scholarly journals Th1/Th17 Plasticity Is a Marker of Advanced β Cell Autoimmunity and Impaired Glucose Tolerance in Humans

2014 ◽  
Vol 194 (1) ◽  
pp. 68-75 ◽  
Author(s):  
Linnea Reinert-Hartwall ◽  
Jarno Honkanen ◽  
Harri M. Salo ◽  
Janne K. Nieminen ◽  
Kristiina Luopajärvi ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Β Cell

Limitations of the fasting proinsulin to insulin ratio as a measure of β‐cell health in people with and without impaired glucose tolerance

2020 ◽  
Author(s):  
Aoife M. Egan ◽  
Marcello C. Laurenti ◽  
Maria Daniela Hurtado Andrade ◽  
Chiara Dalla Man ◽  
Claudio Cobelli ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Β Cell

Pancreatic β-cell function and fetal growth in gestational impaired glucose tolerance

2010 ◽  
Vol 89 (6) ◽  
pp. 769-775 ◽  
Author(s):  
Kei Miyakoshi ◽  
Mamoru Tanaka ◽  
Yoshifumi Saisho ◽  
Akira Shimada ◽  
Kazuhiro Minegishi ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Fetal Growth ◽  
Cell Function ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Β Cell Function

Impact of incretin hormones on β-cell function in subjects with normal or impaired glucose tolerance

2006 ◽  
Vol 291 (6) ◽  
pp. E1144-E1150 ◽  
Author(s):  
Elza Muscelli ◽  
Andrea Mari ◽  
Andrea Natali ◽  
Brenno D. Astiarraga ◽  
Stefania Camastra ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Cell Function ◽  
Oral Glucose ◽  
Incretin Effect ◽  
Β Cell ◽  
Β Cell Function ◽  
Glucose Sensitivity ◽  
Cell Glucose

The mechanisms by which the enteroinsular axis influences β-cell function have not been investigated in detail. We performed oral and isoglycemic intravenous (IV) glucose administration in subjects with normal (NGT; n = 11) or impaired glucose tolerance (IGT; n = 10), using C-peptide deconvolution to calculate insulin secretion rates and mathematical modeling to quantitate β-cell function. The incretin effect was taken to be the ratio of oral to IV responses. In NGT, incretin-mediated insulin release [oral glucose tolerance test (OGTT)/IV ratio = 1.59 ± 0.18, P = 0.004] amounted to 18 ± 2 nmol/m2 (32 ± 4% of oral response), and its time course matched that of total insulin secretion. The β-cell glucose sensitivity (OGTT/IV ratio = 1.52 ± 0.26, P = 0.02), rate sensitivity (response to glucose rate of change, OGTT/IV ratio = 2.22 ± 0.37, P = 0.06), and glucose-independent potentiation were markedly higher with oral than IV glucose. In IGT, β-cell glucose sensitivity (75 ± 14 vs. 156 ± 28 pmol·min−1·m−2·mM−1 of NGT, P = 0.01) and potentiation were impaired on the OGTT. The incretin effect was not significantly different from NGT in terms of plasma glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide responses, total insulin secretion, and enhancement of β-cell glucose sensitivity (OGTT/IV ratio = 1.73 ± 0.24, P = NS vs. NGT). However, the time courses of incretin-mediated insulin secretion and potentiation were altered, with a predominance of glucose-induced vs. incretin-mediated stimulation. We conclude that, under physiological circumstances, incretin-mediated stimulation of insulin secretion results from an enhancement of all dynamic aspects of β-cell function, particularly β-cell glucose sensitivity. In IGT, β-cell function is inherently impaired, whereas the incretin effect is only partially affected.

scholarly journals Baseline Predictors of Glycemic Worsening in Youth and Adults With Impaired Glucose Tolerance or Recently Diagnosed Type 2 Diabetes in the Restoring Insulin Secretion (RISE) Study

2021 ◽  
Author(s):  
Susan Sam ◽  
Sharon L. Edelstein ◽  
Silva A. Arslanian ◽  
Elena Barengolts ◽  
Thomas A. Buchanan ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Age Groups ◽  
Oral Glucose ◽  
Β Cell ◽  
Cox Models ◽  
Cell Responses ◽  
Lower Baseline

Objective: Identify predictors of glycemic worsening among youth and adults with impaired glucose tolerance (IGT) or recently-diagnosed type 2 diabetes in the RISE Study. <p> </p> <p>Research Design and Methods: Ninety-one youth (10-19 years) were randomized 1:1 to 12 months of metformin (MET), or 3 months of glargine followed by 9 months of metformin (G-MET); 267 adults to MET, G-MET, liraglutide plus MET (LIRA+MET) or placebo for 12 months. All participants underwent baseline hyperglycemic clamp and 3-h oral glucose tolerance test (OGTT) at baseline, month-6, month-12 and off treatment at month-15 and month-21. Cox models identified baseline predictors of glycemic worsening (HbA1c increase ≥0.5% from baseline).</p> <p> </p> <p>Results: Glycemic worsening occurred in 17.8% of youth vs. 7.5% of adults at month-12 (p=0.008), and 36% of youth vs. 20% of adults at month-21 (p=0.002). In youth, glycemic worsening did not differ by treatment. In adults, month-12 glycemic worsening was less on LIRA+MET vs. placebo (HR 0.21, CI 0.05-0.96, p=0.044). In both age groups, lower baseline clamp-derived β-cell responses predicted month-12 and month-21 glycemic worsening (p<0.01); lower baseline OGTT-derived β-cell responses predicted month-21 worsening (p<0.05). In youth, higher baseline HbA1c and 2-h glucose predicted month-12 and month-21 glycemic worsening and higher fasting glucose predicted month-21 worsening (p<0.05). In adults, lower clamp and OGTT-derived insulin sensitivity predicted month-12 and month-21 worsening (p<0.05). </p> <p> </p> <p>Conclusions: Glycemic worsening was more common among youth than adults with IGT or recently-diagnosed type 2 diabetes, predicted by lower baseline β-cell responses in both groups, hyperglycemia in youth and insulin resistance in adults. </p>

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