Drugs stimulating insulin secretion in early clinical development for the treatment of type 1 diabetes: what's new?

Abstract

Introduction: Type 1 diabetes is a chronic autoimmune condition characterized by the selective destruction of insulin-producing beta cells in the pancreas. The etiology of T1D is multifactorial, with a combination of genetic susceptibility and environmental triggers believed to underlie beta-cell destruction. Preserving and prolonging beta-cell function in T1D is a pivotal therapeutic objective that can mitigate disease progression and improve glycemic control.

Areas covered: Insulin secretagogues have long been used in the management of type 2 diabetes, but do not have a significant beneficial effect in individuals with long-standing type 1 diabetes. Enhancement of beta-cell function early in the course of type 1 diabetes may offer important benefits in glycemic control and reduced hypoglycemia risk. Glucagon-like peptide-1 receptor agonists, glucokinase activators, free fatty acid receptor agonists, and glimins are drug classes which may offer benefit in enhancing insulin secretion in individuals with type 1 diabetes.

Expert opinion: Drugs which enhance insulin secretion in individuals may offer clinical benefits to individuals with type 1 diabetes. However, the lack of beta-cell capacity introduces a challenge without regeneration of insulin-producing cells. Stem cell therapies combined with regulation of islet autoimmunity may offer the best prospect of increased insulin secretion in individuals with T1D.