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Pancreatic Islets and Diabetes mellitus

The pancreatic islets are cell aggregates of different hormone-secreting endocrine cell types. Their physiologic role is to regulate blood glucose concentrations. The alpha cells (in blue) secrete the hormone glucagon, which temporarily raises the blood glucose. In contrast, the beta cells (in violet) secrete insulin, a vital hormone, to lower the blood glucose concentration. Other endocrine cell types exist in lower numbers and also contribute to glucose metabolism. In pancreatic islets, secretion defects, cell death, and dedifferentiation of the beta cells result in diabetes mellitus. This likely applies to both type 1 (also known as juvenile) and type 2 (also known as adult-onset) diabetes. According to the International Diabetes Federation (IDF), more than 400 million people are currently affected by diabetes worldwide.

Type 1 Diabetes
In general (with few exceptions), diabetes mellitus is a chronic disease, in which individuals can never be cured. This holds particularly true for type 1 diabetes. Here, beta cells are destroyed during an autoimmune reaction and fail to regenerate. We believe that we can interfere with the chronic nature of type 1 diabetes during a specific time called the Honeymoon-Phase. At this time, the newly-diagnosed individual experiences a temporary reduction of the insulin demand, likely due to existing functional beta cells.
Motivated by the goal to improve the situation for individuals with type 1 diabetes, we collaborate with the Department of General Pediatrics in order to explore a pharmacologic approach to maintain their beta cells.   

Type 2 Diabetes
This type of diabetes is often preceded by insulin resistance caused by obesity and a sedentary lifestyle. The insulin resistance challenges the pancreatic beta cells by stimulating increasingly higher insulin production over time. After some time, the islet cells develop secretion defects (besides beta cell death and dedifferentiation). Consequently, blood glucose concentration increases and diabetes is diagnosed.

In collaboration with the Institute for Clinical Diabetology at the German Diabetes Center, we study the development of insulin resistance. Most importantly, we aim to normalize insulin release and optimize blood glucose homeostasis in type 2 diabetes with the help of novel pharmacologic approaches. We also aim to prevent diabetes progression after diagnosis. To this end, we collaborate with the Institute of Beta Cell Biology at the German Diabetes Center, scientists at the German Center for Diabetes Research e.V., the Department of General Pediatrics, the Institute of Neuro- and Sensory Physiology, and the Profil Institute.


Lammert & Zeeb, Metabolism of Human Diseases, Springer-Verlag Wien 2014
International Diabetes Federation (IDF) Diabetes Atlas -7th Edition

Otter & Lammert, Trends Endocrinol Metab 2015

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