scholarly journals Derivation of a quantitative measure of insulin sensitivity from the intravenous tolbutamide test using the minimal model of glucose dynamics

Diabetologia ◽  
1987 ◽  
Vol 30 (5) ◽  
pp. 314-322 ◽  
Author(s):  
N. M. Shennan ◽  
I. F. Godsland ◽  
V. Wynn
Keyword(s):  
Insulin Sensitivity ◽  
Minimal Model ◽  
Quantitative Measure ◽  
Tolbutamide Test ◽  
Intravenous Tolbutamide Test ◽  
Glucose Dynamics

scholarly journals Derivation of a quantitative measure of insulin sensitivity from the intravenous tolbutamide test using the minimal model of glucose dynamics

Diabetologia ◽  
1987 ◽  
Vol 30 (9) ◽  
pp. 755-756
Author(s):  
L. L. Ng ◽  
T. D. R. Hockaday ◽  
I. F. Godsland ◽  
V. Wynn
Keyword(s):  
Insulin Sensitivity ◽  
Minimal Model ◽  
Quantitative Measure ◽  
Tolbutamide Test ◽  
Intravenous Tolbutamide Test ◽  
Glucose Dynamics

Reduced sampling protocols in estimation of insulin sensitivity and glucose effectiveness using the minimal model in NIDDM

Diabetes ◽  
1993 ◽  
Vol 42 (11) ◽  
pp. 1635-1641 ◽  
Author(s):  
P. A. Coates ◽  
R. L. Ollerton ◽  
S. D. Luzio ◽  
I. S. Ismail ◽  
D. R. Owens
Keyword(s):  
Insulin Sensitivity ◽  
Minimal Model ◽  
Glucose Effectiveness ◽  
Sampling Protocols

scholarly journals An empirical index of insulin sensitivity from short IVGTT: validation against the minimal model and glucose clamp indices in patients with different clinical characteristics

Diabetologia ◽  
2009 ◽  
Vol 53 (1) ◽  
pp. 144-152 ◽  
Author(s):  
A. Tura ◽  
S. Sbrignadello ◽  
E. Succurro ◽  
L. Groop ◽  
G. Sesti ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Minimal Model ◽  
Clinical Characteristics ◽  
Glucose Clamp

Insulin sensitivity from the minimal model

Part 2 ◽  
1995 ◽  
pp. 55-70
Keyword(s):  
Insulin Sensitivity ◽  
Minimal Model

scholarly journals Equivalence of the insulin sensitivity index in man derived by the minimal model method and the euglycemic glucose clamp.

1987 ◽  
Vol 79 (3) ◽  
pp. 790-800 ◽  
Author(s):  
R N Bergman ◽  
R Prager ◽  
A Volund ◽  
J M Olefsky
Keyword(s):  
Insulin Sensitivity ◽  
Minimal Model ◽  
Glucose Clamp ◽  
Sensitivity Index ◽  
Insulin Sensitivity Index ◽  
Model Method

Abstract 610: Ineffective Suppression of Adipocyte Lipolysis in Metabolic Syndrome: An in vivo Test for Adipocyte Insulin Resistance

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Jennifer L Ford ◽  
Raymond C Boston ◽  
Rachel E Walker ◽  
Gregory C Shearer
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Insulin Sensitivity ◽  
Lipid Droplet ◽  
Minimal Model ◽  
Initial Rate ◽  
Intravenous Glucose Tolerance Test ◽  
Intravenous Glucose ◽  
In Vivo Test

Background: Insulin resistance is a major contributor to metabolic syndrome, disrupting both glucose and non-esterified fatty acid (NEFA) dynamics through ineffective glucose clearance and decreased suppression of lipid droplet lipolysis. The minimal model of glucose dynamics is used for glycemic insulin sensitivity however it does not measure adipocyte insulin sensitivity, the primary determinant of plasma NEFA. An in-vivo approach to measuring adipocyte insulin sensitivity using NEFA is employed, comparing healthy and metabolic syndrome subjects. Both the models are employed to estimate insulin sensitivity and validate the NEFA approach. Objective: To test the use of NEFA kinetics to measure adipocyte insulin sensitivity compared to the glucose minimal model. Approach and results: Metabolic syndrome (n=56) and optimally healthy (n=14) subjects underwent a frequently sampled intravenous glucose tolerance test, and plasma analyzed for insulin, glucose, and NEFA. Insulin sensitivity ( S I ) and glucose effectiveness ( S G ) were calculated from the glucose minimal model. S I was 1.7 (mU/L) -1 min -1 and 0.40 (mU/L) -1 /min -1 and S G was 0.027 min -1 and 0.017 min -1 for the healthy and metabolic syndrome groups, respectively, indicating substantial glycemic insulin resistance in the latter. A model using glucose as the driver for NEFA kinetics was then applied. We found the initial rate of NEFA utilization by tissues (NU) was less, but the threshold glucose (tG) and glucose concentration required for a unit change in lipolysis inhibition ( G i ) were greater in metabolic syndrome verses healthy (NU: 0.050[0.045, 0.057] vs. 0.068[0.054, 0.086] p=0.03; tG: 6.7[6.2, 7.2] vs. 5.0[4.3, 5.9] p=0.001; G i : 0.30[0.25, 0.35] vs. 0.17[0.07, 0.27] p=0.02). No differences were found in initial rate of NEFA production or glucose utilization. Conclusion: Our results indicate that suppression of lipid-droplet lipolysis requires greater stimulus in metabolic syndrome compared to insulin sensitive adipocytes. Further, the rate of NEFA removal is less in metabolic syndrome. These results reveal components of insulin sensitivity not demonstrated by the glucose model. The NEFA model provides a measurement of adipocyte insulin sensitivity not captured by glycemic indices.

Comparison of Several Insulin Sensitivity Indices Derived from Basal Plasma Insulin and Glucose Levels with Minimal Model Indices

2003 ◽  
Vol 35 (1) ◽  
pp. 13-17 ◽  
Author(s):  
D. A. García-Estévez ◽  
D. Araújo-Vilar ◽  
G. Fiestras-Janeiro ◽  
Á. Saavedra-González ◽  
J. Cabezas-Cerrato
Keyword(s):  
Insulin Sensitivity ◽  
Minimal Model ◽  
Plasma Insulin ◽  
Glucose Levels ◽  
Sensitivity Indices ◽  
Basal Plasma

Modified protocols improve insulin sensitivity estimation using the minimal model

1987 ◽  
Vol 253 (6) ◽  
pp. E595-E602 ◽  
Author(s):  
Y. J. Yang ◽  
J. H. Youn ◽  
R. N. Bergman
Keyword(s):  
Standard Deviation ◽  
Insulin Sensitivity ◽  
Minimal Model ◽  
Insulin Response ◽  
Tolerance Test ◽  
Intravenous Glucose Tolerance Test ◽  
Improve Insulin Sensitivity ◽  
Intravenous Glucose ◽  
Sensitivity Estimation ◽  
Model Technique

We attempted to improve the precision of the estimation of insulin sensitivity (S1) from the minimal model technique by modifying insulin dynamics during a frequently sampled intravenous glucose tolerance test (FSIGT). Tolbutamide and somatostatin (SRIF) were used to change the insulin dynamics without directly affecting insulin sensitivity. Injection of tolbutamide (100 mg) at t = 20 min provoked an immediate secondary peak in insulin response, resulting in a greater integrated incremental insulin than the standard FSIGT. SRIF, injected at t = -1 min, delayed insulin secretion in proportion to the dose without any change in magnitude. Computer simulation was used to assess the precision of S1 estimation. Insulin dynamics from both standard and modified protocols were adjusted in magnitude, with the shape unchanged and analyzed to determine the effect of the magnitude of insulin response. Fractional standard deviation was reduced from 73% with the standard insulin profile to 23% with tolbutamide and 18% with the highest dose of SRIF. In addition, the fractional standard deviation of S1 estimates decreased exponentially with increasing magnitude of insulin response. Modified FSIGTs require a smaller insulin response than the standard protocol to achieve the same precision.

Fetal growth and the physiological control of glucose tolerance in adults: a minimal model analysis

2000 ◽  
Vol 278 (4) ◽  
pp. E700-E706 ◽  
Author(s):  
Daniel E. Flanagan ◽  
Vivienne M. Moore ◽  
Ian F. Godsland ◽  
Richard A. Cockington ◽  
Jeffrey S. Robinson ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Body Mass ◽  
Fetal Growth ◽  
Minimal Model ◽  
Adult Life ◽  
Fat Distribution ◽  
Birth Size

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.

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