Relationship between homeostasis model assessment of insulin resistance and beta cell function and serum 25-hydroxyvitamin D in non-diabetic Korean adults

Abstract Background: Abnormal lipids are strong predictive factors of cardiovascular disease (CVD) in both type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM). However, the potential associations of insulin resistance (IR) and beta cell function (BCF) in diabetes and abnormal lipids, i.e. high triglyceride (TG), low high-density lipoprotein cholesterol (HDL-C) and high low-density lipoprotein cholesterol (LDL-C) are not fully understood. In this study, we aim to explore whether decreased BCF and increased IR in newly diagnosed T1DM or T2DM are associated with abnormal lipids.Methods: Clinical and laboratory data were collected from 16334 adults with newly diagnosed diabetes in this cross-sectional study. Types of diabetes were diagnosed based on clinical characteristics and diabetes-related biochemical measurement results. Homeostasis model assessment were used to estimate IR and BCF. Restricted cubic spline and binary logistic regression were used to examine the associations of IR or BCF and abnormal lipids in T1DM and T2DM, respectively. Results: High TG, low HDL-C and high LDL-C accounted for 49.7%, 47.7% and 59.2%, respectively. In multivariable analysis, high IR was associated with increased risk of high TG (Odds ratios (ORs) of homeostasis model assessment of insulin resistance (HOMA2-IR) ≥2, ≥1-<2 vs <1: 4.77, 95% CI 2.69-8.57; 2.31, 95% CI 1.54-3.47, p for trend < 0.001) in T1DM and was associated with elevated risk of high TG, low HDL-C and high LDL-C (all p for trend <0.01) in T2DM. Low BCF, i.e., homeostasis model assessment of beta-cell function (HOMA2-B) <30 versus ≥30, was associated with marginally increased risk of high TG (OR 1.42, 95% CI 0.98-2.10, p = 0.07) in T1DM and associated with increased risk of high TG (OR 1.21, 95% CI 1.09-1.34, p <0.001) and high LDL-C (OR 1.23, 95% CI 1.12-1.36, p <0.001) in T2DM.Conclusions: In patients with newly diagnosed diabetes, high IR and low BCF had different associations with risk of dyslipidemia in T1DM and T2DM, suggesting that early treatment that improve IR or BCF may have a benefit for abnormal lipid metabolism.

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The Dynamic Roles of Visfatin and Obestatin Serum Concentration in Pancreatic Beta Cells Dysfunction (HOMA-beta) and Insulin Resistance (HOMA-IR) in Centrally Obese Men

The Indonesian Biomedical Journal ◽

10.18585/inabj.v4i1.161 ◽

2012 ◽

Vol 4 (1) ◽

pp. 43

Author(s):

Bayu Winata Putera ◽

Cynthia Retna Sartika ◽

Andi Wijaya

Keyword(s):

Insulin Resistance ◽

Type 2 Diabetes ◽

Beta Cell ◽

Beta Cell Function ◽

Cell Function ◽

Model Assessment ◽

Homeostasis Model Assessment ◽

Cell Dysfunction ◽

Pancreas Cell

BACKGROUND: Obesity is a major health problem in the world today. Obesity is closely associated with insulin resistance and type 2 diabetes. Epidemiological studies have shown that obese persons are in a state of insulin resistance, however, most of them do not progress to type 2 diabetes. This occurs because the beta cell function is still good enough for maintaining normal glucose level. Obestatin and visfatin are cytokines that are known to have a role in beta cell function. The aim of this study was to assess the relationship between visfatin and obestatin and Homeostasis Model Assessment of beta cell function (HOMA-β) and Homeostasis Model Assessment of insulin resistance (HOMA-IR).METHODS: This was a cross-sectional study involving 80 central obesity men with waist circumference >90 cm, age 30-65 years old. Visfatin and obestatin were measured by ELISA method. Beta pancreas cell dysfunction and insulin resistance were calculated by HOMA model.RESULTS: Our study showed a correlation between visfatin and HOMA-β (r=0.244 and p = 0.029) and visfatin with HOMA-IR (r=0.287 and p=0.001) and no correlation was found between obestatin with HOMA-β (r=0.010 and p=0.990) and obestatin with HOMA-IR (r=0.080 and p=0.480). We also found visfatin and obestatin concentrations were fluctuative depending on the measurements of the waist circumferences.CONCLUSIONS: High visfatin and low obestatin concentration were independently associated with increased beta pancreas cell dysfunction and insulin resistance.KEYWORDS: obesity. visfatin, obestatin, beta cell dysfunction (HOMA-β), insulin resistance (HOMA-IR)

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Dipeptidyl-Peptidase-IV Inhibitors, Imigliptin and Alogliptin, Improve Beta-Cell Function in Type 2 Diabetes

Frontiers in Endocrinology ◽

10.3389/fendo.2021.694390 ◽

2021 ◽

Vol 12 ◽

Author(s):

Xu Liu ◽

Yang Liu ◽

Hongzhong Liu ◽

Haiyan Li ◽

Jianhong Yang ◽

...

Keyword(s):

Insulin Resistance ◽

Type 2 Diabetes ◽

Beta Cell ◽

Beta Cell Function ◽

Cell Function ◽

Dipeptidyl Peptidase ◽

Chinese Patients ◽

Oral Glucose ◽

Model Assessment

ObjectsImigliptin is a novel dipeptidyl peptidase-4 inhibitor. In the present study, we aimed to evaluate the effects of imigliptin and alogliptin on insulin resistance and beta-cell function in Chinese patients with type-2 diabetes mellitus (T2DM).MethodsA total of 37 Chinese T2DM patients were randomized to receive 25 mg imigliptin, 50 mg imigliptin, placebo, and 25 mg alogliptin (positive drug) for 13 days. Oral glucose tolerance tests were conducted at baseline and on day 13, followed by the oral minimal model (OMM).ResultsImigliptin or alogliptin treatment, compared with their baseline or placebo, was associated with higher beta-cell function parameters (φs and φtot) and lower glucose area under the curve (AUC) and postprandial glucose levels. The changes in the AUC for the glucose appearance rate between 0 and 120 min also showed a decrease in imigliptin or alogliptin groups. However, the insulin resistance parameter, fasting glucose, was not changed. For the homeostatic model assessment (HOMA-β and HOMA-IR) parameters or secretory units of islets in transplantation index (SUIT), no statistically significant changes were found both within treatments and between treatments.ConclusionsAfter 13 days of treatment, imigliptin and alogliptin could decrease glycemic levels by improving beta-cell function. By comparing OMM with HOMA or SUIT results, glucose stimulation might be more sensitive for detecting changes in beta-cell function.

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Caffeine and Caffeine Metabolites in Relation to Insulin Resistance and Beta Cell Function in U.S. Adults

Nutrients ◽

10.3390/nu12061783 ◽

2020 ◽

Vol 12 (6) ◽

pp. 1783

Author(s):

Sohyae Lee ◽

Jin-young Min ◽

Kyoung-bok Min

Keyword(s):

Insulin Resistance ◽

Beta Cell ◽

Beta Cell Function ◽

High Performance ◽

Cell Function ◽

Cross Sectional Study ◽

Caffeine Intake ◽

Model Assessment ◽

Cross Sectional ◽

Glucose Levels

The relationship between caffeine and insulin resistance (IR) has been assessed only in terms of caffeine intake, and the association between caffeine and beta cell function (BCF) remains unclear. This study examines the association between urinary caffeine and its metabolites, IR, and BCF in nondiabetic, noninstitutionalized US adults in order to account for the inter-individual differences in caffeine metabolism. Data on urinary caffeine and its metabolites, IR and BCF from adults aged 20 years and older who participated in the 2009–2010 and 2011–2012 National Health and Nutrition Examination Surveys were analyzed (n for caffeine = 994). IR and BCF were assessed using homeostatic model assessment (HOMA) and urinary caffeine and its metabolites were measured using high-performance liquid chromatography-electrospray ionization-tandem quadrupole mass spectrometry. After adjusting for all covariates, increases in urinary 1,3-DMU, 1,7-DMU, 1,3,7-TMU, theophylline, paraxanthine, caffeine, and AAMU were significantly associated with increased HOMA-IR and HOMA-β (HOMA of insulin resistance and beta cell function). Compared with individuals in the lowest quartile of urinary 1,3-DMU, 1,7-DMU, 1,3,7-TMU, theophylline, paraxanthine, caffeine, and AAMU, the regression coefficients for HOMA-IR and HOMA-β were significantly higher among those in the highest quartile. After stratification by prediabetes status, HOMA-IR and HOMA-β showed significant positive associations with urinary caffeine and its metabolites among subjects with normal fasting plasma glucose levels. Our cross-sectional study showed that caffeine and its metabolites were positively related to IR and BCF.

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Large birth size, infancy growth pattern, insulin resistance and β-cell function

Acta Endocrinologica ◽

10.1530/eje-20-1332 ◽

2021 ◽

Author(s):

Rong Huang ◽

Yu Dong ◽

Anne Monique Nuyt ◽

Emile Levy ◽

Shu-Qin Wei ◽

...

Keyword(s):

Insulin Resistance ◽

Beta Cell ◽

Gestational Age ◽

Growth Pattern ◽

Beta Cell Function ◽

Cell Function ◽

Birth Size ◽

Model Assessment ◽

Β Cell ◽

Β Cell Function

Objective: Large birth size programs an elevated risk of type 2 diabetes in adulthood, but data are absent concerning glucose metabolic health impact in infancy. We sought to determine whether large birth size is associated with insulin resistance and β-cell function in infancy, and evaluate the determinants. Design and Participants: In the Canadian 3D birth cohort, we conducted a nested matched (1:2) study of 70 large-for-gestational-age (LGA, birth weight >90th percentile) and 140 optimal-for-gestational-age (OGA, 25th-75th percentiles) control infants. The primary outcomes were homeostasis model assessment of insulin resistance (HOMA-IR) and beta-cell function (HOMA-β) at age 2-years. Results: HOMA-IR and HOMA-β were similar in LGA and OGA infants. Adjusting for maternal and infant characteristics, decelerated growth in length during early infancy (0-3 months) was associated a 25.8% decrease (95% confidence intervals 6.7-41.0%) in HOMA-β. During mid-infancy (3-12 months), accelerated growth in weight was associated with a 25.5% (0.35-56.9%) increase in HOMA-IR, in length with a 69.3% increase (31.4-118.0%) in HOMA-IR and a 24.5% (0.52-54.3%) increase in HOMA-β. Decelerated growth in length during late infancy (1-2 years) was associated with a 28.4% (9.5-43.4%) decrease in HOMA-IR and a 21.2% (3.9-35.4%) decrease in HOMA-β. Female sex was associated with higher HOMA-β, Caucasian ethnicity with lower HOMA-IR, and maternal smoking with lower HOMA-β. Conclusions: The study is the first to demonstrate that large birth size is not associated with insulin resistance and β-cell function in infancy, but infancy growth pattern matters. Decelerated infancy growth may be detrimental to beta-cell function.

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Abstract MP74: Understanding the Higher Diabetes Prevalence in South Asians Compared to Four U.S. Racial/Ethnic Groups: The MASALA and MESA Studies

Circulation ◽

10.1161/circ.129.suppl_1.mp74 ◽

2014 ◽

Vol 129 (suppl_1) ◽

Author(s):

Alka M Kanaya ◽

David Herrrington ◽

Kiang Liu ◽

Michael J Blaha ◽

Namratha R Kandula

Keyword(s):

Insulin Resistance ◽

Waist Circumference ◽

Beta Cell ◽

Ethnic Group ◽

Ethnic Groups ◽

Beta Cell Function ◽

Cell Function ◽

South Asians ◽

Chinese Americans ◽

Model Assessment

Background: South Asians (SA) have a high prevalence of diabetes (DM) which may be due to differences in insulin resistance (IR) or beta-cell function. We compared the prevalence of DM, IR, and beta cell function between SA and four race/ethnic groups. We also determined whether the association between age and adiposity with IR and beta cell function differed by ethnicty. Methods: We conducted a cross-sectional analysis of two cohorts aged 44-84 years without CVD: the Mediators of Atherosclerosis in South Asians Living in America (MASALA) study and the Multi-Ethnic Study of Atherosclerosis (MESA). We compared 799 SA with 2,611 Whites, 1,879 African Americans (AA), 1,493 Latinos and 801 Chinese Americans (CA). DM was classified by fasting plasma glucose ≥126 mg/dL or use of a diabetes medication. Insulin resistance was estimated by the homeostasis model assessment (HOMA)-IR and beta cell function by the HOMA-ß model. Spline curves displayed the effect of age and waist with HOMA-IR and HOMA- ß stratified by ethnic group among those not on diabetes medications. Results: SA had significantly higher age-adjusted prevalence of DM (23%) compared to each MESA group (6% Whites; 18% AA; 17% Latino; 13% CA, p<0.001 each compared to SA), which were further enhanced after adjusting for all covariates of DM. Median HOMA-IR was higher and HOMA-β was lower in SA compared to other groups. Patterns of insulin resistance and ß cell function with age and waist circumference differed by ethnic group (Figure). SA had higher HOMA-IR to age 65, and lower HOMA-ß across the all ages compared to other groups. SA had higher HOMA-IR and lower HOMA-β after adjusting for waist circumference compared to other groups. Conclusions: There are ethnic differences in IR and beta cell that vary by age and adiposity. South Asians may have lower innate beta cell function and an inability to compensate adequately for high levels of IR with increasing adiposity. Longitudinal follow-up can assess whether IR and beta cell function explain the higher diabetes rates in South Asians.

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