Associations of Glucose Control with Insulin Sensitivity and Pancreatic  -Cell Responsiveness in Newly Presenting Type 2 Diabetes

2002 ◽  
Vol 87 (1) ◽  
pp. 198-203 ◽  
Author(s):  
A. I. Albarrak
2002 ◽  
Vol 87 (1) ◽  
pp. 198-203 ◽  
Author(s):  
Ahmed I. Albarrak ◽  
Stephen D. Luzio ◽  
Ludovic J. Chassin ◽  
Rebecca A. Playle ◽  
David R. Owens ◽  
...  

We examined the ability of indices of insulin sensitivity and pancreatic β-cell responsiveness to explain interindividual variability of clinical measures of glucose control in newly presenting type 2 diabetes. Subjects with newly presenting type 2 diabetes (n = 65; 53 males and 12 females; age, 54 ± 1 yr; body mass index, 30.5 ± 0.7 kg/m2; mean ± se) underwent an insulin-modified iv glucose tolerance test to determine minimal model-derived insulin sensitivity (SI), glucose effectiveness, first-phase insulin secretion, and disposition index. Subjects also underwent a standard meal tolerance test (MTT) to measure fasting/basal (M0) and postprandial (MI) pancreatic β-cell responsiveness. Stepwise linear regression used these indices to explain interindividual variability of fasting and postprandial plasma glucose and insulin concentrations and glycated hemoglobin (HbA1C). All measures of pancreatic β-cell responsiveness (M0, MI, and first-phase insulin secretion) were negatively correlated with fasting plasma glucose (P < 0.01) and positively correlated with fasting plasma insulin (FPI) and insulin responses to MTT (P < 0.05). SI demonstrated negative correlation with FPI (P < 0.001) but failed to correlate with any glucose variable. MI followed by disposition index (composite index of insulin sensitivity and pancreatic β-cell responsiveness) were most informative in explaining interindividual variability. It was possible to explain 70–80% interindividual variability of fasting plasma glucose, FPI, HbA1C, and insulin responses to MTT, and only 25–40% interindividual variability of postprandial glucose. In conclusion, postprandial insulin deficiency is the most powerful explanatory factor of deteriorating glucose control in newly presenting type 2 diabetes. Indices of insulin sensitivity and pancreatic β-cell responsiveness explain fasting glucose and HbA1C well but fail to explain postprandial glucose.


2019 ◽  
Vol 51 (Supplement) ◽  
pp. 425
Author(s):  
Juan F. Ortega ◽  
Miguel Ramirez-Jimenez ◽  
Felix Morales-Palomo ◽  
Ricardo Mora-Rodriguez

2011 ◽  
Vol 108 (7) ◽  
pp. 1286-1291 ◽  
Author(s):  
Linda M. Morgan ◽  
Jiang-Wen Shi ◽  
Shelagh M. Hampton ◽  
Gary Frost

Shiftworkers have a higher risk of CHD and type 2 diabetes. They consume a large proportion of their daily energy and carbohydrate intake in the late evening or night-time, a factor which could be linked to their increase in disease risk. We compared the metabolic effects of varying both dietary glycaemic index (GI) and the time at which most daily energy intake was consumed. We hypothesised that glucose control would be optimal with a low-GI diet, consumed predominantly early in the day. A total of six healthy lean volunteers consumed isoenergetic meals on four occasions, comprising either high- or low-GI foods, with 60 % energy consumed predominantly early (breakfast) or late (supper). Interstitial glucose was measured continuously for 20 h. Insulin, TAG and non-esterified fatty acids were measured for 2 h following every meal. Highest glucose values were observed when large 5021 kJ (1200 kcal) high-GI suppers were consumed. Glucose levels were also significantly higher in predominantly late high- v. low-GI meals (P < 0·01). Using an estimate of postprandial insulin sensitivity throughout the day, we demonstrate that this follows the same trend, with insulin sensitivity being significantly worse in high energy consumed in the evening meal pattern. Both meal timing and GI affected glucose tolerance and insulin secretion. Avoidance of large, high-GI meals in the evening may be particularly beneficial in improving postprandial glucose profiles and may play a role in reducing the risk of type 2 diabetes; however, longer-term studies are needed to confirm this.


2015 ◽  
Vol 10 (S 01) ◽  
Author(s):  
M Apostolopoulou ◽  
K Strassburger ◽  
B Knebel ◽  
J Kotzka ◽  
J Szendroedi ◽  
...  

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 946-P
Author(s):  
TZVETELINA TOTOMIROVA ◽  
IVONA DASKALOVA ◽  
MILA ARNAUDOVA

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