QUICKI is a useful index of insulin sensitivity in subjects with hypertension

2003 ◽  
Vol 284 (4) ◽  
pp. E804-E812 ◽  
Author(s):  
Hui Chen ◽  
Gail Sullivan ◽  
Lilly Q. Yue ◽  
Arie Katz ◽  
Michael J. Quon
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Minimal Model ◽  
Fasting Blood Glucose ◽  
Glucose Clamp ◽  
Model Assessment ◽  
Antihypertensive Medications ◽  
Intravenous Glucose ◽  
Glucose Tolerance Tests ◽  
Intravenous Glucose Tolerance Tests

Insulin resistance may link disorders of metabolic homeostasis such as diabetes and obesity with disorders of hemodynamic homeostasis such as hypertension. Thus it is of interest to validate simple methods for quantifying insulin sensitivity in hypertensive patients. The quantitative insulin-sensitivity check index (QUICKI) is a novel mathematical transformation of fasting blood glucose and insulin levels. In obese and diabetic subjects, QUICKI has a significantly better linear correlation with glucose clamp determinations of insulin sensitivity than minimal-model estimates. To determine whether QUICKI is also useful in hypertensive subjects, we performed glucose clamps and frequently sampled intravenous glucose tolerance tests (FSIVGTT) on 27 hypertensive subjects taken off antihypertensive medication. Indexes of insulin sensitivity derived from glucose clamp studies (SIClamp) were compared with QUICKI, minimal-model analysis of FSIVGTTs (SIMM), and homeostasis model assessment (HOMA). The correlation between QUICKI and SIClamp ( r = 0.84) was significantly better than that between SIMM and SIClamp( r = 0.65; P < 0.028). The correlation between QUICKI and SIClamp was comparable to that between 1/HOMA and SIClamp ( r = 0.82). When studies were repeated in 14 subjects who had resumed antihypertensive medications, the percent changes in SIClamp for each of these patients were significantly correlated with percent changes in QUICKI ( r = 0.61) and HOMA ( r = −0.54) but not SIMM ( r = −0.18). We conclude that QUICKI is a simple, robust index of insulin sensitivity that is useful for evaluating and following the insulin resistance of hypertensive subjects in both research studies and clinical practice.

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.

Evaluation of four mathematical models of glucose and insulin dynamics with analysis of effects of age and obesity

1992 ◽  
Vol 262 (5) ◽  
pp. E755-E762 ◽  
Author(s):  
C. Walton ◽  
I. F. Godsland ◽  
A. J. Proudler ◽  
C. Felton ◽  
V. Wynn
Keyword(s):  
Insulin Secretion ◽  
Mathematical Models ◽  
Minimal Model ◽  
Pancreatic Secretion ◽  
Insulin Delivery ◽  
Intravenous Glucose ◽  
Glucose Disappearance ◽  
Glucose Tolerance Tests ◽  
Intravenous Glucose Tolerance Tests ◽  
Insulin Uptake

Despite there being a number of mathematical models of glucose and insulin dynamics, there have been no evaluations of their operation in large groups of subjects. We have carried out intravenous glucose tolerance tests on a group of 182 healthy males, with determination of plasma glucose, insulin, and C-peptide concentrations. Parameters of glucose and insulin dynamics were determined using the minimal model of glucose disappearance, a minimal model of peripheral insulin delivery, and two different models of pancreatic insulin secretion (models I and II). Successful identifications were obtained in 96, 95, 76, and 100% of cases, respectively. The models were evaluated in terms of their ability to recover effects of obesity and aging on carbohydrate metabolism. The glucose disappearance model successfully detected the insulin resistance of both obesity and aging, whereas the peripheral insulin delivery model indicated an increased responsiveness of insulin delivery to glucose in obesity but detected no significant change associated with age. No parameter of pancreatic secretion model I exhibited a significant association with either age or obesity. Insulin secretion model II indicated that the hyperinsulinemia accompanying obesity resulted from both increased pancreatic secretion and decreased hepatic insulin uptake.

scholarly journals The effect of pregnancy on nitrogen retention, maternal insulin sensitivity, and mRNA abundance of genes involved in energy and amino acid metabolism in gilts

2019 ◽  
Vol 97 (12) ◽  
pp. 4912-4921 ◽  
Author(s):  
Emily G Miller ◽  
Lee-Anne Huber ◽  
John P Cant ◽  
Crystal L Levesque ◽  
Cornelis F M de Lange
Keyword(s):  
Insulin Sensitivity ◽  
Estrogen Receptor Alpha ◽  
Plasma Concentrations ◽  
Nitrogen Retention ◽  
Mrna Abundance ◽  
Whole Body ◽  
Intravenous Glucose ◽  
Estrone Sulfate ◽  
Glucose Tolerance Tests ◽  
Intravenous Glucose Tolerance Tests

Abstract Twenty-one of each pregnant (P) and nonserviced, nonpregnant (NP) sister-pairs of gilts were selected to investigate the effect of pregnancy on protein deposition (Pd; whole body and maternal), insulin sensitivity, and mRNA abundance of genes involved in energy and AA metabolism. Between breeding (study day 0) and day 111, P and NP gilts received 2.16 kg of the experimental diet (3.34 Mcal ME/kg, 17.6% crude protein, 0.78% standardized ileal digestible lysine) that was formulated to meet the estimated ME requirements of pregnant gilts (and meet or exceed AA requirements). Nitrogen balances were conducted on day 63 and 102 ± 0.2 of the study during 4-d periods. Blood samples were collected on day 43, 56, 71, 85, 98, and 108 ± 0.3 of the study to determine plasma concentrations of fasted IGF-1, estradiol (E2), and estrone sulfate (E1S). Frequently sampled intravenous glucose tolerance tests (FSIGTT) were conducted on day 75 ± 0.7 in 6 P and 5 NP gilts and on day 107 ± 0.4 in 17 P and 17 NP gilts and the MINMOD approach was applied to evaluate whole body insulin sensitivity and pancreatic responsiveness. Longissimus muscle (LM) and s.c. adipose tissue (AD) samples were excised from 12 P and 12 NP gilts at day 111 ± 0.4 of the study after euthanasia to determine mRNA abundance of key genes. Whole body Pd was greater (P &lt; 0.001) at day 102 and maternal Pd was lower (P &lt; 0.002) at day 63 and 102 for P compared to NP gilts. Plasma concentrations of E1S and E2 increased (P &lt; 0.05) with study day for P gilts and remained constant for NP gilts, which coincided with reduced plasma concentrations of IGF-1 and increased estrogen receptor alpha (ESR1) mRNA abundance in LM of P gilts. Glucose effectiveness was not different between P and NP gilts, but whole body insulin sensitivity was lower (P = 0.004) in P compared to NP gilts on day 75 and 107, which corresponded with reduced mRNA abundances of SLC2A4, HK2, SREBF1, and FASN, and increased abundances of PDK4 and PPARGC1A in LM and AD. When fed identically, P gilts had greater whole body Pd at day 102, which reflects Pd in the pregnancy-associated tissues (at the expense of maternal Pd), likely driven by estrogen-stimulated insulin resistance in peripheral tissue and subsequent modulation of gene expression relating to glucose metabolism.

scholarly journals The biochemical assessment of insulin resistance

2007 ◽  
Vol 44 (4) ◽  
pp. 324-342 ◽  
Author(s):  
Anwar Borai ◽  
Callum Livingstone ◽  
Gordon A A Ferns
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Model Assessment ◽  
Intravenous Glucose ◽  
Gold Standard Method ◽  
The Metabolic Syndrome ◽  
Increased Risk

Insulin resistance is a common condition, recognized to be a central feature of the metabolic syndrome, and strongly associated with an increased risk of cardiovascular disease and diabetes. The quantitative assessment of insulin sensitivity is not used for routine clinical purposes, but the emerging importance of insulin resistance has led to its wider application to research studies that have examined its pathogenesis, aetiology and consequences. The gold standard method for the determination of insulin sensitivity is the euglycaemic hyperinsulinaemic clamp from which indices of insulin sensitivity can be derived. The clamp technique is both expensive and complex to undertake and has prompted the use of surrogate methods, notably the insulin tolerance test and frequently sampled intravenous glucose tolerance test. Indices may be derived from these methods and correlate well with those derived from clamp studies. Indices can also be derived from measurements made during a standard oral glucose tolerance test and from one-off fasting specimens (e.g. homeostasis model assessment and quantitative insulin sensitivity check index). These indices lend themselves for use in large population studies where a relatively simple, inexpensive assessment is necessary. However, these tests all suffer from important limitations, including poor precision. Insulin resistance is increasingly being assessed in clinical situations, where relatively simple markers are required. Insulin-like growth factor binding protein-1 is an emerging marker which may be useful in this context.

GLUCOSE TOLERANCE AND INSULIN RESPONSE DURING DAILY CONTINUOUS LOW-DOSE ORAL CONTRACEPTIVE TREATMENT

1969 ◽  
Vol 62 (2) ◽  
pp. 242-250 ◽  
Author(s):  
U. Larsson-Cohn ◽  
B. Tengström ◽  
L. Wide
Keyword(s):  
Glucose Tolerance ◽  
Blood Glucose Concentration ◽  
Fasting Blood Glucose ◽  
Insulin Response ◽  
Continuous Treatment ◽  
Intravenous Glucose ◽  
Dose Oral ◽  
Glucose Tolerance Tests ◽  
Insulin Response To Glucose ◽  
Intravenous Glucose Tolerance Tests

ABSTRACT Intravenous glucose tolerance tests and insulin determinations were performed on 37 women at different stages of the menstrual cycle and after one, three and twelve months of daily continuous treatment with 0.5 mg of norethindrone or 0.5 mg of chlormadinone acetate. The fasting blood glucose concentration, the k-values (percentage disappearance rate of glucose per minute) and the insulin response to glucose administration were compared. No statistically significant differences were found between the values obtained on two occasions before treatment, and during treatment.

scholarly journals Quantitative Insulin Sensitivity Check Index: A Simple, Accurate Method for Assessing Insulin Sensitivity In Humans

2000 ◽  
Vol 85 (7) ◽  
pp. 2402-2410 ◽  
Author(s):  
Arie Katz ◽  
Sridhar S. Nambi ◽  
Kieren Mather ◽  
Alain D. Baron ◽  
Dean A. Follmann ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Minimal Model ◽  
Accurate Method ◽  
Model Analysis ◽  
Glucose Clamp ◽  
Clinical Investigations ◽  
Glucose Tolerance Tests ◽  
Type 2 Diabetic

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.

scholarly journals Adiposity and Insulin Sensitivity Derived from Intravenous Glucose Tolerance Tests in Antipsychotic-Treated Patients

2007 ◽  
Vol 32 (12) ◽  
pp. 2561-2569 ◽  
Author(s):  
Dan W Haupt ◽  
Peter A Fahnestock ◽  
Karen A Flavin ◽  
Julie A Schweiger ◽  
Angela Stevens ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Intravenous Glucose ◽  
Intravenous Glucose Tolerance ◽  
Glucose Tolerance Tests ◽  
Intravenous Glucose Tolerance Tests

scholarly journals SAT-624 Predictive Ability of Lipoprotein Insulin Resistance (LPIR) Score in South Asians: A Comparison of Surrogate Indices of Insulin Sensitivity/Resistance

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Andin Fosam ◽  
Shivraj Grewal ◽  
Abdul-Latif Armiyaw ◽  
Camila Sarcone ◽  
Antoinette Rabel ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Mean Squared Error ◽  
Predictive Accuracy ◽  
South Asians ◽  
Model Analysis ◽  
Calibration Model ◽  
Model Assessment ◽  
Intravenous Glucose ◽  
Insulin Resistant

Abstract South Asians (SA) are at higher risk for developing insulin resistance (IR) and type 2 diabetes. Consequently, identifying IR in this population is important. Lack of standardization and harmonization of insulin assays limit the clinical use of insulin-based surrogate indexes of insulin resistance. The lipoprotein insulin resistance (LPIR) score, a metabolomic marker, reflects the lipoprotein abnormalities observed in insulin-resistant states. The reliability of the LPIR score to predict IR in South Asians is currently unknown. In this study, we aimed to evaluate the predictive accuracy of LPIR compared to other fasting-based surrogate indices in SA. In a cross-sectional study of 59 non-diabetic SA subjects (age 36 ± 8 years, BMI 26.5 ± 5.2 kg/m2), we used calibration model analysis to assess the ability of the LPIR score and other simple surrogate indices [homeostasis model assessment (HOMA-IR), quantitative insulin sensitivity check index (QUICKI) and Adipose tissue insulin sensitivity (Adipo-SI)] to predict insulin sensitivity derived from the reference frequently sampled intravenous glucose tolerance test (FSIVGTT) and Minimal Model analysis (SiMM). LPIR scores were calculated using six lipoprotein particle concentrations and sizes measured by nuclear magnetic resonance (NMR) spectroscopy. Further, quantitative predictive accuracy and index comparisons were determined by root mean squared error (RMSE) of prediction and leave-one-out cross-validation-type RMSE of prediction (CVPE). Receiver operating characteristic (ROC) curve analysis was performed to determine how well LPIR distinguished insulin resistant individuals, categorized as an SiMM &lt; 3. As determined by calibration model analysis, Adipo-SI, HOMA-IR, and QUICKI showed moderate correlations with for SiMM (Adipo-SI: r = 0.66; HOMA-IR: r = 0.60; QUICKI: r = 0.57, p = &lt;0.0001). No significant differences were noted among CVPE or RMSE from any of the routinely used surrogate indices when compared with LPIR. The ROC area under the curve was 0.76 (95% CI 0.64–0.87) suggesting that LPIR performed well in identifying insulin resistant subjects. The optimal cut-off in IR individuals was LPIR &gt;46 (sensitivity: 75.9 %, specificity: 70.0%). We conclude that NMR-derived LPIR may be an appropriate index to assess insulin resistance in South Asians.

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