scholarly journals Stability analysis of insulin-glucose feedback in the Glucosafe pancreas model of endogenous insulin production

2014 ◽  
Vol 47 (3) ◽  
pp. 10959-10963 ◽  
Author(s):  
Mark Lillelund Rousing ◽  
Ulrike Pielmeier ◽  
Steen Andreassen
Keyword(s):  
Stability Analysis ◽  
Insulin Production ◽  
Endogenous Insulin ◽  
Endogenous Insulin Production

Abstract #791: Repaglinide Stimulation of C-Peptide Test to Assess Endogenous Insulin Production

2005 ◽  
Vol 11 ◽  
pp. 17
Author(s):  
Stanley Andrew Tan ◽  
Marilyn Kay Wilson ◽  
John Stephan Pasztor ◽  
Linda Giles Tan
Keyword(s):  
Insulin Production ◽  
C Peptide ◽  
Endogenous Insulin ◽  
Endogenous Insulin Production ◽  
Stimulation Of

Urinary C-Peptide: A Useful Tool for Evaluating the Endogenous Insulin Reserve in Cohort and Longitudinal Studies of Diabetes in Childhood

1988 ◽  
Vol 25 (5) ◽  
pp. 552-559 ◽  
Author(s):  
C E de Beaufort ◽  
N C den Boer ◽  
G J Bruining ◽  
G A M Eilers ◽  
R van Strik ◽  
...  
Keyword(s):  
Linear Correlation ◽  
Type I Diabetes ◽  
Insulin Dose ◽  
Type I ◽  
Exogenous Insulin ◽  
Insulin Production ◽  
C Peptide ◽  
Endogenous Insulin ◽  
Diabetic Children ◽  
Endogenous Insulin Production

Increasing research into the remission phase of type I diabetes mellitus stresses the importance of a non-traumatic and reliable method for the evaluation of endogenous insulin production. We compared 24-h urinary C-peptide excretion (UCE) with plasma C-peptide values before and after stimulation with 1 mg glucagon in 24 type I diabetic children. Fasting plasma C-peptide values and stimulated plasma C-peptide values showed a linear correlation with 24 h UCE. Mean plasma C-peptide levels correlated inversely with the exogenous insulin dose. A slightly better correlation was found between the exogenous insulin dose and 24 h UCE. Control data of 24 h UCE were obtained from healthy siblings. A linear correlation with age was found up to 10 years of age above which UCE values seem to reach a plateau. This effect of age, as well as the frequency of sampling was taken into account in the derivation of 95% reference intervals for UCE. The measurement of 24 h UCE appears to be a useful parameter to assess endogenous insulin production in diabetic children, provided that age is taken into account.

scholarly journals N-3 PUFA and Pregnancy Preserve C-Peptide in Women with Type 1 Diabetes Mellitus

Pharmaceutics ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2082
Author(s):  
Josip Delmis ◽  
Marina Ivanisevic ◽  
Marina Horvaticek
Keyword(s):  
Type 1 Diabetes ◽  
Immune System ◽  
Pregnant Women ◽  
Cell Function ◽  
Insulin Production ◽  
Β Cell ◽  
C Peptide ◽  
Endogenous Insulin ◽  
Endogenous Insulin Production

Type 1 diabetes (T1DM) is an autoimmune disease characterized by the gradual loss of β-cell function and insulin secretion. In pregnant women with T1DM, endogenous insulin production is absent or minimal, and exogenous insulin is required to control glycemia and prevent ketoacidosis. During pregnancy, there is a partial decrease in the activity of the immune system, and there is a suppression of autoimmune diseases. These changes in pregnant women with T1DM are reflected by Langerhans islet enlargement and improved function compared to pre-pregnancy conditions. N-3 polyunsaturated fatty acids (n-3 PUFA) have a protective effect, affect β-cell preservation, and increase endogenous insulin production. Increased endogenous insulin production results in reduced daily insulin doses, better metabolic control, and adverse effects of insulin therapy, primarily hypoglycemia. Hypoglycemia affects most pregnant women with T1DM and is several times more common than that outside of pregnancy. Strict glycemic control improves the outcome of pregnancy but increases the risk of hypoglycemia and causes maternal complications, including coma and convulsions. The suppression of the immune system during pregnancy increases the concentration of C-peptide in women with T1DM, and n-3 PUFA supplements serve as the additional support for a rise in C-peptide levels through its anti-inflammatory action.

scholarly journals Increase of Neutrophil Extracellular Traps, Mitochondrial DNA and Nuclear DNA in Newly Diagnosed Type 1 Diabetes Children but Not in High-Risk Children

2021 ◽  
Vol 12 ◽  
Author(s):  
Camilla Skoglund ◽  
Daniel Appelgren ◽  
Ingela Johansson ◽  
Rosaura Casas ◽  
Johnny Ludvigsson
Keyword(s):  
High Risk ◽  
Nuclear Dna ◽  
Extracellular Dna ◽  
Healthy Children ◽  
Newly Diagnosed ◽  
Endogenous Insulin ◽  
Hla Genotypes ◽  
Endogenous Insulin Production

Neutrophil extracellular traps (NETs) and mitochondrial DNA (mtDNA) are inflammatory mediators involved in the development of type 1 diabetes (T1D). Pancreas-infiltrating neutrophils can release NETs, contributing to the inflammatory process. Levels of NETs are increased in serum from patients with T1D and mtDNA is increased in adult T1D patients. Our aim was to investigate extracellular DNA (NETs, mtDNA and nuclear DNA) in children with newly diagnosed T1D and in children at high risk of the disease. We also elucidated if extracellular DNA short after diagnosis could predict loss of endogenous insulin production. Samples were analysed for mtDNA and nuclear DNA using droplet digital PCR and NETs were assessed by a NET-remnants ELISA. In addition, in vitro assays for induction and degradation of NETs, as well as analyses of neutrophil elastase, HLA genotypes, levels of c-peptide, IL-1beta, IFN and autoantibodies (GADA, IA-2A, IAA and ZnT8A) were performed. In serum from children 10 days after T1D onset there was an increase in NETs (p=0.007), mtDNA (p<0.001) and nuclear DNA (p<0.001) compared to healthy children. The elevated levels were found only in younger children. In addition, mtDNA increased in consecutive samples short after onset (p=0.017). However, levels of extracellular DNA short after onset did not reflect future loss of endogenous insulin production. T1D serum induced NETs in vitro and did not deviate in the ability to degrade NETs. HLA genotypes and autoantibodies, except for ZnT8A, were not associated with extracellular DNA in T1D children. Serum from children with high risk of T1D showed fluctuating levels of extracellular DNA, sometimes increased compared to healthy children. Therefore, extracellular DNA in serum from autoantibody positive high-risk children does not seem to be a suitable biomarker candidate for prediction of T1D. In conclusion, we found increased levels of extracellular DNA in children with newly diagnosed T1D, which might be explained by an ongoing systemic inflammation.

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