The so-called incretin hormones, GIP (short for glucose-dependent insulin-releasing polypeptide) and GLP-1 (glucagon-like peptide 1), are produced in the intestine after ingestion of a meal, and are transported via the circulation to the pancreas. There they stimulate the synthesis and secretion of insulin by binding to specific receptor molecules on the beta cells. GLP-1 has already proven effective in the treatment of diabetes. GIP, on the other hand, has shown very limited efficacy in patients with diabetes, and whether this lack of responsiveness is a cause or a consequence of the diabetic condition itself remains controversial. "In our genetically modified (transgenic) pigs, which produce a partially defective GIP receptor, the response to GIP is also very weak", reports Dr. Simone Renner, who is first author on the new publication and research associate at the chair for Molecular Animal Breeding and Biotechnology. "Our results suggest that inability to respond to GIP leads not only to a fall in glucose utilization and insulin secretion, but is also associated with a reduction in the mass of beta cells in the pancreas. This would argue that impaired response to GIP is more likely to be a cause rather than a consequence of diabetes. We hope that our model will help to accelerate the translation of the latest research findings into clinical applications."
The pig is a particularly suitable model, because its metabolism and physiology closely resemble our own. The transgenic pigs not only display a weak response to GIP, they also display other traits that are typical of type 2 diabetes in humans. For instance, the efficiency of both glucose utilization and insulin secretion falls off with increasing age, as in humans. The number of insulin-producing beta cells in the pancreas is also lower t
|Contact: Prof. Dr. Eckhard Wolf|