Type 2 diabetes (T2D) is associated with metabolic inflexibility during not only food intake, but also during exercise. Furthermore, substrate recruitment from adipose tissue and liver is essential during challenges like exercise and fasting. However, knowledge of the underlying mechanisms behind exercise- and fasting-induced regulation of liver and adipose tissue metabolism and substrate recruitment during metabolic challenges as well as the alterations with T2D is limited.
The endocrine pancreas plays a key role in regulating the nutrient uptake and metabolism. The pancreatic β-cells respond to nutrients in the blood by increasing the insulin secretion, which in turn increases the storage of nutrients.
Exercise elicits phenotypic alterations in skeletal muscle which impact positively on muscle function and metabolic health. Many of these adaptations are orchestrated by AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTORC)1, but the subcellular locations of the signaling and its exact molecular links to Diabetes-relevant downstream processes such as autophagy and mitochondrial function remain unclear.
Dual-hormone treatment with insulin and low-dose glucagon is a sparsely explored area except in artificial pancreas (automated) systems. However, dual-hormone treatment has the potential to improve the quality of life and glycemic control in a majority of patients with type 1 diabetes, including both patients treated with multiple daily insulin injections and with insulin pumps. Stable, liquid glucagon formulations with similar action profile as the current unstable glucagon products are under development by more companies including our collaborator Zealand Pharma.
In vitro produced pancreatic β-cells are a potential source for cell replacement therapies, but in order to produce safe cells for therapeutic purposes the biology underlying β-cell specification should be addressed. The objective of this project is to determine the mechanisms underlying pancreatic endocrine lineage allocation with focus on the principal endocrine lineages involved in glucose homeostasis, the α- and β-cell lineages.
Type 2 diabetes is a widespread and escalating disease worldwide. It is associated with a physiological inability to handle glucose, which leads to disease in the heart, vasculature, nerves, kidneys and eyes. Fatty liver disease is also closely related to diabetes.
Background: Obesity and type 2 diabetes represent a world-wide problem and their treatment is a growing concern. Roux-en-Y gastric bypass surgery (RYGB) is currently the most successful treatment with diabetes remission rates of 50-80 % and weight loss of 30% in obese individuals. Most importantly, mortality is reduced about 30 %. These results show that there are mechanisms within our own body that can cure diabetes and obesity.
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