The goal of this clinical trial is to investigate the etiopathogenesis of isolated hypoglycemia and hypoglycemia with abnormal glucose tolerance in children with Cystic Fibrosis (CF) and to evaluate the role of glucagon and pancreatic insufficiency on hypoglycemia in CF. The main questions it aims to answer are:

1. Do isolated hypoglycemia and hypoglycemia with abnormal glucose tolerance have different etiopathogenesis?
2. What is the role of pancreatic insufficiency in these two conditions? Participants were asked to perform 3-h OGTT and to take blood samples. Researchers compared with healthy peers to see if there is isolated hypoglycemia in OGTT and how is the glucagon response to OGTT in healthy peers.

The exact underlying mechanism of hypoglycemia in CF is still unknown. Some recent studies support the delayed and prolonged insulin secretion and impaired counterregulatory hormone response as the reason of reactive hypoglycemia, whereas the others argued an additive effect of an intrinsic factor.

However, the weakness of these limited studies is that nearly all of them included CF patients who had pancreatic insufficiency (PI) and could not reveal the mechanism of hypoglycemia seen in those without PI. In addition, there were no healthy controls for comparison of glucagon secretion in CF patients with hypoglycemia. Moreover, the studies that evaluate the role of glucagon in hypoglycemic CF patients were performed in hypoglycemic adult patients with abnormal glucose tolerance (AGT) and the delayed and prolonged insulin release is expected to be more likely as the reason of hypoglycemia in this setting. Previously, the investigators had demonstrated isolated hypoglycemia in some of the pediatric CF patients during OGTT. In this study, the investigators aimed to further investigate possible mechanisms of hypoglycemia. The investigators hypothesized that the mechanism of isolated hypoglycemia might be different from hypoglycemia seen in patients with AGT. Furthermore, the investigators evaluated the role of pancreatic insufficiency in hypoglycemia of CF patients by analyzing glucose, insulin and glucagon response to a glucose load in CF patients with and without PI.

Inclusion Criteria:

• 10-18 year-old children genetically diagnosed with Cystic Fibrosis
• Regularly followed by the department of pediatric endocrinology

Exclusion Criteria:

• Using corticosteroid therapy in the last 3 months
• Those who had acute exacerbation in the last 3 months
• Previously diagnosed with diabetes

The study population is the children and adolescents aged 10-18 years with CF who were regularly followed-up at the Pediatric Endocrinology and Diabetes Units.

The control group was age-matched healthy, diabetes non-diabetic siblings of patients with type 1 diabetes. All the controls were negative for β-cell autoantibodies (anti-glutamic acid decarboxylase, islet cell antibody, and insulin antibody).

All data except the participants' name-surname can be shared with the other researchers