, Nakas, Christos T, Hepprich, Matthias, Donath, Marc Y, Herzig, David, Bally, Lia; https://orcid.org/0000-0003-1993-7672, Ferreira, Antonio, Schönenberger, Katja A; https://orcid.org/0000-0002-2122-4746, Potoczna, Natascha, Vogt, Andreas, Gerber, Philipp A, Zehetner, Jörg, Giachino, Daniel, Nett, Philipp, Gawinecka, Joanna, Cossu, Luca; https://orcid.org/0000-0002-8804-0722, Fuster, Daniel G, Dalla Man, Chiara, Facchinetti, Andrea, Melmer, Andreas, Nakas, Christos T, Hepprich, Matthias, Donath, Marc Y, Herzig, David, and Bally, Lia; https://orcid.org/0000-0003-1993-7672

Abstract

Aims: To investigate the effect of empagliflozin on glucose dynamics in individuals suffering from postbariatric hypoglycemia (PBH) after Roux-en-Y gastric bypass (RYGB). Methods: Twenty-two adults with PBH after RYGB were randomized to empagliflozin 25 mg or placebo once daily over 20 days in a randomized, double-blind, placebo-controlled, crossover trial. The primary efficacy outcome was the amplitude of plasma glucose excursion (peak to nadir) during a mixed-meal tolerance test (MMTT). Outcomes of the outpatient period were assessed using continuous glucose monitoring (CGM) and an event-tracking app. Results: The amplitude of glucose excursion during the MMTT was 8.1 ± 2.4 mmol/L with empagliflozin versus 8.1 ± 2.6 mmol/L with placebo (mean ± standard deviation, P = 0.807). CGM-based mean amplitude of glucose excursion during the 20-day period was lower with empagliflozin than placebo (4.8 ± 1.3 vs. 5.2 ± 1.6. P = 0.028). Empagliflozin reduced the time spent with CGM values >10.0 mmol/L (3.8 ± 3.5% vs. 4.7 ± 3.8%, P = 0.009), but not the time spent with CGM values <3.0 mmol/L (1.7 ± 1.6% vs. 1.5 ± 1.5%, P = 0.457). No significant difference was observed in the quantity and quality of recorded symptoms. Eleven adverse events occurred with empagliflozin (three drug-related) and six with placebo. Conclusions: Empagliflozin 25 mg reduces glucose excursions but not hypoglycemia in individuals with PBH.

Published
2023

45. A guiding map for inflammation

Author

Netea, Mihai G, Balkwill, Frances, Chonchol, Michel, Cominelli, Fabio, Donath, Marc Y, Giamarellos-Bourboulis, Evangelos J, Golenbock, Douglas, Gresnigt, Mark S, Heneka, Michael T, Hoffman, Hal M, Hotchkiss, Richard, Joosten, Leo A B, Kastner, Daniel L, Korte, Martin, Latz, Eicke, Libby, Peter, Mandrup-Poulsen, Thomas, Mantovani, Alberto, Mills, Kingston H G, Nowak, Kristen L, O'Neill, Luke A, Pickkers, Peter, van der Poll, Tom, Ridker, Paul M, Schalkwijk, Joost, Schwartz, David A, Siegmund, Britta, Steer, Clifford J, Tilg, Herbert, van der Meer, Jos W M, van de Veerdonk, Frank L, and Dinarello, Charles A

Published
2017
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46. Author Correction: A guiding map for inflammation

Author

Netea, Mihai G., Balkwill, Frances, Chonchol, Michel, Cominelli, Fabio, Donath, Marc Y., Giamarellos-Bourboulis, Evangelos J., Golenbock, Douglas, Gresnigt, Mark S., Heneka, Michael T., Hoffman, Hal M., Hotchkiss, Richard, Joosten, Leo A. B., Kastner, Daniel L., Korte, Martin, Latz, Eicke, Libby, Peter, Mandrup-Poulsen, Thomas, Mantovani, Alberto, Mills, Kingston H. G., Nowak, Kristen L., O’Neill, Luke A., Pickkers, Peter, van der Poll, Tom, Ridker, Paul M., Schalkwijk, Joost, Schwartz, David A., Siegmund, Britta, Steer, Clifford J., Tilg, Herbert, van der Meer, Jos W. M., van de Veerdonk, Frank L., and Dinarello, Charles A.

Published
2021
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