# Cells Co-Producing Insulin and Glucagon in Congenital Hyperinsulinism

## TL;DR

The study found unusual insulin and glucagon-producing cells in infants with congenital hyperinsulinism, suggesting changes in pancreatic cell behavior under hypoglycemic conditions.

## Contribution

The study identifies increased bi-hormonal insulin+/glucagon+ cells in CHI, revealing novel islet cell phenotype alterations in hypoglycemic conditions.

## Key findings

- Diffuse CHI showed increased insulin+/glucagon+ cells.
- Insulin+ cells lacking PDX1 were more common in diffuse CHI and focal CHI.
- Altered β-cell phenotypes may occur under hypoglycemic conditions.

## Abstract

Alterations of pancreatic islet cell phenotypes are well established in diabetic conditions and considered to be one of the possible causes of insulin deficiency. However, there is limited information about alterations of islet cell phenotypes in opposite metabolic conditions such as hypoglycemia in infants with congenital hyperinsulinism (CHI). Surgical biopsies of the pancreas from six infants with diffuse CHI and five infants with focal CHI were examined using double immunofluorescence with antibodies against insulin, glucagon and the key transcriptional factor responsible for β-cell differentiation and maturation—PDX1. The phenotypes of cells within the pancreatic islets in diffuse CHI and within the focus in focal CHI were compared to those in unaltered pancreatic islets located outside the focus. In diffuse CHI, the proportion of bi-hormonal insulin+/glucagon+ cells was increased. Additionally, an increase in the proportion of insulin+ cells lacking PDX1 was observed in diffuse CHI and within the focus. It can be assumed that alterations of the phenotype of β-cells may occur under hypoglycemic conditions, but the role of islet cell plasticity in infants with CHI remains to be established.