Vivid follows an interdisciplinary approach to investigate mechanisms involved in the early steps of diabetes development, interconnecting different disciplines of life sciences including biochemistry, biology, molecular biology, pharmacology, pediatrics, endocrinology and diabetology.
Outline of the different projects
Maternal overweigt is a strong risk factors for type 2 diabetes in the offspring. This project investigates the underlying mechanisms of prenatal programming of liver and adipose cells in a peri-conceptional diabetogenic environment.
Bone marrow adipose tissue (MAT) is a distinct specialized compartment contributing to systemic metabolism. The project studies the role of MAT in the early development of insulin resistance.
Changes in oxidative phosphorylation and formation of mitochondrial cristae and crista junctions have been implicated in the pathogenesis of type 2 diabetes. The project focuses on these processes and their role in the progression of insulin resistance.
An impaired balance of glucose and fatty acids as energy source in skeletal muscle is an early indicator of insulin resistance and diabetes. The project analyzes the impact of early nutritional challenges on energy substrate preference and metabolic health.
Type 2 diabetes is accompanied by a chronic, low-grade metabolic inflammation (‘meta-inflammation’) which may already occur in early developmental stages and impact metabolism and disease progression throughout different stages of life. The project investigates the role of different (IL)-6 signaling routes and their role in diet-induced meta-inflammation early in life.
Physical exercise improves skeletal muscle insulin sensitivity. The project aims at identifying novel exercise-associated regulatory factors, cytokines/myokines and metabolites that explain the diabetes-protective effect.
Blockade of N-methyl-D-aspartate (NMDA) receptors has been shown to improve insulin secretion and survival of beta cells. The project aims to elucidate the molecular mechanism of NMDA receptor signaling, its modulation by inflammatory cytokines and protective effect of antagonists.