Obesity; Type 2 Diabetes; Weight loss; Incretin hormones; Glucose-dependent insulinotropic polypeptide (GIP); Glucagon-like peptide 1 (GLP-1); Gut hormones; Enteroendocrine cells; Pancreatic alpha and beta cell secretion. 

To clarify additional core mechanisms in type 2 diabetes pathophysiology, our scientific efforts within the next years encompass studies on the role of the gastrointestinal tract in human physiology and diabetic pathophysiology.

Hepatic steatosis glucagon resistance

Obese and/or prediabetic individuals are also characterised by fasting hyperglucagonaemia and increased hepatic glucose production, supporting the view that glucagon secretory abnormalities constitute an early part of the type 2 diabetic pathophysiology. In individuals with fasting hyperglucagonaemia, the hepatic sensitivity to glucagon may be compromised due to hepatic steatosis and perhaps provide a feedback mechanism acting on the level of pancreatic alpha cells. If true, our ‘steatosis-induced glucagon resistance hypothesis’ would constitute a parallel to the obesity-induced insulin resistance in muscle and liver tissue

Hypo-Heart

Many patients with diabetes will die or be disabled as a consequence of vascular complications. Prospective studies have shown continuous associations of improved glycaemic control with the risk of major vascular events. We think that patients with type 2 diabetes have clinically relevant, but often unrecognised, episodes of arrhythmias, which correlate to episodes of hypoglycaemia. Also, we think that hypoglycaemia may identify patients at higher risk of adverse cardiovascular events.