A Comparison Between the Minimal Model and the Glucose Clamp in the Assessment of Insulin Sensitivity Across the Spectrum of Glucose Tolerance

Diabetes ◽  
1994 ◽  
Vol 43 (9) ◽  
pp. 1114-1121 ◽  
Author(s):  
M. F. Saad ◽  
R. L. Anderson ◽  
A. Laws ◽  
R. M. Watanabe ◽  
W. W. Kades ◽  
...  
Diabetologia ◽  
2009 ◽  
Vol 53 (1) ◽  
pp. 144-152 ◽  
Author(s):  
A. Tura ◽  
S. Sbrignadello ◽  
E. Succurro ◽  
L. Groop ◽  
G. Sesti ◽  
...  

2000 ◽  
Vol 278 (4) ◽  
pp. E700-E706 ◽  
Author(s):  
Daniel E. Flanagan ◽  
Vivienne M. Moore ◽  
Ian F. Godsland ◽  
Richard A. Cockington ◽  
Jeffrey S. Robinson ◽  
...  

Although there is now substantial evidence linking low birthweight with impaired glucose tolerance and type 2 diabetes in adult life, the extent to which reduced fetal growth is associated with impaired insulin sensitivity, defective insulin secretion, or a combination of both factors is not clear. We have therefore examined the relationships between birth size and both insulin sensitivity and insulin secretion as assessed by an intravenous glucose tolerance test with minimal model analysis in 163 men and women, aged 20 yr, born at term in Adelaide, South Australia. Birth size did not correlate with body mass index or fat distribution in men or women. Men who were lighter or shorter as babies were less insulin sensitive ( P = 0.03 and P = 0.01, respectively), independently of their body mass index or body fat distribution. They also had higher insulin secretion ( P = 0.007 and P = 0.006) and increased glucose effectiveness ( P = 0.003 and P = 0.003). Overall glucose tolerance, however, did not correlate with birth size, suggesting that the reduced insulin sensitivity was being compensated for by an increase in insulin secretion and insulin-independent glucose disposal. There were no relationships between birth size and insulin sensitivity or insulin secretion in women. These results show that small size at birth is associated with increased insulin resistance and hyperinsulinemia in young adult life but that these relationships are restricted to the male gender in this age group.


2009 ◽  
Vol 296 (5) ◽  
pp. R1316-R1324 ◽  
Author(s):  
Giovanni Pacini ◽  
Maria Ahrén ◽  
Bo Ahrén

Mice are increasingly used in studies where measuring insulin sensitivity (IS) is a common procedure. The glucose clamp is labor intensive, cannot be used in large numbers of animals, cannot be repeated in the same mouse, and has been questioned as a valid tool for IS in mice; thus, the minimal model with 50-min intravenous glucose tolerance test (IVGTT) data was adapted for studies in mice. However, specific software and particular ability was needed. The aim of this study was to establish a simple procedure for evaluating IS during IVGTT in mice (CSI). IVGTTs ( n = 520) were performed in NMRI and C57BL/6J mice (20–25g). After glucose injection (1 g/kg), seven samples were collected for 50 min for glucose and insulin measurements, analyzed with a minimal model that provided the validated reference IS (SI). By using the regression CSI = α1 + α2 × KG/AUCD, where KG is intravenous glucose tolerance index and AUCd is the dynamic area under the curve, IS was calculated in 134 control animals randomly selected (regression CSI vs. SI: r = 0.66, P < 0.0001) and yielded α1 = 1.93 and α2 = 0.24. KG is the slope of log (glucose5-20) and AUCD is the mean dynamic area under insulin curve in the IVGTT. By keeping fixed α1 and α2, CSI was validated in 143 control mice (4.7 ± 0.2 min·μU−1·ml−1, virtually identical to SI: 4.7 ± 0.3, r = 0.89, P < 0.0001); and in 123 mice in different conditions: transgenic, addition of neuropeptides, incretins, and insulin (CSI: 6.0 ± 0.4 vs. SI: 6.1 ± 0.4, r = 0.94, P < 0.0001). In the other 120 animals, CSI revealed its ability to segregate different categories, as does SI. This easily usable formula for calculating CSI overcomes many experimental obstacles and may be a simple alternative to more complex procedures when large numbers of mice or repeated experiments in the same animals are required.


2000 ◽  
Vol 85 (7) ◽  
pp. 2402-2410 ◽  
Author(s):  
Arie Katz ◽  
Sridhar S. Nambi ◽  
Kieren Mather ◽  
Alain D. Baron ◽  
Dean A. Follmann ◽  
...  

Insulin resistance plays an important role in the pathophysiology of diabetes and is associated with obesity and other cardiovascular risk factors. The “gold standard” glucose clamp and minimal model analysis are two established methods for determining insulin sensitivity in vivo, but neither is easily implemented in large studies. Thus, it is of interest to develop a simple, accurate method for assessing insulin sensitivity that is useful for clinical investigations. We performed both hyperinsulinemic isoglycemic glucose clamp and insulin-modified frequently sampled iv glucose tolerance tests on 28 non-obese, 13 obese, and 15 type 2 diabetic subjects. We obtained correlations between indexes of insulin sensitivity from glucose clamp studies (SIClamp) and minimal model analysis (SIMM) that were comparable to previous reports (r = 0.57). We performed a sensitivity analysis on our data and discovered that physiological steady state values [i.e. fasting insulin (I0) and glucose (G0)] contain critical information about insulin sensitivity. We defined a quantitative insulin sensitivity check index (QUICKI = 1/[log(I0) + log(G0)]) that has substantially better correlation with SIClamp (r = 0.78) than the correlation we observed between SIMM and SIClamp. Moreover, we observed a comparable overall correlation between QUICKI and SIClamp in a totally independent group of 21 obese and 14 nonobese subjects from another institution. We conclude that QUICKI is an index of insulin sensitivity obtained from a fasting blood sample that may be useful for clinical research.


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