Publications of the PLID

Here you can find all articles of PLID scientists that were published within the last 5 years. By law we are prevented from posting the pdf files of recent publications on our website.
Please contact us directly if you are interested in a reprint. Thank you.

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Featured Publications

Graphical Abstract Panzer et a. JCI insights

New approach to study human pancreas pathogenesis in the development and progression of T1D

In type 1 diabetes (T1D), autoimmune destruction of pancreatic beta cells leads to insulin deficiency and loss of glycemic control. However, knowledge about pathophysiology in T1D remains incomplete, also due to a lack of technologies to study the live human pancreas in T1D.

Mass or function - PLID scientists provide new puzzle piece for the controversial debate on early type-2 diabetes pathogenesis

Type-2 diabetes (T2D) is characterized by peripheral insulin resistance and insufficient insulin release from pancreatic islet beta cells. However, it is still unclear if the inadequate insulin levels during T2D development are the result of beta cell dysfunction and/or loss of beta cell numbers.

How insulin interacts with its receptor

One goal of modern diabetes research is to improve the effect of therapeutic insulin on the body. In a new study, the researchers have now solved a critical part of the puzzle by showing how insulin interacts with its receptor at a second binding site.

Graphical Abstract Binger et al.2019 PNAS

International research team identified new important player in insulin homeostasis

Researchers from La Trobe University in Australia and the PLID have identified that the protein Atp6ap2 is essential for the correct functioning of pancreatic beta cells. When this protein was switched off in the beta cells of mice their blood glucose levels dramatically increased.

Metabolically phenotyped surgical patients represent a novel and complementary source of pancreatic tissue for diabetes research

Contemporary research of beta cell biology in context of type-2 diabetes is based mainly on the long-standing technique for isolation of the pancreatic islets of Langerhans. Scientists of the PLID developed a new approach to isolate islets from snap frozen surgical specimens donated by metabolically phenotyped pancreatectomized patients. A new review article published in “Molecular Metabolism” explains how this platform may represent a paradigmatic shift for the study of human islets and diabetes research.

Widespread disease diabetes: Why do beta cells refuse to release insulin?

Researchers from PLID together with colleagues from Imperial College London and other research institutes from the UK, Canada and Italy have observed amazing cell interactions: The beta cells of the pancreas work as highly-connected clusters, known as islets, and their responses to rising blood glucose levels are coordinated by small teams of “leader cells”. To show that, the research teams developed an innovative imaging technique which allowed them to observe beta cells’ hierarchical relationship in live animals including in zebrafish and mouse.

New drug reduces risk of death in patients with type 2 diabetes

In Germany, about one in ten people suffer from diabetes and diabetes patients still die two to three times more frequently from cardiovascular diseases such as heart attacks and strokes. Newly developed drugs for diabetes therapy are therefore expected to reduce the number of cardiovascular deaths. Scientists from the PLID have, together with international colleagues, investigated for the first time whether semaglutide in tablet form leads to a reduction in cardiovascular events. An international, randomized double-blind study with 3,183 participants was therefore conducted in 21 countries in parallel.

Better efficacy of an orally available GLP-1 agonist compared to DPP-IV inhibitor

With the participation of researchers from the PLID, a GLP-1 receptor agonist in the form of tablets could for the first time be compared with the most common second-line therapy of T2D, a DPP-IV inhibitor. The results of the PIONEER-3 trial have now been published in the renowned journal ´Journal of the American Medical Association (JAMA)´.

Publikation_Grzybek_AdiposeTissueLipidomics

New shotgun lipidomics method for molecular profiling of adipose tissue

Scientists from PLID, University Hospital Carl Gustav Carus and Lipotype GmbH joined their forces and developed a new shotgun lipidomics method for the molecular profiling of brown and white adipose tissue.

How a protein promotes the healing of inflammation

Inflammatory processes are a natural defense reaction of the immune system against pathogens. If they get out of control, they can however lead to diseases themselves. The protein DEL-1, is a central actor that ensures that excessive inflammation subsides. Scientists from the Medical Faculty Carl Gustav Carus of the TU Dresden and the National Center for Tumor Diseases Dresden (NCT/UCC), together with an international team of researchers, were able to demonstrate the importance and basic function of this protein.

How the insulin receptor works

Scientists at PLID have found out how cells react to insulin. It was previously known that insulin transmits a signal through receptors on the cell surface, however the Coskun group was now able to observe a change in the shape of the receptors.

Largest collection of islet cells reveals new diabetes genes

A collaborative study has identified a novel cluster of dysregulated genes in the pancreatic islets of patients with type 2 diabetes. The study is part of the EU-Innovative Medicine Initiative (IMI) research consortium IMIDIA.

Rainbow colors reveal cell history

Dr. Nikolay Ninov and his group developed a system called “Beta-bow”, which allows the history of β-cells to be traced by genetic bar-coding and multicolor imaging.

Pancreas lineage allocation and specification

Sphingosine-1-phosphate has a key role in mouse pancreas progenitor survival and the generation of the endocrine and acinar lineages. S1p signaling promotes endocrine specification by stabilizing YAP and attenuating Notch signaling.

Recent Publications

Here you can find the 10 latest publications of our institute. If you are looking for older publications, please follow the link below to our publications form 2013 until today.

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Kaptan et al., Exogenous ethanol induces a metabolic switch that prolongs the survival of Caenorhabditis elegans dauer larva and enhances its resistance to desiccation. Aging Cell. 2020 Sep 8:e13214. doi: 10.1111/acel.13214.
Vasiljević et al., The making of insulin in health and disease. Diabetologia. 2020 Oct;63(10):1981-1989. doi: 10.1007/s00125-020-05192-7
Höfner et al., Tolerance of Stored Boar Spermatozoa to Autologous Seminal Plasma: A Proteomic and Lipidomic Approach. Int J Mol Sci. 2020 Sep 4;21(18):E6474. doi: 10.3390/ijms21186474.
Hollstein et al., Autoantibody-negative insulin-dependent diabetes mellitus after SARS-CoV-2 infection: a case report. Nat Metab. 2020 Sep 2. doi: 10.1038/s42255-020-00281-8.
Bornstein et al., New Horizons: Novel Adrenal Regenerative Therapies. J Clin Endocrinol Metab. 2020 Sep 1;105(9):dgaa438. doi: 10.1210/clinem/dgaa438.
Buitinga et al., Non-Invasive Monitoring of Glycemia-Induced Regulation Of GLP-1R Expression in Murine and Human Islets of Langerhans. Diabetes. 2020 Aug 25:db200616. doi: 10.2337/db20-0616.
Stefanovic et al., Hox-dependent coordination of mouse cardiac progenitor cell patterning and differentiation. Elife. 2020 Aug 17;9:e55124. doi: 10.7554/eLife.55124.
Bornstein et al., Management of diabetes in patients with COVID-19 - Authors' reply. Lancet Diabetes Endocrinol. 2020 Aug;8(8):669-670. doi: 10.1016/S2213-8587(20)30223-0.
Pinkert et al., Development of a new mouse model for coxsackievirus-induced myocarditis by attenuating coxsackievirus B3 virulence in the pancreas. Cardiovasc Res. 2020 Aug 1;116(10):1756-1766. doi: 10.1093/cvr/cvz259.
Qadir et al., Publisher Correction: Long-term culture of human pancreatic slices as a model to study real-time islet regeneration. Nat Commun. 2020 Jul 22;11(1):3742. doi: 10.1038/s41467-020-17574-x.