The Molecular Traumatology Group investigates the molecular and cellular bases of clinically relevant questions in musculoskeletal surgery, focusing on pharmacologically exploitable signaling events.
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Trauma and Obesity (Leptin)
Frank Graef, Ricarda Seemann, Serafeim Tsitsilonis
In contrast to the long-held belief of bone being a sole organ of locomotion we now know that it is also an endocrine organ which is tightly integrated in energy metabolism. Bone is able to influence insulin and glucose homeostasis via insulin and sympathetic signaling pathways in osteoblasts and a leptin-related feedback mechanism. This is important since patients with diabetes are known to have impaired bone healing. Leptin is an adipocyte-derived hormone which is essential for bone healing. Our research group could show that mice lacking the hormone leptin have impaired fracture healing. Moreover, leptin seems to be major signaling factor increasing callus formation in fracture healing after traumatic brain injury. Our studies focus on the morphological and molecular changes of obesity and deficiency or resistance of leptin on bone and its implications in fracture healing.
PCT and Obesity (Calca)
Jessika Appelt, Paul Köhli, Johannes Keller, Serafeim Tsitsilonis
Metabolic diseases such as obesity and diabetes mellitus (DM) are evolving to a pandemic. Being a main risk factor for myocardial infarction, arterial hypertension, early death and impaired healing after trauma, sufficient treatment could improve general health and recovery after trauma of affected patients. Obesity and DM are associated with a state of chronic low-grade inflammation, which is suspected to be a potential mediator in disease progression and development of accompanying diseases. PCT, a marker of systemic inflammation, has been shown to be elevated in patients with metabolic syndrome. Our recent studies in a genetic model of PCT-inactivation subjected to high fat diet revealed an improved glucose-tolerance, a reduced weight-gain and a reduction of inflammatory state. Thus, we aim to analyze the molecular mechanisms underlying this phenomenon, identify the relevant biologic PCT-receptor in metabolic diseases, and target it pharmacologically to improve general health and trauma-recovery of affected patients.