Ignite Creation Date:
2024-05-06 @ 7:53 PM
Last Modification Date:
2024-10-26 @ 3:15 PM
Study NCT ID:
NCT06163482
Status:
RECRUITING
Last Update Posted:
2024-06-07
First Post:
2023-11-27
Brief Title:
Hormonal Responses to a Mixed Meal in People With Cystic Fibrosis
Sponsor:
University of Cincinnati
Organization:
University of Cincinnati
Study Overview
Official Title:
Changes in Postprandial Hormone Levels in Cystic Fibrosis Related Diabetes
Status:
RECRUITING
Status Verified Date:
2024-06
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
In this exploratory study the hormonal responses to a mixed meal will be examined in people with cystic fibrosis The aim of this study is to find correlates with impaired glucose tolerance that is associated with this population
Detailed Description:
The pancreas plays a key role in the regulation of whole-body glucose metabolism in humans It contains 1 to 3 million islets each of which contains several types of endocrine cells including insulin-secreting beta cells glucagon-secreting alpha cells and somatostatin- secreting delta cells Insulin is released in response to a rise in blood glucose after a meal and promotes glucose utilization by peripheral tissues eg skeletal muscle which allows the return of blood glucose to a fasting level Glucagon is released when blood glucose falls below a normal fasting level 80-100 mgdL and it acts on the liver in opposition to insulin enhancing hepatic glucose production Somatostatins role in whole body glucose homeostasis is somewhat more complex The role it plays in acutely regulating whole-body glucose homeostasis is small in healthy humans On the other hand it is capable of inhibiting the secretion of both insulin and glucagon regardless of ambient metabolic conditions In addition to its ability to regulate hormone secretion somatostatin is also known to reduce glucose absorption from the gastrointestinal tract
CF is the most common life-limiting genetic disease in Caucasians It is caused by recessive mutations in the gene encoding CF transmembrane conductance regulator CFTR The primary pathologic change is secretion of thick ductular mucus which leads to progressive obstructive damage to the lungs and exocrine pancreas Damage to the exocrine pancreas which is responsible for the secretion of digestive enzymes leads to exocrine pancreas insufficiency PI manifested as diarrhea and malabsorption of ingested nutrients requiring pancreatic enzyme replacement Pathological changes of exocrine PI occur as early as the first few months of life and most CF patients are diagnosed with PI before they reach adulthood
The degree of exocrine PI correlates with risk of developing cystic fibrosis related diabetes CFRD However not all CF patients with PI have diabetes Patients with CFRD have impaired pancreatic beta cell function which is characterized most prominently by a loss of insulin secretion in response to the ingestion of glucose Furthermore it has been reported that glucagon responses to insulin induced hypoglycemia are reduced in CFRD thereby providing evidence that pancreatic alpha cell function is also impaired in CFRD One hypothesis for impaired endocrine function in CFRD is a reduction in islet count andor altered islet-structure These changes which are hallmark characteristics of CF are thought to be preceded by obstructive damage to the exocrine pancreas by thick viscous pancreatic secretions that result in progressive fibrosis and fatty infiltration of the pancreas Indeed immunohistochemical studies of islets from patients with CFRD show significantly reduced insulin-producing cells compared to those of CF patients without diabetes and controls
It is clear that metabolic regulation becomes progressively worse as the CF phenotype progresses from mild to severe from exocrine pancreatic sufficiency to exocrine pancreatic insufficiency to diabetes However the mechanism through which this worsening of metabolic regulation occurs is unclear In fact it is possible that in addition to changes in islet morphology another important factor that could lead to deteriorating metabolic regulation in CF is the mucosal secretions that result in fibrosis and fat infiltration in the pancreas The aim of the current study is to examine how hormone responses to a mixed meal differ between healthy controls and people with cystic fibrosis and how these changes correlate with deteriorating glucose tolerance
CF is the most common life-limiting genetic disease in Caucasians It is caused by recessive mutations in the gene encoding CF transmembrane conductance regulator CFTR The primary pathologic change is secretion of thick ductular mucus which leads to progressive obstructive damage to the lungs and exocrine pancreas Damage to the exocrine pancreas which is responsible for the secretion of digestive enzymes leads to exocrine pancreas insufficiency PI manifested as diarrhea and malabsorption of ingested nutrients requiring pancreatic enzyme replacement Pathological changes of exocrine PI occur as early as the first few months of life and most CF patients are diagnosed with PI before they reach adulthood
The degree of exocrine PI correlates with risk of developing cystic fibrosis related diabetes CFRD However not all CF patients with PI have diabetes Patients with CFRD have impaired pancreatic beta cell function which is characterized most prominently by a loss of insulin secretion in response to the ingestion of glucose Furthermore it has been reported that glucagon responses to insulin induced hypoglycemia are reduced in CFRD thereby providing evidence that pancreatic alpha cell function is also impaired in CFRD One hypothesis for impaired endocrine function in CFRD is a reduction in islet count andor altered islet-structure These changes which are hallmark characteristics of CF are thought to be preceded by obstructive damage to the exocrine pancreas by thick viscous pancreatic secretions that result in progressive fibrosis and fatty infiltration of the pancreas Indeed immunohistochemical studies of islets from patients with CFRD show significantly reduced insulin-producing cells compared to those of CF patients without diabetes and controls
It is clear that metabolic regulation becomes progressively worse as the CF phenotype progresses from mild to severe from exocrine pancreatic sufficiency to exocrine pancreatic insufficiency to diabetes However the mechanism through which this worsening of metabolic regulation occurs is unclear In fact it is possible that in addition to changes in islet morphology another important factor that could lead to deteriorating metabolic regulation in CF is the mucosal secretions that result in fibrosis and fat infiltration in the pancreas The aim of the current study is to examine how hormone responses to a mixed meal differ between healthy controls and people with cystic fibrosis and how these changes correlate with deteriorating glucose tolerance
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None