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

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1783
Author(s):  
Sohyae Lee ◽  
Jin-young Min ◽  
Kyoung-bok Min

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.

Metabolism ◽  
2004 ◽  
Vol 53 (11) ◽  
pp. 1462-1466 ◽  
Author(s):  
Daniel A. Garcı́a-Estévez ◽  
David Araújo-Vilar ◽  
Ángeles Saavedra-González ◽  
Gloria Fiestras-Janeiro ◽  
José Cabezas-Cerrato

2016 ◽  
Vol 53 (5) ◽  
pp. 268
Author(s):  
Raynald Takumansang ◽  
Sarah M. Warouw ◽  
Hesti Lestari

Background Obesity has become a rapidly growing epidemic worldwide, increasing the risk of morbidity and mortality in adolescents. Obesity is due to an expansion of adipose tissue mass, which is an important source of cytokines and contributes to an increase in pro-inflammatory cytokines, such as interleukin-6 (IL-6). Interleukin-6 is significantly increased in obesity and may lead to a state of insulin resistance.Objective To assess for a correlation between IL-6 levels and insulin resistance in obese adolescentsMethods We conducted a cross-sectional study from January to April 2012 in Manado, North Sulawesi. Subjects were either obese or normal body mass index (BMI) teens aged 13-18 years. Data collected were anthropometric status, BMI, and blood specimens for fasting plasma glucose levels, fasting insulin levels, and IL-6 levels. Insulin resistance was expressed as homeostatic model assessment of insulin resistance (HOMA-IR) level >2.77. Data was analyzed by Pearson’s correlation and linear regression tests to assess for a possible correlation between IL-6 levels and insulin resistance.Results The mean BMI in the obese group was 31.21 (SD 3.61) kg/m2 while the mean BMI in the normal group was 19.52 (SD 2.38) kg/m2. There was no significant association between IL-6 and the occurrence of insulin resistance (P=0.309). The log regression coefficient value of IL-6 was negative (b = -0.329).Conclusion There is no correlation between IL-6 levels and incidence of insulin resistance in obese adolescents.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A319-A320
Author(s):  
Vishwanath Pattan ◽  
Maria Chang Villacreses ◽  
Rudruidee Karnchanasorn ◽  
Wei Feng ◽  
Raynald Samoa ◽  
...  

Abstract Trace element is essential for the proper growth, development, and physiology of the organism and the primary source of trace element is dietary intake. Among trace elements, the role of copper (Cu), selenium (Se), and zinc (Zn) in the pathogenesis of diabetes have been widely recognized. However, there is little information available about these 3 trace elements across the different states of glucose tolerance. We examined associations between serum levels of trace elements - Cu, Zn, and Se with various stages of glucose tolerance in a representative, cross-sectional sample of US adults. Our sample included 5,087 adults (≥20 years) with available serum concentrations of Cu, Zn and Se as well as states of glucose tolerance, defined by history, HbA1c, fasting, and 2-hour plasma glucose concentrations. Serum concentrations of trace elements were compared with glucose tolerance status with the consideration of covariates. Regression analyses was used to examine the relationship of trace elements with HOMA-IR, HOMA-B, and BMI in non-diabetic subjects with the consideration of appropriate covariates. Serum Se (P<0.0001) and Zn (P<0.0001) concentrations differed significantly among 3 groups based on the states of glucose tolerance, while no difference was noted in serum Cu concentration. In non-diabetic subjects, serum Cu concentration was positively correlated with BMI (P<0.0001) with a possible compensatory increased beta cell function (P=0.018). Serum Se concentration was negatively correlated with insulin resistance (P=0.016) but not with beta cell function or BMI. Serum Zn concertation was negatively correlated with beta cell function (P=0.0023) and BMI (P=0.018), but not with insulin resistance. We found that a higher serum concentration of trace elements was associated with negative glucose and fuel homeostasis in a non-deficiency population possibly through different mechanisms. Although the casual relationship remains to be elucidated, we recommend against trace element supplementation in a non-deficiency population.


2021 ◽  
Vol 12 ◽  
Author(s):  
Xu Liu ◽  
Yang Liu ◽  
Hongzhong Liu ◽  
Haiyan Li ◽  
Jianhong Yang ◽  
...  

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.


2021 ◽  
Author(s):  
Rong Huang ◽  
Yu Dong ◽  
Anne Monique Nuyt ◽  
Emile Levy ◽  
Shu-Qin Wei ◽  
...  

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.


2021 ◽  
Vol 12 ◽  
Author(s):  
Hui Guo ◽  
Chiyu Wang ◽  
Boren Jiang ◽  
Shaohong Ge ◽  
Jian Cai ◽  
...  

BackgroundThe interrelation between glucose and bone metabolism is complex and has not been fully revealed. This study aimed to investigate the association between insulin resistance, β-cell function and bone turnover biomarker levels among participants with abnormal glycometabolism.MethodsA total of 5277 subjects were involved through a cross-sectional study (METAL study, http://www.chictr.org.cn, ChiCTR1800017573) in Shanghai, China. Homeostasis model assessment of insulin resistance (HOMA-IR) and β-cell dysfunction (HOMA-%β) were applied to elucidate the nexus between β-C-terminal telopeptide (β-CTX), intact N-terminal propeptide of type I collagen (P1NP) and osteocalcin (OC). β-CTX, OC and P1NP were detected by chemiluminescence.ResultsHOMA-IR was negatively associated with β-CTX, P1NP and OC (regression coefficient (β) -0.044 (-0.053, -0.035), Q4vsQ1; β -7.340 (-9.130, -5.550), Q4vsQ1 and β -2.885 (-3.357, -2.412), Q4vsQ1, respectively, all P for trend <0.001). HOMA-%β was positively associated with β-CTX, P1NP and OC (β 0.022 (0.014, 0.031), Q4vsQ1; β 6.951 (5.300, 8.602), Q4vsQ1 and β 1.361 (0.921, 1.800), Q4vsQ1, respectively, all P for trend <0.001).ConclusionsOur results support that lower bone turnover biomarker (β-CTX, P1NP and OC) levels were associated with a combination of higher prevalence of insulin resistance and worse β-cell function among dysglycemia patients. It is feasible to detect bone turnover in diabetes or hyperglycemia patients to predict the risk of osteoporosis and fracture, relieve patients’ pain and reduce the expenses of long-term cure.


Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Alka M Kanaya ◽  
David Herrrington ◽  
Kiang Liu ◽  
Michael J Blaha ◽  
Namratha R Kandula

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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