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Meeting Abstracts
Journal: Diabetes
Diabetes 2020;69(Supplement_1):1473-P
Published: 01 June 2020
... and laboratory parameters were recorded. IR was calculated using TyG index and HOMA IR using following formulae: TyG = ln (Triglycerides in mg/dL x Glucose in mg/dL/2)8 IRHOMA = (I0 × G0)/405 (I0 -fasting insulin in mIU/L, G0-fasting glucose in mg/dL)1 IR was defined as HOMA-IR >2.8 or TyG index >4.65...
Meeting Abstracts
Journal: Diabetes
Diabetes 2019;68(Supplement_1):2499-PUB
Published: 01 June 2019
... cholesterol increased moderate to severe HOMA-IR by 50% and 90% respectively (aOR 1.999, 95% CI: 1.123-3.56; P = 0.019). Insulin level among female (aOR1.051, 95% CI: 1.005-1.098; P = 0.028) and HbA1c among male (aOR1.427, 95% CI: 1.06-1.921; P =0.019) increased 5% and 42% of metabolic syndrome risk...
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Tree model for <span class="search-highlight">insulin</span> <span class="search-highlight">resistance</span> using <span class="search-highlight">HOMA</span>-<span class="search-highlight">IR</span>, BMI, LDL, and waist circum...
Published: 01 February 2005
FIG. 2. Tree model for insulin resistance using HOMA-IR, BMI, LDL, and waist circumference. Using the regression equation, fasting plasma insulin (pmol/l) = 6.786 + (25.314 × HOMA-IR), the approximate insulin concentrations corresponding to the HOMA-IR cutoffs of 7.40 and 3.11 are 194.1 and 85.5 p... More
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Diet-induced changes in <span class="search-highlight">insulin</span> sensitivity, measured from EGC (<em>A</em>...
Published: 15 May 2014
Figure 2 Diet-induced changes in insulin sensitivity, measured from EGC (A), IVGTT (B), or HOMA-IR (C). Both clamp and IVGTT detected substantial diet-induced insulin resistance. In contrast, changes in HOMA-IR did not reflect development of resistance after fat feeding. ***, P < 0.0001. Figure 2. Diet-induced changes in insulin sensitivity, measured from EGC (A), IVGTT (B), or HOMA-IR (C). Both clamp and IVGTT detected substantial diet-induced insulin resistance. In contrast, changes in HOMA-IR did not reflect development of resistance after fat feeding. ***, P < 0.0001. More
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Associations between <span class="search-highlight">insulin</span> secretion indicators (<em>A</em>–
Published: 18 July 2017
Figure 2 Associations between insulin secretion indicators (AE) and concentrations of PCBs stratified by the level of HOMA-IR. ∑PCBs: rank sum of six PCBs (PCB118, PCB138, PCB153, PCB170, PCB180, and PCB187) adjusted for age, sex, BMI, cigarette smoking, alcohol consumption, physical activity, total cholesterol, triglycerides, and insulin sensitivity. For the analyses in which the static and dynamic DIs are dependent variables, insulin sensitivity was excluded from the preceding covariates. ●, insulin-sensitive group (HOMA-IR <1.95); □, insulin-resistant group (HOMA-IR ≥1.95). Figure 2. Associations between insulin secretion indicators (A–E) and concentrations of PCBs stratified by the level of HOMA-IR. ∑PCBs: rank sum of six PCBs (PCB118, PCB138, PCB153, PCB170, PCB180, and PCB187) adjusted for age, sex, BMI, cigarette smoking, alcohol consumption, physical activity, total cholesterol, triglycerides, and insulin sensitivity. For the analyses in which the static and dynamic DIs are dependent variables, insulin sensitivity was excluded from the preceding covariates. ●, insulin-sensitive group (HOMA-IR <1.95); □, insulin-resistant group (HOMA-IR ≥1.95). More
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Associations between <span class="search-highlight">insulin</span> secretion indicators (<em>A</em>–
Published: 18 July 2017
Figure 1 Associations between insulin secretion indicators (AE) and concentrations of OCPs stratified by the level of HOMA-IR. ∑OCPs: rank sum of four OCPs (p,p′-DDT; p,p′-DDE; β-HCH; and trans-nonachlor) adjusted for age, sex, BMI, cigarette smoking, alcohol consumption, physical activity, total cholesterol, triglycerides, and insulin sensitivity. For the analyses in which the static and dynamic DIs are dependent variables, insulin sensitivity was excluded from the preceding covariates. ●, insulin-sensitive group (HOMA-IR <1.95); □, insulin-resistant group (HOMA-IR ≥1.95). Figure 1. Associations between insulin secretion indicators (A–E) and concentrations of OCPs stratified by the level of HOMA-IR. ∑OCPs: rank sum of four OCPs (p,p′-DDT; p,p′-DDE; β-HCH; and trans-nonachlor) adjusted for age, sex, BMI, cigarette smoking, alcohol consumption, physical activity, total cholesterol, triglycerides, and insulin sensitivity. For the analyses in which the static and dynamic DIs are dependent variables, insulin sensitivity was excluded from the preceding covariates. ●, insulin-sensitive group (HOMA-IR <1.95); □, insulin-resistant group (HOMA-IR ≥1.95). More
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Circulating factors measured before pregnancy and in the first trimester th...
Published: 12 October 2016
Figure 1 Circulating factors measured before pregnancy and in the first trimester that have been associated with the subsequent diagnosis of GDM in late second/third trimester. GGT, γ-glutamyl transferase; HOMA-IR, HOMA of insulin resistance; TPA, tissue plasminogen activator. Figure 1. Circulat... More
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Notch-dependent gene expression is progressively increased in <span class="search-highlight">insulin</span> resis...
Published: 16 November 2013
FIG. 4. Notch-dependent gene expression is progressively increased in insulin resistance and NAFLD severity. Quantitative PCR for HES1 and other Notch target genes from liver biopsy samples from patients with pathologically confirmed SS, NASH, or normal liver, further subdivided as insulin-sensitive (HOMA-IR <2.5) vs. insulin-resistant (HOMA-IR >2.5) (A), or T2D patients (B), are shown. C: Hepatocyte Notch target expression is increased in patients with NASH. Scale bars are 50 µm long. Data show means ± SEM. *P < 0.05 vs. T2D/SS; ***P < 0.001 by ANOVA. AU, arbitrary units. FIG. 4. Notch-dependent gene expression is progressively increased in insulin resistance and NAFLD severity. Quantitative PCR for HES1 and other Notch target genes from liver biopsy samples from patients with pathologically confirmed SS, NASH, or normal liver, further subdivided as insulin-sensitive (HOMA-IR <2.5) vs. insulin-resistant (HOMA-IR >2.5) (A), or T2D patients (B), are shown. C: Hepatocyte Notch target expression is increased in patients with NASH. Scale bars are 50 µm long. Data show means ± SEM. *P < 0.05 vs. T2D/SS; ***P < 0.001 by ANOVA. AU, arbitrary units. More
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Depot-specific release of 16:1<em>n</em>-7 from lower- and upper-bo...
Published: 14 May 2012
FIG. 1. Depot-specific release of 16:1n-7 from lower- and upper-body subcutaneous AT depots. A: The release of 16:1n-7 relative to 16:0 was greater from gluteofemoral AT compared with abdominal AT in both sexes (P ≤ 0.001). B: When grouped according to insulin-resistance status (as calculated by HOMA-IR), the release of 16:1n-7 relative to 16:0 from the gluteofemoral depot was higher in individuals with a HOMA-IR<2.4 (P < 0.05). Release of 16:1n-7 relative to 16:0 from abdominal AT was not different between HOMA-IR groups. All data are represented as mean ± SEM. FIG. 1. Depot-specific release of 16:1n-7 from lower- and upper-body subcutaneous AT depots. A: The release of 16:1n-7 relative to 16:0 was greater from gluteofemoral AT compared with abdominal AT in both sexes (P ≤ 0.001). B: When grouped according to insulin-resistance status (as calculated by HOMA-IR), the release of 16:1n-7 relative to 16:0 from the gluteofemoral depot was higher in individuals with a HOMA-IR<2.4 (P < 0.05). Release of 16:1n-7 relative to 16:0 from abdominal AT was not different between HOMA-IR groups. All data are represented as mean ± SEM. More
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Serum <span class="search-highlight">insulin</span> levels 10 min after glucose challenge (<em>A</em>), H...
Published: 01 May 2007
FIG. 4. Serum insulin levels 10 min after glucose challenge (A), HOMA of β-cell index (B), insulin tolerance test (C), and HOMA of insulin resistance (IR) index (D) at 1, 3, and 6 months of age. Serum insulin levels (A) and HOMA of β-cell indices (B) of Munich Ins2C95S mutant (mt) mice are significantly lower than those of wild-type (wt) mice. C: Blood glucose decrease from basal is significantly less in mutants versus wild-type mice. D: One-month-old female (f) mutants and 3- and 6-month-old male (m) mutants show significantly higher HOMA of insulin resistance indices than wild-type mice. Data represent means and SE. *P < 0.05. FIG. 4. Serum insulin levels 10 min after glucose challenge (A), HOMA of β-cell index (B), insulin tolerance test (C), and HOMA of insulin resistance (IR) index (D) at 1, 3, and 6 months of age. Serum insulin levels (A) and HOMA of β-cell indices (B) of Munich Ins2C95S mutant (mt) mice are significantly lower than those of wild-type (wt) mice. C: Blood glucose decrease from basal is significantly less in mutants versus wild-type mice. D: One-month-old female (f) mutants and 3- and 6-month-old male (m) mutants show significantly higher HOMA of insulin resistance indices than wild-type mice. Data represent means and SE. *P < 0.05. More
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<span class="search-highlight">Insulin</span> sensitivity determined by the <span class="search-highlight">HOMA</span>-<span class="search-highlight">IR</span> (<em>A</em>) and β-ce...
Published: 01 July 2002
FIG. 1. Insulin sensitivity determined by the HOMA-IR (A) and β-cell function quantified as ΔI30/ΔG30 (B) and (ΔI30/ΔG30)/HOMA-IR (C) from an OGTT in 531 first-degree relatives with NGT (n = 240), IFG/IGT (n = 191), and diabetes (n = 100). Individuals who had IFG or IGT and had diabetes by the 2-h or fasting glucose criteria, respectively, were classified as having diabetes. As glucose tolerance declined, insulin resistance increased and β-cell function deteriorated. FIG. 1. Insulin sensitivity determined by the HOMA-IR (A) and β-cell function quantified as ΔI30/ΔG30 (B) and (ΔI30/ΔG30)/HOMA-IR (C) from an OGTT in 531 first-degree relatives with NGT (n = 240), IFG/IGT (n = 191), and diabetes (n = 100). Individuals who had IFG or IGT and had diabetes by the 2-h or fasting glucose criteria, respectively, were classified as having diabetes. As glucose tolerance declined, insulin resistance increased and β-cell function deteriorated. More
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Relationship of <span class="search-highlight">insulin</span> sensitivity determined by the <span class="search-highlight">HOMA</span>-<span class="search-highlight">IR</span> (<em>A</em>...
Published: 01 July 2002
FIG. 3. Relationship of insulin sensitivity determined by the HOMA-IR (A), β-cell function quantified as ΔI30/ΔG30 (B) and (ΔI30/ΔG30)/HOMA-IR (C) to glucose disposal after an oral glucose load quantified as AUCg in 531 first-degree relatives. The relationship between insulin sensitivity and glucose disposal is linear in nature (r2 = 0.084, P < 0.001), whereas that between β-cell function and glucose disposal is nonlinear and best described by a log-linear fit (ΔI30/ΔG30: r2 = 0.29, P < 0.001; (ΔI30/ΔG30)/HOMA resistance: r2 = 0.45, P < 0.001) The means for each glucose tolerance category (NGT [shaded circle], IFG/IGT [shaded diamond], and diabetes [shaded square]) are illustrated. FIG. 3. Relationship of insulin sensitivity determined by the HOMA-IR (A), β-cell function quantified as ΔI30/ΔG30 (B) and (ΔI30/ΔG30)/HOMA-IR (C) to glucose disposal after an oral glucose load quantified as AUCg in 531 first-degree relatives. The relationship between insulin sensitivity and glucose disposal is linear in nature (r2 = 0.084, P < 0.001), whereas that between β-cell function and glucose disposal is nonlinear and best described by a log-linear fit (ΔI30/ΔG30: r2 = 0.29, P < 0.001; (ΔI30/ΔG30)/HOMA resistance: r2 = 0.45, P < 0.001) The means for each glucose tolerance category (NGT [shaded circle], IFG/IGT [shaded diamond], and diabetes [shaded square]) are illustrated. More
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The BCAA catabolic pathway shows a strong correlation with <span class="search-highlight">insulin</span> resistan...
Published: 14 August 2019
The BCAA catabolic pathway shows a strong correlation with insulin resistance in a mouse population. Correlation of individual BCAA catabolic genes in different tissues for fasting glucose, fasting insulin, and HOMA-IR in HMDP mice fed an HFD. Red indicates a positive correlation, whereas blue indic... More
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Increasing 5α-reductase activity is associated with increased <span class="search-highlight">insulin</span> secre...
Published: 01 October 2008
FIG. 2. Increasing 5α-reductase activity is associated with increased insulin secretion across an OGTT in men (•) and women (□)—fasting insulin (A), 2-h insulin (B), area under curve insulin (C), and increased insulin resistance as measured by HOMA-IR (D). FIG. 2. Increasing 5α-reductase activity is associated with increased insulin secretion across an OGTT in men (•) and women (□)—fasting insulin (A), 2-h insulin (B), area under curve insulin (C), and increased insulin resistance as measured by HOMA-IR (D). More
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Obese patients with <span class="search-highlight">insulin</span> <span class="search-highlight">resistance</span> display significantly decreased
Published: 17 October 2011
FIG. 1. Obese patients with insulin resistance display significantly decreased Helios but increased FOXP3 mRNA expression in their hVAT. A: hVAT of lean control subjects (white bar, n = 14), obese patients with normal insulin sensitivity (HOMA <2.5, gray bar, n = 39), and obese patients with impaired insulin sensitivity (HOMA >5, black bar, n = 39) was analyzed for Helios and FOXP3 mRNA expression. P < 0.025 was considered significant; n.s., not significant. Correlation of the Helios-to-FOXP3 mRNA ratio in hVAT (n = 92) with BMI (P = 0.121) (B), HOMA-IR (P = 0.003) (C), and fasting blood glucose levels (P = 0.045) (D) was analyzed using Spearman ρ. P < 0.05 was considered significant. FIG. 1. Obese patients with insulin resistance display significantly decreased Helios but increased FOXP3 mRNA expression in their hVAT. A: hVAT of lean control subjects (white bar, n = 14), obese patients with normal insulin sensitivity (HOMA <2.5, gray bar, n = 39), and obese patients with impaired insulin sensitivity (HOMA >5, black bar, n = 39) was analyzed for Helios and FOXP3 mRNA expression. P < 0.025 was considered significant; n.s., not significant. Correlation of the Helios-to-FOXP3 mRNA ratio in hVAT (n = 92) with BMI (P = 0.121) (B), HOMA-IR (P = 0.003) (C), and fasting blood glucose levels (P = 0.045) (D) was analyzed using Spearman ρ. P < 0.05 was considered significant. More
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An overview of the study design, analytical steps, and questions addressed....
Published: 03 November 2014
Figure 1 An overview of the study design, analytical steps, and questions addressed. The strategy addressed a number of key questions about the relationship between human genetic associations with T2D or related glycemic traits and antidiabetes drug targets. A similar strategy can be applied to other diseases and traits. 2-h glucose and 2-h insulin, glucose or insulin plasma levels measured 2 h after an oral glucose tolerance test; HbA1c, a measure for long-term glycemia; HOMA-B, a measure for β-cell function; HOMA-IR, a measure for insulin resistance. Figure 1. An overview of the study design, analytical steps, and questions addressed. The strategy addressed a number of key questions about the relationship between human genetic associations with T2D or related glycemic traits and antidiabetes drug targets. A similar strategy can be applied to other diseases and traits. 2-h glucose and 2-h insulin, glucose or insulin plasma levels measured 2 h after an oral glucose tolerance test; HbA1c, a measure for long-term glycemia; HOMA-B, a measure for β-cell function; HOMA-IR, a measure for insulin resistance. More
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Association of serum adipokine levels and <span class="search-highlight">HOMA</span>-<span class="search-highlight">IR</span> with BMI SDS, adipocyte d...
Published: 12 November 2014
Figure 5 Association of serum adipokine levels and HOMA-IR with BMI SDS, adipocyte diameter, and macrophage infiltration. Adiponectin serum levels decrease with BMI SDS (A), whereas no association with adipocyte diameter was observed (B). Furthermore, we observed a negative association with macrophage infiltration (C). Serum leptin levels were positively associated with BMI SDS (D), adipocyte diameter (E), and macrophage infiltration (F). The insulin resistance marker HOMA-IR showed a positive correlation with BMI SDS (G), adipocyte size (H), and macrophage infiltration (I). Pearson correlation coefficient R and P values are given in each scatter plot. Significant P values (P < 0.05) are indicated in bold. Lean children are represented as open circles and obese as closed circles. Figure 5. Association of serum adipokine levels and HOMA-IR with BMI SDS, adipocyte diameter, and macrophage infiltration. Adiponectin serum levels decrease with BMI SDS (A), whereas no association with adipocyte diameter was observed (B). Furthermore, we observed a negative association with macrophage infiltration (C). Serum leptin levels were positively associated with BMI SDS (D), adipocyte diameter (E), and macrophage infiltration (F). The insulin resistance marker HOMA-IR showed a positive correlation with BMI SDS (G), adipocyte size (H), and macrophage infiltration (I). Pearson correlation coefficient R and P values are given in each scatter plot. Significant P values (P < 0.05) are indicated in bold. Lean children are represented as open circles and obese as closed circles. More
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SF exposure in utero increases <span class="search-highlight">insulin</span> <span class="search-highlight">resistance</span> in offspring mice. GTT (...
Published: 15 September 2014
Figure 2 SF exposure in utero increases insulin resistance in offspring mice. GTT (A), ITT (B), and HOMA-IR (C) values at 24 weeks of age in SC and SF were determined. Data are mean ± SE (n = 8/experimental group). *P < 0.01 for SF vs. SC, **P < 0.001. Figure 2. SF exposure in utero increases insulin resistance in offspring mice. GTT (A), ITT (B), and HOMA-IR (C) values at 24 weeks of age in SC and SF were determined. Data are mean ± SE (n = 8/experimental group). *P < 0.01 for SF vs. SC, **P < 0.001. More
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Circulating LECT2 correlates with adiposity and <span class="search-highlight">insulin</span> <span class="search-highlight">resistance</span>. Graphs ...
Published: 12 April 2014
Figure 1 Circulating LECT2 correlates with adiposity and insulin resistance. Graphs show individual correlations between serum levels of LECT2 and BMI (A), waist circumference (B), HOMA-IR index (C), insulin sensitivity (Matsuda index) (D), selenoprotein P (SeP) (E), HbA1c (F), and systolic blood pressure (G) in humans (n = 200). Figure 1. Circulating LECT2 correlates with adiposity and insulin resistance. Graphs show individual correlations between serum levels of LECT2 and BMI (A), waist circumference (B), HOMA-IR index (C), insulin sensitivity (Matsuda index) (D), selenoprotein P (SeP) (E), HbA1c (F), and systolic blood pressure (G) in humans (n = 200). More
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Irradiation alters body weight and whole-body metabolism. Ten-week-old C57B...
Published: 20 September 2016
Figure 1 Irradiation alters body weight and whole-body metabolism. Ten-week-old C57Bl/6 mice were irradiated or sham treated. A: Body weight throughout the study (N = 7–15). Oral glucose tolerance was tested 6 weeks into HFD (11 weeks postirradiation; N = 11–15) (B) and 19 weeks into HFD (N = 7 to 8) (C). D: HOMA index of insulin resistance (HOMA-IR) was calculated 28 weeks into HFD (N = 7 to 8). Error bars are SEM. *P < 0.05, **P < 0.05 for irradiation only; #P < 0.05 for HFD only. AU, arbitrary units; Ctrl, nonirradiated; Irr, irradiated. Figure 1. Irradiation alters body weight and whole-body metabolism. Ten-week-old C57Bl/6 mice were irradiated or sham treated. A: Body weight throughout the study (N = 7–15). Oral glucose tolerance was tested 6 weeks into HFD (11 weeks postirradiation; N = 11–15) (B) and 19 weeks into HFD (N = 7 to 8) (C). D: HOMA index of insulin resistance (HOMA-IR) was calculated 28 weeks into HFD (N = 7 to 8). Error bars are SEM. *P < 0.05, **P < 0.05 for irradiation only; #P < 0.05 for HFD only. AU, arbitrary units; Ctrl, nonirradiated; Irr, irradiated. More