Inulin might exceed incretin based drugs in the treatment of type 2 diabetes mellitus

Abstract

Glucagon hormone being catabolic and hyperglycemic, it acts in an opposite manner to insulin and adds to insulin resistance. The oligosaccharide inulin fructans is indigestible in the small bowel. When it reaches the large intestine, it encourages beneficial microbacteria strains. These latter produce certain peptides which when absorbed they reach the endlocrine L-cells of the small gut. These peptides stimulate L-cells to release glucagon like peptide 1 (GLP-1) which suppresses glucagon and stimulates insulin secretion in a glucose dependant manner. Our aim is to find how inulin suppresses glucagon and to what extent this improves insulin resistance. Fasting serum glucagon and homeostasis model assessment for insulin resistance (HOMA-IR) were estimated in 28 type 2 diabetic female patients before and after twenty one days of daily inulin intake. Fasting serum glucagon and HOMA-IR decreased significantly after the inulin intake period. In conclusion inulin stimulates the release of GLP-1. This acts in a glucose dependant manner thus simulating the novel incretin based drugs in reducing insulin resistance. However, owing to inulin other actions on insulin resistance, it might exceed these novel drugs.