scholarly journals Association of Baseline Characteristics With Insulin Sensitivity and β-Cell Function in the Glycemia Reduction Approaches in Diabetes: A Comparative Effectiveness (GRADE) Study Cohort

2020 ◽  
Author(s):  
Neda Rasouli ◽  
Naji Younes ◽  
Kristina M. Utzschneider ◽  
Silvio E. Inzucchi ◽  
Ashok Balasubramanyam ◽  
...  

<b>Objective:</b> We investigated sex and racial differences in insulin sensitivity, β-cell function and HbA1c, and the associations with selected phenotypic characteristics. <p><b>Research Design and Methods:</b> This is a cross-sectional analysis of baseline data from 3,108 GRADE participants. All had type 2 diabetes diagnosed <10 years and were on metformin monotherapy. Insulin sensitivity and β-cell function were evaluated using the homeostasis model assessment of insulin sensitivity (HOMA2-S) and estimates from oral glucose tolerance tests including the Matsuda index, insulinogenic index (IGI), C-peptide index (CPI) and oral disposition index (DI).</p> <p><b>Results:</b> The cohort was 56.6±10 years of age (mean±SD), 63.8% male, with BMI 34.2±6.7 kg/m<sup>2</sup>, HbA1c 7.5±0.5% and type 2 diabetes duration 4.0±2.8 years. Women had higher DI than men but similar insulin sensitivity. DI was the highest in Black/African Americans, followed by American Indians/Alaska Natives, Asians and Whites in descending order. Compared to white, American Indian/Alaska Native had significantly higher HbA1c but Black/African Americans and Asians had lower HbA1c. However, when adjusted for glucose levels, Black/African Americans had higher HbA1c than whites. Insulin sensitivity correlated inversely with BMI, waist to hip ratio, triglyceride to HDL cholesterol ratio (TG/HDL- C) and the presence of metabolic syndrome; whereas DI was associated directly with age and inversely with BMI, HbA1c and TG/HDL-C. </p> <p><b>Conclusion</b>: In the GRADE cohort, β-cell function differed by sex and race and was associated with the concurrent level of HbA1c. HbA1c also differed among the races, but not sex. Age, BMI and TG/HDL-C were associated with multiple measures of β-cell function and insulin sensitivity.<br> </p>

2020 ◽  
Author(s):  
Neda Rasouli ◽  
Naji Younes ◽  
Kristina M. Utzschneider ◽  
Silvio E. Inzucchi ◽  
Ashok Balasubramanyam ◽  
...  

<b>Objective:</b> We investigated sex and racial differences in insulin sensitivity, β-cell function and HbA1c, and the associations with selected phenotypic characteristics. <p><b>Research Design and Methods:</b> This is a cross-sectional analysis of baseline data from 3,108 GRADE participants. All had type 2 diabetes diagnosed <10 years and were on metformin monotherapy. Insulin sensitivity and β-cell function were evaluated using the homeostasis model assessment of insulin sensitivity (HOMA2-S) and estimates from oral glucose tolerance tests including the Matsuda index, insulinogenic index (IGI), C-peptide index (CPI) and oral disposition index (DI).</p> <p><b>Results:</b> The cohort was 56.6±10 years of age (mean±SD), 63.8% male, with BMI 34.2±6.7 kg/m<sup>2</sup>, HbA1c 7.5±0.5% and type 2 diabetes duration 4.0±2.8 years. Women had higher DI than men but similar insulin sensitivity. DI was the highest in Black/African Americans, followed by American Indians/Alaska Natives, Asians and Whites in descending order. Compared to white, American Indian/Alaska Native had significantly higher HbA1c but Black/African Americans and Asians had lower HbA1c. However, when adjusted for glucose levels, Black/African Americans had higher HbA1c than whites. Insulin sensitivity correlated inversely with BMI, waist to hip ratio, triglyceride to HDL cholesterol ratio (TG/HDL- C) and the presence of metabolic syndrome; whereas DI was associated directly with age and inversely with BMI, HbA1c and TG/HDL-C. </p> <p><b>Conclusion</b>: In the GRADE cohort, β-cell function differed by sex and race and was associated with the concurrent level of HbA1c. HbA1c also differed among the races, but not sex. Age, BMI and TG/HDL-C were associated with multiple measures of β-cell function and insulin sensitivity.<br> </p>


2019 ◽  
Vol 105 (3) ◽  
pp. e285-e294 ◽  
Author(s):  
Zhila Semnani-Azad ◽  
Philip W Connelly ◽  
Luke W Johnston ◽  
Ravi Retnakaran ◽  
Stewart B Harris ◽  
...  

Abstract Context Chronic inflammation arising from adipose tissue macrophage (ATM) activation may be central in type 2 diabetes etiology. Our objective was to assess the longitudinal associations of soluble CD163 (sCD163), a novel biomarker of ATM activation, with insulin sensitivity, β-cell function, and dysglycemia in high-risk subjects. Methods Adults at risk for type 2 diabetes in the Prospective Metabolism and Islet Cell Evaluation (PROMISE) study had 3 assessments over 6 years (n = 408). Levels of sCD163 were measured using fasting serum. Insulin sensitivity was assessed by HOMA2-%S and the Matsuda index (ISI). β-cell function was determined by insulinogenic index (IGI) over HOMA-IR and insulin secretion-sensitivity index-2 (ISSI-2). Incident dysglycemia was defined as the onset of impaired fasting glucose, impaired glucose tolerance, or type 2 diabetes. Generalized estimating equations (GEE) evaluated longitudinal associations of sCD163 with insulin sensitivity, β-cell function, and incident dysglycemia adjusting for demographic and lifestyle covariates. Areas under receiver-operating-characteristic curve (AROC) tested whether sCD163 improved dysglycemia prediction in a clinical model. Results Longitudinal analyses showed significant inverse associations between sCD163 and insulin sensitivity (% difference per standard deviation increase of sCD163 for HOMA2-%S (β = −7.01; 95% CI, −12.26 to −1.44) and ISI (β = −7.60; 95% CI, −11.09 to −3.97) and β-cell function (ISSI-2 (β = −4.67; 95 %CI, −8.59 to −0.58) and IGI/HOMA-IR (β = −8.75; 95% CI, −15.42 to −1.56)). Increased sCD163 was associated with greater risk for incident dysglycemia (odds ratio = 1.04; 95% CI, 1.02-1.06; P &lt; 0.001). Adding sCD163 data to a model with clinical variables improved prediction of incident dysglycemia (AROC=0.6731 vs 0.638; P &lt; 0.05). Conclusions sCD163 was longitudinally associated with core disorders that precede the onset of type 2 diabetes.


2017 ◽  
Vol 103 (2) ◽  
pp. 514-522 ◽  
Author(s):  
Ebenezer Nyenwe ◽  
Ibiye Owei ◽  
Jim Wan ◽  
Sam Dagogo-Jack

Abstract Context There are ethnic differences in glucoregulation and prevalence of type 2 diabetes, but studies on the role of genetics in modifying ethnic effects in normoglycemic African-Americans and Caucasians are limited. Therefore, we investigated glucoregulation in normoglycemic African-Americans and Caucasians with or without parental diabetes. Design Fifty subjects with parental diabetes (from the Pathobiology of Prediabetes in a Biracial Cohort Study) and 50 subjects without parental diabetes were matched in age, sex, ethnicity, and body mass index (BMI). Subjects underwent a 75-g oral glucose tolerance test (OGTT), physical examination, anthropometry, biochemistries, indirect calorimetry and assessment of body composition, insulin sensitivity by euglycemic clamp (Si-clamp), and β-cell function by Disposition index. Results The mean age was 40.5 ± 11.6 years, BMI 28.7 ± 5.9 kg/m2, fasting plasma glucose 90.2 ± 5.9 mg/dL, and 2-hour postglucose 120.0 ± 26.8 mg/dL. Offspring with parental diabetes showed higher glycemic excursion during OGTT–area under the curve–glucose (16,005.6 ± 2324.7 vs 14,973.8 ± 1819.9, P &lt; 0.005), lower Si-clamp (0.132 ± 0.068 vs 0.162 ± 0.081 µmol/kg fat-free mass/min/pmol/L, P &lt; 0.05), and lower Disposition index (8.74 ± 5.72 vs 11.83 ± 7.49, P &lt; 0.05). Compared with lean subjects without parental diabetes, β cell function was lower by ∼30% in lean subjects with parental diabetes, ∼40% in obese subjects without parental diabetes, and ∼50% in obese individuals with parental diabetes (P &lt; 0.0001). African-Americans without parental diabetes had ∼40% lower insulin sensitivity (P &lt; 0.001), twofold higher acute insulin secretion (P &lt; 0.001), but ∼30% lower Disposition index (P &lt; 0.01) compared with Caucasians without parental diabetes. Remarkably, there were no significant differences by ethnicity in these glucoregulatory measures among subjects with parental diabetes. Conclusion Offspring with parental diabetes harbor substantial impairments in glucoregulation compared with individuals without parental diabetes. Ethnic disparities in glucoregulation were abrogated by parental diabetes.


Healthcare ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 1010
Author(s):  
Wei-Hao Hsu ◽  
Chin-Wei Tseng ◽  
Yu-Ting Huang ◽  
Ching-Chao Liang ◽  
Mei-Yueh Lee ◽  
...  

Prediabetes should be viewed as an increased risk for diabetes and cardiovascular disease. In this study, we investigated its prevalence among the relatives and spouses of patients with type 2 diabetes or risk factors for prediabetes, insulin resistance, and β-cell function. A total of 175 individuals were included and stratified into three groups: controls, and relatives and spouses of type 2 diabetic patients. We compared clinical characteristics consisting of a homeostatic model assessment for insulin resistance (HOMA-IR) and beta cell function (HOMA-β), a quantitative insulin sensitivity check index (QUICKI), and triglyceride glucose (TyG) index. After a multivariable linear regression analysis, the relative group was independently correlated with high fasting glucose, a high TyG index, and low β-cell function; the relatives and spouses were independently associated with a low QUICKI. The relatives and spouses equally had a higher prevalence of prediabetes. These study also indicated that the relatives had multiple factors predicting the development of diabetes mellitus, and that the spouses may share a number of common environmental factors associated with low insulin sensitivity.


2019 ◽  
Vol 74 (2) ◽  
pp. 125-131 ◽  
Author(s):  
Ting Chen ◽  
Fengyun Wang ◽  
Zhenyu Chu ◽  
Ling Sun ◽  
Haitao Lv ◽  
...  

Objectives: Spexin (SPX) is a novel peptide that has recently emerged as an important regulatory adipokine of obesity and related metabolic disease. Little is known about its role in children. The aim of the current study was to determine the potential role of SPX in obese children and explore its relationships with obesity-related markers, insulin sensitivity and pancreatic β cell function. Method: We studied the levels of serum SPX in 40 obese and 32 normal weight pre-puberty children (mean age was 8.59 ± 1.82 and 8.15 ± 2.03 years in obesity and control groups respectively). We investigated the levels of body mass index, blood pressure, lipids, glucose, insulin, Homeostasis model assessment for insulin-resistant (HOMA-IR, HOMA for β-cell function [HOMA-β]), insulinogenic index and C-peptide index and analyzed their correlations with SPX levels. Results: SPX levels were significantly decreased in obese children compared to controls. Moreover, serum SPX levels were lower in IR obese subjects in contrast with the non-IR obese subjects. Serum SPX concentrations correlated negatively and significantly with triglycerides, systolic blood pressure, diastolic blood pressure, fasting insulin level, HOMA-IR, insulinogenic index, and HOMA-β levels in obese children. Conclusions: In summary, serum SPX levels significantly decreased in obese children and negatively correlated with insulin resistance and pancreatic β cell function indicators. Therefore, SPX may play a protective role in the process of glucose homeostasis and is closely related to β cell function in obese children.


2015 ◽  
Vol 308 (6) ◽  
pp. E535-E544 ◽  
Author(s):  
Christoffer Martinussen ◽  
Kirstine N. Bojsen-Møller ◽  
Carsten Dirksen ◽  
Siv H. Jacobsen ◽  
Nils B. Jørgensen ◽  
...  

Roux-en-Y gastric bypass surgery (RYGB) in patients with type 2 diabetes often leads to early disease remission, and it is unknown to what extent this involves improved pancreatic β-cell function per se and/or enhanced insulin- and non-insulin-mediated glucose disposal (glucose effectiveness). We studied 30 obese patients, including 10 with type 2 diabetes, 8 with impaired glucose tolerance, and 12 with normal glucose tolerance before, 1 wk, and 3 mo after RYGB, using an intravenous glucose tolerance test (IVGTT) to estimate first-phase insulin response, insulin sensitivity (Si), and glucose effectiveness with Bergman's minimal model. In the fasting state, insulin sensitivity was estimated by HOMA-S and β-cell function by HOMA-β. Moreover, mixed-meal tests and oral GTTs were performed. In patients with type 2 diabetes, glucose levels normalized after RYGB, first-phase insulin secretion in response to iv glucose increased twofold, and HOMA-β already improved 1 wk postoperatively, with further enhancements at 3 mo. Insulin sensitivity increased in the liver (HOMA-S) at 1 wk and at 3 mo in peripheral tissues (Si), whereas glucose effectiveness did not improve significantly. During oral testing, GLP-1 responses and insulin secretion increased regardless of glucose tolerance. Therefore, in addition to increased insulin sensitivity and exaggerated postprandial GLP-1 levels, diabetes remission after RYGB involves early improvement of pancreatic β-cell function per se, reflected in enhanced first-phase insulin secretion to iv glucose and increased HOMA-β. A major role for improved glucose effectiveness after RYGB was not supported by this study.


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