scholarly journals Erratum to: Effect of Sitagliptin on Islet Function in Pancreatic Insufficient Cystic Fibrosis With Abnormal Glucose Tolerance

2021 ◽  
Author(s):  
Andrea Kelly ◽  
Saba Sheikh ◽  
Darko Stefanovski ◽  
Amy J Peleckis ◽  
Sarah C Nyirjesy ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Glucose Tolerance ◽  
Islet Function ◽  
Abnormal Glucose Tolerance

scholarly journals Abnormal glucose tolerance in children with cystic fibrosis: the predictive role of continuous glucose monitoring system

2010 ◽  
Vol 162 (4) ◽  
pp. 705-710 ◽  
Author(s):  
Riccardo Schiaffini ◽  
Claudia Brufani ◽  
Beatrice Russo ◽  
Danilo Fintini ◽  
Antonella Migliaccio ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Monitoring System ◽  
Continuous Glucose Monitoring ◽  
Glucose Monitoring ◽  
Continuous Glucose Monitoring System ◽  
Abnormal Glucose Tolerance ◽  
Altered Glucose

A long pre-diabetic phase of abnormal glucose tolerance is described in subjects with cystic fibrosis (CF) since childhood.ObjectiveThe aims of the study were to compare oral glucose tolerance test (OGTT) and continuous glucose monitoring system (CGMS) in the diagnosis of altered glucose metabolism, and to longitudinally evaluate the role of CGMS in predicting glucose metabolism deterioration in children with CF.MethodsSeventeen children with CF and 14 controls were enrolled (mean age 13.3±3.0 years). All subjects underwent OGTT and CGMS registration. On the basis of OGTT, children were classified as normal glucose tolerance, impaired glucose tolerance (IGT), IGT plus at least one glucose value above 200 mg/dl at intermediate OGTT points (IGT+200) and CF-related diabetes (CFRD). HbA1c, glucose area under the curve, insulin sensitivity, and insulinogenic and disposition indexes were also considered. Subjects with CF underwent another OGTT after 2.5 years.ResultsBaseline OGTT revealed 3/17 (7.6%) children with CF with at least one glucose value above 200 mg/dl (1 CFRD and 2 IGT+200), while CGMS revealed 6/17 (35.3%) children with glucose excursions above 200 mg/dl (P=0.010). None of the controls showed glucose over 200 mg/dl either at OGTT or at CGMS. At the 2.5-year follow-up OGTT, all the six subjects who had diabetic glucose excursion (i.e. >200 mg/dl) at baseline CGMS presented IGT+200 or CFRD. In logistic regression analysis, CGMS diabetic excursion was the strongest predictor of IGT+200 and CFRD (P<0.001).ConclusionsCGMS could be a useful tool to predict glucose metabolism derangements in children affected by CF.

Normal adiponectin levels despite abnormal glucose tolerance (or diabetes) and inflammation in adult patients with cystic fibrosis

2007 ◽  
Vol 33 (3) ◽  
pp. 213-219 ◽  
Author(s):  
I. Hammana ◽  
A. Malet ◽  
M. Costa ◽  
E. Brochiero ◽  
Y. Berthiaume ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Glucose Tolerance ◽  
Adult Patients ◽  
Abnormal Glucose Tolerance

scholarly journals Abnormal Glucose Tolerance in Infants and Young Children with Cystic Fibrosis

2016 ◽  
Vol 194 (8) ◽  
pp. 974-980 ◽  
Author(s):  
Yaling Yi ◽  
Andrew W. Norris ◽  
Kai Wang ◽  
Xingshen Sun ◽  
Aliye Uc ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Young Children ◽  
Glucose Tolerance ◽  
Abnormal Glucose Tolerance ◽  
Infants And Young Children

Elevated Gluconeogenesis and Lack of Suppression by Insulin Contribute to Cystic Fibrosis-Related Diabetes

2008 ◽  
Vol 56 (3) ◽  
pp. 567-573 ◽  
Author(s):  
Dana S. Hardin ◽  
Chul Ahn ◽  
Julie Rice ◽  
Mark Rice ◽  
Randall Rosenblatt
Keyword(s):  
Cystic Fibrosis ◽  
Glucose Tolerance ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Normal Glucose Tolerance ◽  
Abnormal Glucose Tolerance ◽  
Protein Breakdown ◽  
Relative Contribution ◽  
Hepatic Glucose ◽  
Normal Glucose

The incidence of diabetes is high in cystic fibrosis (CF) and is an important cause of morbidity and mortality. Understanding the pathophysiology is imperative. Studies have documented increased endogenous (mostly hepatic) glucose production (HGP) but have not distinguished the relative contribution of gluconeogenesis (GNG). The purpose of this study was to quantitate GNG, to determine its contribution to high HGP, and to measure insulin's suppression of GNG.We recruited 31 adult CF subjects (age, 26.2 ± 7.9 years; 12 female subjects) and quantified GNG by measuring the incorporation of 2H into the second and fifth carbons of glucose. Hepatic glucose production was measured using [6,6-2H2]glucose. Protein breakdown was measured using [1-13C]leucine. Data were compared with that from 11 healthy volunteers (age, 27.5 ± 7.0 years) who underwent both GNG and clamp studies. Thirteen CF subjects and all controls had a hyperinsulinemic euglycemic clamp during measures of GNG. Other measures included glucose tolerance and glucagon and cortisol levels.Rate of GNG was higher in CF subjects than controls and comprised a greater percentage of fasting HGP (GNG as percent of HGP: CF = 68%; controls = 44%; P = 0.034). Suppression of GNG by insulin was significantly lower in CF than in controls and was lower in CF subjects with abnormal glucose tolerance than in those with normal glucose tolerance. Gluconeogenesis correlated with protein breakdown.These studies suggest that high HGP in CF is mostly from elevated rates of GNG and that resistance to insulin's suppression of GNG may contribute to abnormal glucose tolerance in CF.

scholarly journals Abnormal glucose tolerance and the 50-gram glucose challenge test in Cystic fibrosis

2020 ◽  
Vol 19 (5) ◽  
pp. 696-699 ◽  
Author(s):  
Saba Sheikh ◽  
A Russell Localio ◽  
Andrea Kelly ◽  
Ronald C Rubenstein
Keyword(s):  
Cystic Fibrosis ◽  
Glucose Tolerance ◽  
Challenge Test ◽  
Abnormal Glucose Tolerance ◽  
Glucose Challenge Test ◽  
Glucose Challenge

scholarly journals Randomized, Controlled Trial Of Sitagliptin And Islet Function In Cystic Fibrosis With Abnormal Glucose Tolerance

2021 ◽  
Author(s):  
Andrea Kelly ◽  
Saba Sheikh ◽  
Darko Stefanovski ◽  
Amy J Peleckis, C R N P ◽  
Sarah C Nyirjesy ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Insulin Response ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Second Phase ◽  
Abnormal Glucose Tolerance ◽  
Study Objective ◽  
Glucagon Suppression

Abstract Purpose Impaired incretin secretion may contribute to the defective insulin secretion and abnormal glucose tolerance (AGT) that associate with worse clinical outcomes in pancreatic insufficient cystic fibrosis (PI-CF). The study objective was to test the hypothesis that dipeptidyl peptidase-4 (DPP-4) inhibitor-induced increases in intact incretin hormone (glucagon-like peptide-1 [GLP-1] and glucose-dependent insulinotropic polypeptide [GIP]) concentrations augment insulin secretion and glucagon suppression and lower post-prandial glycemia in PI-CF with AGT. Methods Twenty-six adults from Children’s Hospital of Philadelphia and University of Pennsylvania CF Center with PI-CF and AGT (defined by oral glucose tolerance test glucose [mg/dL]: early glucose intolerance [1-hour ≥155 & 2-hour &lt;140], impaired glucose tolerance [2-hour ≥140 and &lt;200 mg/dl], or diabetes [2-hour ≥200]) were randomized to a 6-month double-blind trial of DPP-4 inhibitor sitagliptin 100 mg daily or matched-placebo; 24 completed the trial (n=12 sitagliptin; n=12 placebo). Main outcome measures were mixed-meal tolerance test (MMTT) responses for intact GLP-1 and GIP, insulin secretory rates (ISR), glucagon suppression, and glycemia and glucose-potentiated arginine (GPA) test-derived measures of β- and α-cell function. Results Following 6-months of sitagliptin vs. placebo, MMTT intact GLP-1 and GIP responses increased (P &lt;0.001), ISR dynamics improved (P &lt;0.05), and glucagon suppression was modestly enhanced (P &lt;0.05) while GPA test responses for glucagon were lower. No improvements in glucose tolerance or β-cell sensitivity to glucose, including for second-phase insulin response were found. Conclusions In glucose intolerant PI-CF, sitagliptin intervention augmented meal-related incretin responses with improved early insulin secretion and glucagon suppression without affecting post-prandial glycemia.

Sign in / Sign up

Export Citation Format

Share Document