scholarly journals Improved indices of insulin resistance and insulin secretion for use in genetic and population studies of type2 diabetes mellitus

Twin Research ◽  
2000 ◽  
Vol 3 (3) ◽  
pp. 148-151 ◽  
Author(s):  
Arthur B Jenkins ◽  
Katherine Samaras ◽  
David GP Carey ◽  
Paul Kelly ◽  
Lesley V Campbell
Keyword(s):  
Insulin Resistance ◽  
Insulin Secretion ◽  
Plasma Glucose ◽  
Fasting Plasma Glucose ◽  
Statistical Modelling ◽  
Model Assessment ◽  
Fasting Plasma ◽  
Significant Heritability ◽  
A Minor ◽  
Direct Measures

AbstractHomeostasis model assessment (HOMA) provides indices of insulin secretion (β) and insulin resistance (R) derived from fasting plasma glucose (FPG) and fasting plasma insulin (FPI) levels. However, these indices could not account for a significant heritability of fasting plasma glucose (FPG) (h2 = 0.75, P < 0.01) in a group of 214 female twins. This result is consistent with a misclassification between effects due to insulin secretion and resistance in the HOMA indices. We report here evidence of such misclassification in the HOMA indices and describe a minor modification to the model which corrects it. Direct measures of insulin resistance (euglycaemic clamp) and secretion (i.v. glucose bolus) were obtained in 43 non-diabetic subjects. Heritability was estimated by statistical modelling of genetic and environmental influences in data from 214 non-diabetic female subjects. Modified HOMA (HOMA′) indices were obtained from β′ = (Ln(FPI)–c)/FPG and R′ = (Ln(FPI)–c)* FPG where c is a constant derived from regression analysis of Ln(FPI) vs FPG. Indices from both models correlated with the direct measures similarly (r = 0.63 (R), 0.49 (R′), 0.45 (β), 0.39 (β′), all P < 0.01). Directly measured insulin resistance and secretion were not significantly correlated (r = 0.13, P = 0.21). However, unmodified HOMA- and R were strongly related (r = 0.78, P < 0.0001 vs 0.13) demonstrating substantial misclassification. The relationship between β′ and R′ (r = 0.13) was not different from that between the two direct measures and significant heritability of β′ (h2 = 0.68, P < 0.01) and R′ (h2 = 0.59, P < 0.05) was evident in the twin data. The proposed modification to HOMA significantly reduces misclassification and reveals separate components of insulin resistance and insulin secretion in the heritability of FPG. Twin Research (2000) 3, 148–151.

THE RELATIONSHIP BETWEEN DIFFERENT DIABETIC FACTORS IN IMPAIRED FASTING PLASMA GLUCOSE OBESE ELDERLY

2021 ◽  
pp. 10-12
Author(s):  
Ming-Chieh Ma ◽  
Dee Pei
Keyword(s):  
Insulin Resistance ◽  
Insulin Secretion ◽  
Plasma Glucose ◽  
Fasting Plasma Glucose ◽  
Demographic Data ◽  
Fasting Blood Glucose ◽  
Second Phase ◽  
Male And Female ◽  
Fasting Plasma ◽  
The Relationship

Background: In both developed and developing countries, the relationship between aging an obesity is similar and studies appear to be more important at all ages. Therefore, we focused on patients with impaired fasting blood glucose levels to see the baseline changes in insulin homeostasis. The current study seeks to explain the relationship between insulin secretion, insulin resistance, and glucose effects in obese elderly people. Methods: We randomly enrolled 31subjects who were aged 65 years old. All these patients were obese (body mass index ≥ 25 2 kg/m ) and the fasting plasma glucose (FPG) was between 100 and 125 mg/dl. Four diabetic factors were calculated and included rst phase insulin secretion (PFIS), second phase insulin secretion (SFIS), insulin resistance (IR) and glucose effectiveness (GE). Results: In the current study, we enrolled 18 male and 13 female subjects. The mean FPG was 108 (mg/dl) in both male and female. All the demographic data were non-signicant when compared with male and female except the hemoglobin. When we compared these four diabetic factors with FPG, we found only SPIS was signicantly negative correlated with FPG in both genders. Discussion: FPG was correlated with SPIS only. FPIS, IR and GE were not correlated with FPG in impaired fasting plasma glucose obese elderly. Further study is needed for understating the underlying mechanisms.

scholarly journals Homeostasis model assessment: insulin resistance and ?-cell function from fasting plasma glucose and insulin concentrations in man

Diabetologia ◽  
1985 ◽  
Vol 28 (7) ◽  
pp. 412-419 ◽  
Author(s):  
D. R. Matthews ◽  
J. P. Hosker ◽  
A. S. Rudenski ◽  
B. A. Naylor ◽  
D. F. Treacher ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Plasma Glucose ◽  
Fasting Plasma Glucose ◽  
Cell Function ◽  
Model Assessment ◽  
Homeostasis Model Assessment ◽  
Fasting Plasma

Variation of Fasting Plasma Glucose, Insulin, and Insulin Resistance in Thai Adults According to the New BMI Criteria for Asians

2008 ◽  
Vol 78 (2) ◽  
pp. 57-63 ◽  
Author(s):  
Komindr ◽  
Viroonudomphol ◽  
Cherdchu
Keyword(s):  
Insulin Resistance ◽  
Nutritional Status ◽  
Plasma Glucose ◽  
Fasting Plasma Glucose ◽  
Plasma Lipid ◽  
Model Assessment ◽  
Lower Middle Class ◽  
Lipid Status ◽  
Fasting Plasma ◽  
Relationship Of

For a group of 73 males and 247 females, being health-conscious and from the lower middle class of Bangkok, with various degrees of the nutritional status defined by the new criteria for Asians, the relationship of anthropometric indicators and the plasma lipid status to fasting glucose, fasting plasma insulin, and the homeostasis model assessment for insulin-resistance (HOMA-IR) has been studied. For assessing differences among groups either the Mann-Whitney U-test or the Kruskal-Wallis analysis of variance for multiple comparisons were applied. Multivariate regression models were computed to assess variation of glucose, insulin, and the HOMA-IR due to the nutritional status and serum lipids. A significant increase in fasting plasma glucose for both sexes and for females for the HOMA-IR models could be observed for the group with a body-mass index (BMI) range of 23 to less than 25. Insulin concentrations and HOMA-IR correlated for both sexes, especially with BMI and hip circumference, while the variation of fasting plasma glucose is less dependent on anthropometric nutritional indicators in comparison to insulin and HOMA-IR. Only the lipid status of females weakly correlated with insulin and HOMA-IR.

scholarly journals Estimates of Insulin Secretory Function in Apparently Healthy Volunteers Vary as a Function of How the Relevant Variables Are Quantified

2011 ◽  
Vol 57 (4) ◽  
pp. 627-632 ◽  
Author(s):  
Barry R Johns ◽  
Fahim Abbasi ◽  
Gerald M Reaven
Keyword(s):  
Insulin Resistance ◽  
Insulin Secretion ◽  
Plasma Glucose ◽  
Insulin Action ◽  
Cell Function ◽  
Model Assessment ◽  
Pancreatic Β Cell ◽  
Homeostasis Model Assessment ◽  
Β Cell ◽  
Β Cell Function

BACKGROUND Several surrogate estimates have been used to define relationships between insulin action and pancreatic β-cell function in healthy individuals. Because it is unclear how conclusions about insulin secretory function depend on specific estimates used, we evaluated the effect of different approaches to measurement of insulin action and secretion on observations of pancreatic β-cell function in individuals whose fasting plasma glucose (FPG) was &lt;7.0 mmol/L (126 mg/dL). METHODS We determined 2 indices of insulin secretion [homeostasis model assessment of β-cell function (HOMA-β) and daylong insulin response to mixed meals], insulin action [homeostasis model assessment of insulin resistance (HOMA-IR) and steady-state plasma glucose (SSPG) concentration during the insulin suppression test], and degree of glycemia [fasting plasma glucose (FPG) and daylong glucose response to mixed meals] in 285 individuals with FPG &lt;7.0 mmol/L. We compared the relationship between the 2 measures of insulin secretion as a function of the measures of insulin action and degree of glycemia. RESULTS Assessment of insulin secretion varied dramatically as a function of which of the 2 methods was used and which measure of insulin resistance or glycemia served as the independent variable. For example, the correlation between insulin secretion (HOMA-β) and insulin resistance varied from an r value of 0.74 (when HOMA-IR was used) to 0.22 (when SSPG concentration was used). CONCLUSIONS Conclusions about β-cell function in nondiabetic individuals depend on the measurements used to assess insulin action and insulin secretion. Viewing estimates of insulin secretion in relationship to measures of insulin resistance and/or degree of glycemia does not mean that an unequivocal measure of pancreatic β-cell function has been obtained.

scholarly journals Effect of Exenatide on Splanchnic and Peripheral Glucose Metabolism in Type 2 Diabetic Subjects

2011 ◽  
Vol 96 (6) ◽  
pp. 1763-1770 ◽  
Author(s):  
E. Cersosimo ◽  
A. Gastaldelli ◽  
A. Cervera ◽  
E. Wajcberg ◽  
A. Sriwijilkamol ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Gastric Emptying ◽  
Glucose Uptake ◽  
Plasma Glucose ◽  
Fasting Plasma Glucose ◽  
Plasma Insulin ◽  
Hepatic Insulin Resistance ◽  
Oral Glucose ◽  
Fasting Plasma

Objective: Our objective was to examine the mechanisms via which exenatide attenuates postprandial hyperglycemia in type 2 diabetes mellitus (T2DM). Study Design: Seventeen T2DM patients (44 yr; seven females, 10 males; body mass index = 33.6 kg/m2; glycosylated hemoglobin = 7.9%) received a mixed meal followed for 6 h with double-tracer technique ([1-14C]glucose orally; [3-3H]glucose iv) before and after 2 wk of exenatide. In protocol II (n = 5), but not in protocol I (n = 12), exenatide was given in the morning of the repeat meal. Total and oral glucose appearance rates (RaT and RaO, respectively), endogenous glucose production (EGP), splanchnic glucose uptake (75 g − RaO), and hepatic insulin resistance (basal EGP × fasting plasma insulin) were determined. Results: After 2 wk of exenatide (protocol I), fasting plasma glucose decreased (from 10.2 to 7.6 mm) and mean postmeal plasma glucose decreased (from 13.2 to 11.3 mm) (P &lt; 0.05); fasting and meal-stimulated plasma insulin and glucagon did not change significantly. After exenatide, basal EGP decreased (from 13.9 to 10.8 μmol/kg · min, P &lt; 0.05), and hepatic insulin resistance declined (both P &lt; 0.05). RaO, gastric emptying (acetaminophen area under the curve), and splanchnic glucose uptake did not change. In protocol II (exenatide given before repeat meal), fasting plasma glucose decreased (from 11.1 to 8.9 mm) and mean postmeal plasma glucose decreased (from 14.2 to 10.1 mm) (P &lt; 0.05); fasting and meal-stimulated plasma insulin and glucagon did not change significantly. After exenatide, basal EGP decreased (from 13.4 to 10.7 μmol/kg · min, P = 0.05). RaT and RaO decreased markedly from 0–180 min after meal ingestion, consistent with exenatide's action to delay gastric emptying. Conclusions: Exenatide improves 1) fasting hyperglycemia by reducing basal EGP and 2) postmeal hyperglycemia by reducing the appearance of oral glucose in the systemic circulation.

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