1,721,057 research outputs found
The revolving door of 'residual beta cell function': Cause or effect in medical reports?
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Incretin Effect in Youths with Normal and Impaired Glucose Tolerance
Full text linkBackground. Prediabetes includes a broad range of glucose metabolism alterations that increase the risk for diabetes in youths. Analogues of gut-derived hormones (incretins) have been paved as a promising therapeutic option for youths with diabetes. Though, we lack in vivo studies assessing the incretin effect in prediabetes and early diabetes in youths as well as longitudinal assessment of the incretin response in this age.
We estimated the incretin effect in obese youths with normal and impaired glucose tolerance, by the use of the gold standard matched oral glucose tolerance test (OGTT) and iso-glycemic intravenous glucose tolerance test (iso-IVGTT).
Methods. We enrolled 30 overweight/obese youths with normal (NGT) and impaired (IGT) glucose tolerance. Each participant underwent a 180-minutes OGTT and an iso-IVGTT to quantify the incretin effect, followed by a hyperglycemic clamp to measure glucose and arginine induced insulin secretion. Seriated samples for plasma glucose, insulin, C-peptide and active GLP-1(7-36) were collected. The minimal model and deconvolution were adopted to estimate insulin secretion based on glucose and C-peptide. The hyperglycemic clamp-derived indices were A) M/I for insulin sensitivity, B) acute (0–10 min [first phase]) C-peptide response to glucose (ACPRg), C) steady-state C-peptide concentrations at plasma glucose of 11.1 mmol/L, and D) arginine-stimulated maximum C-peptide response at plasma glucose >25 mmol/L (ACPRmax).
Results. We completed the three tests in 28 youths (15.9±2.4y, 14F, 13 NGT, 15 IGT). The NGT and IGT groups did not differ with respect to age, ethnicity, BMI, fasting glucose. No significant differences were observed between the two groups in either measure of β-cell function [ACPRg, steady- state C-peptide, ACPRmax, (p=0.372, p=0.478 and p=0.230)] or in insulin sensitivity [M/I] (p=0.106). The incretin effect was higher in the NGT than IGT group (+28.3%[-4, 62] and -10.3%[-34.3, 14.2], p=0.022), in spite of a lower GLP-1 secretion rate during the OGTT in the NGT group (p<0.001).
Conclusion. Impairment of glucose tolerance in youths is associated with a reduced incretin effect in the absence of a significant impairment of β-cell function. The higher secretion rate of GLP-1 is suggestive for a primary incretin resistance. The incretin pathway could represent potential target for therapeutic interventions in youth onset prediabetes
A Technological Revolution: The Integration of New Treatments to Manage Type 1 Diabetes
No full textIntensive insulin treatment and frequent self-monitoring of blood glucose (SMBG) have been recognized as pillars of diabetes treatment. Many patients with type 1 diabetes (T1D) struggle to achieve targeted glycemic control. Technology has vastly changed how these tenets to treatment can occur. Continuous subcutaneous insulin infusion (CSII) pumps and continuous glucose monitoring (CGM) can be used in place of their counterparts, multiple daily injections and SMBG. We present a review of CSII, CGM, and of different levels of integration among these two therapies, ranging from low glucose suspension devices to hybrid closed loop insulin delivery. Analysis of the various tools, their effect on glycemic control, and a guide to integrate them into pediatric clinical practice is presented. Although a cure for T1D remains the ultimate goal, technology holds the promise of keeping youth with T1D in targeted control and minimize the burden of this chronic medical condition. [Pediatr Ann. 2019;48(8):e311-e318.]
The Neonate Glucose Simulator: A New Tool for Testing a Nutritional Clinical Advisor to Regulate Glycemia in Preterm Infants admitted to the Neonatal Intensive Care Unit
Full text linkPreterm birth is the leading cause of death in young children, and is often associated with long-term neurodevelopmental impairment in children that reach school age. Parenteral and enteral nutrition play a crucial role in the development of the infant admitted to the neonatal intensive care unit (NICU), as it is the only mean of nutrition for the neonates. However, standard nutrition protocols, not individualized to the neonate's specific needs, are followed. A personalization of parenteral and enteral nutrition could help in the development of the infant brain, and be associated to better clinical outcomes. In particular, hypoglycaemic and hyperglycaemic episodes have to be avoided, as they are associated with cognitive impairments and increased mortality rates. Therefore, the availability of a nutritional clinical advisor, able to suggest the optimal amount of glucose to feed the hospitalized neonates, would be of great help in the NICU. Needless to say, the preterm neonates are very fragile and glycaemic control algorithms have to be carefully tested before being applied in this population. Therefore, the first step toward the design of these tools, is to build up a model able to simulate reliable glucose traces of neonates, to safely and effectively test such advisory systems. The aim of this study is thus to build a Neonate Glucose Simulator, able to generate reliable glucose time courses and usable to optimize the control strategy and avoid hyperglycaemic and hypoglycaemic episodes. The simulator must include a model of glucose-insulin-C-peptide interaction, possibly accounting for the metabolic processes known to be altered in infants born preterm, a model of both parenteral and enteral nutrition and a set of virtual neonates representative of real ones. The proposed Neonate Glucose Simulator was equipped with a population of 100 virtual neonates and the glucose time courses obtained for the virtual subjects were compared with real data collected on a population of infants born preterm, monitored during their stay in the NICU, demonstrating the reliability of the newly built tool
Cardiac Autoimmunity as a Novel Biomarker, Mediator, and Therapeutic Target of Heart Disease in Type 1 Diabetes
Full text linkPatients with type 1 diabetes (T1D) suffer excess mortality from cardiovascular disease (CVD) that has persisted despite substantial reductions in microvascular complications. Although T1D and type 2 diabetes (T2D) are etiologically distinct, it has generally been assumed that CVD in T1D is “the same disease” as that found in T2D. Here, we review the most recent epidemiological and clinical studies on heart disease in T1D, highlighting differences between CVD in T1D and T2D. In addition, we discuss experimental and clinical evidence for a post-myocardial infarction (MI) autoimmune heart syndrome in T1D, including the development of diagnostic assays which we believe can, for the first time, differentiate between heart disease in T1D and T2D. We postulate that a clinically unrecognized form of chronic myocardial inflammation (“myocarditis”) triggered by MI contributes to the poor CVD outcomes in T1D. These findings provide a conceptual shift in our understanding of CVD in T1D and have important diagnostic and therapeutic implications.Version of Recor
Keeping Up with the Diabetes Technology: 2016 Endocrine Society Guidelines of Insulin Pump Therapy and Continuous Glucose Monitor Management of Diabetes
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