Serum Uric Acid Levels were Dynamically Coupled with Hemoglobin A1c in the Development of Type 2 Diabetes.
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ABSTRACT:
SUBMITTER: Wei F
PROVIDER: S-EPMC4916504 | biostudies-literature | 2016 Jun
REPOSITORIES: biostudies-literature
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Serum Uric Acid Levels were Dynamically Coupled with Hemoglobin A1c in the Development of Type 2 Diabetes.
Wei Fengjiang F Chang Baocheng B Yang Xilin X Wang Yaogang Y Chen Liming L Li Wei-Dong WD
Scientific reports 20160622
The aim of the study was to decipher the relationship between serum uric acid (SUA) and glycated hemoglobin A1c (HbA1c) or fasting plasma glucose (FPG) in both type 2 diabetes mellitus (T2DM) patients and normal subjects. A total of 2,250 unrelated T2DM patients and 4,420 Han Chinese subjects from a physical examination population were recruited for this study. In T2DM patients SUA levels were negatively correlated with HbA1c (rs = -0.109, P = 0.000) and 2 h plasma glucose levels (rs = -0.178, P ...[more]
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Project description:BackgroundHemoglobin glycation index (HGI), which is calculated by blood glucose and hemoglobin A1c(HbA1c), reflects the individual discrepancy in HbA1c. This study aimed to investigate the association between HGI/HbA1c and serum uric acid(SUA) stratified by sex and diabetes.MethodsThe study recruited 33772 participants who underwent physical examinations between April 2016 and August 2021 in Beijing Chao-Yang Hospital. A random subsample of 3000 subjects was utilized to calculate the formula of HGI and data of the remaining 30772 participants were used for analysis. HGI and HbA1c were categorized according to quartiles (Q1, Q2, Q3, Q4), using Q1 as the reference. We used multiple linear regression and restricted cubic splines for data analysis.Results30772 participants with a mean age of 44.4 years old were included in the analysis, 48.6% (N = 14944) of which were female and 7.7% (N = 2363) with diabetes. Associations of HGI, HbA1c and SUA were modified by sex and diabetes. The relationship between SUA levels and HGI was positive in women without diabetes, with one unit increase in HGI associating with an 11.3 μmol/L increase in SUA (P < 0.001) after adjusting for other confounders. On average, each one-unit increase in HbA1c was associated with a 14.3 μmol/L decrease in SUA in women with diabetes, a 14.9 μmol/L decrease in SUA in men with diabetes, and a 16.5 μmol/L increase in SUA in women without diabetes (all P < 0.001). The SUA levels in men without diabetes showed a bell-shaped relation with HbA1c, increasing as the HbA1c rose to around 5.7% and then falling with a further increase of HbA1c (P < 0.001).ConclusionsSUA levels were inversely correlated with HbA1c in diabetic patients, also in men with prediabetes (HbA1c ≥ 5.7%), but positively correlated with HbA1c and HGI in women without diabetes. Glycemic control may help to reduce the risk of hyperuricemia in non-diabetes women.
| S-EPMC9719659 | biostudies-literature
Project description:Hemoglobin A1c (HbA1c) is a biomarker used for population-level screening of type 2 diabetes (T2D) and risk stratification. Large-scale, genome-wide association studies have identified multiple genomic loci influencing HbA1c. We discuss the challenges of classifying these genomic loci as influencing HbA1c through glycemic or nonglycemic pathways, based on their probable biology and pleiotropic associations with erythrocyte traits. We show that putative nonglycemic genetic variants have a measurable, albeit small, impact on the classification of T2D status by HbA1c in white and Asian populations. Accounting for their effect on HbA1c may be relevant when screening populations with higher frequencies of nonglycemic HbA1c-altering alleles. As carriers of such HbA1c-altering alleles have HbA1c levels that may not accurately reflect overall glycemia, we describe how accounting for genotype may improve the performance of HbA1c in T2D prediction models and risk stratification, allowing for lifestyle intervention strategies to be directed towards those who are truly at elevated risk for developing T2D. In a Mendelian randomization framework, genetic variants can be used as instrumental variables to estimate causal relationships between HbA1c and T2D-related complications. This approach may help to support or refute HbA1c as an appropriate biomarker for long-term health outcomes in the general population.
| S-EPMC5275759 | biostudies-literature
Project description:ObjectiveTo systematically evaluate the association between serum uric acid (SUA) level and subsequent development of type 2 diabetes.Research design and methodsWe searched Medline (31 March from 1966 to 2009) and Embase (31 March from 1980 to 2009) for observational cohort studies examining the association between SUA and the risk of type 2 diabetes by manual literature search. Relative risks (RRs) for each 1 mg/dl increase in SUA were pooled by using a random-effects model. The studies included were stratified into subgroups representing different study characteristics, and meta-regression analyses were performed to investigate the effect of these characteristics on the association between SUA level and type 2 diabetes risk.ResultsThe search yielded 11 cohort studies (42,834 participants) that reported 3,305 incident cases of type 2 diabetes during follow-up periods ranging from 2.0 to 13.5 years. The pooled RR of a 1 mg/dl increase in SUA was 1.17 (95% CI 1.09-1.25). Study results were consistently significant (i.e., >1) across characteristics of participants and study design. Publication bias was both visually and statistically suggested (P = 0.03 for Egger's test, 0.06). Adjustment for publication bias attenuated the pooled RR per mg/dl increase in SUA (RR 1.11 [95% CI 1.03-1.20]), but the association remained statistically significant (P = 0.009).ConclusionsThe current meta-analysis suggests that SUA level is positively associated with the development of type 2 diabetes regardless of various study characteristics. Further research should attempt to determine whether it is effective to utilize SUA level as a predictor of type 2 diabetes for its primary prevention.
| S-EPMC2732137 | biostudies-literature
Project description:Background and objectiveSerum uric acid may predict the onset and progression of kidney disease, but it is unclear whether uric acid is an independent risk factor for diabetic nephropathy. Our aim was to study the relationship between uric acid levels and the development of CKD components in patients with type 2 diabetes.Design, setting, participants, & measurementsLongitudinal study of a cohort of patients with type 2 diabetes from the database of the Italian Association of Clinical Diabetologists network. From a total of 62,830 patients attending the diabetes centers between January 1, 2004, and June 30, 2008, we considered those with baseline eGFR values ≥60 ml/min per 1.73 m2 and normal albumin excretion (n=20,142). Urinary albumin excretion, GFR, and serum uric acid were available in 13,964 patients. We assessed the association of serum uric acid quintiles with onset of CKD components by multinomial logistic regression model adjusting for potential confounders. We calculated the relative risk ratios (RRRs) for eGFR <60 ml/min per 1.73 m2, albuminuria, and their combination at 4 years.ResultsAt 4-year follow-up, 1109 (7.9%) patients developed GFR <60 ml/min per 1.73 m2 with normoalbuminuria, 1968 (14.1%) had albuminuria with eGFR ≥60 ml/min per 1.73 m2, and 286 (2.0%) had albuminuria with eGFR <60 ml/min per 1.73 m2. The incidence of eGFR <60 ml/min per 1.73 m2 increased in parallel with uric acid quintiles: Compared with the lowest quintile, RRRs were 1.46 (95% confidence interval [CI], 1.14 to 1.88; P=0.003), 1.44 (95% CI, 1.11 to 1.87; P=0.006), 1.95 (95% CI, 1.48 to 2.58; P<0.001), and 2.61 (95% CI, 1.98 to 3.42; P<0.001) for second, third, fourth, and fifth quintiles, respectively. Serum uric acid was significantly associated with albuminuria only in presence of eGFR <60 ml/min per 1.73 m2.ConclusionsMild hyperuricemia is strongly associated with the risk of CKD in patients with type 2 diabetes.
| S-EPMC4633786 | biostudies-literature
Project description:In the present study, the aim was to investigate the association between serum 25-hydroxyvitamin D concentration and measures of glycemic control including hemoglobin A1c (HbA1c) and fasting blood glucose (FBG) in adult patients with diabetes mellitus (DM) from the north of Jordan. Another aim was to compare serum levels of 25-hydroxyvitamin D between patients with good glycemic control and patients with uncontrolled DM. This was a cross-sectional study that included 261 participants with DM. The concentration of 25-hydroxyvitamin D was measured using electrochemiluminescence immunoassay, HbA1c was measured using turbidimetric inhibition immunoassay and FBG was measured using the hexokinase method. Data regarding other clinical variables were obtained from medical records or by self-reporting. Participants with good glycemic control exhibited significantly higher levels of 25-hydroxyvitamin D compared with participants with uncontrolled DM (P=0.03). Participants with sufficient vitamin D status (>30 ng/ml in serum) exhibited significantly lower HbA1c level compared with participants with deficient vitamin D (<20 ng/ml) status (P=0.02). Correlation analysis determined significant inverse correlations between 25-hydroxyvitamin D levels and HbA1c and FBG levels (r=-0.23 and -0.17, respectively, both P<0.01). There were also significant correlations between duration of DM and HbA1c and FBG levels (both r=0.21, P<0.01). HbA1c level was also inversely correlated with participants' age (r=-0.19, P<0.01). Further multiple linear regression analysis revealed an inverse significant association between HbA1c and 25-hydroxyvitamin D levels (F=12.95, R2=0.48, P<0.01) but did not identify a similar association between FBG and 25-hydroxyvitamin D levels. These findings may encourage further research to identify if vitamin D supplementation may improve measures of glycemic control, and how vitamin D may affect glucose homeostasis in patients with DM.
| S-EPMC6256128 | biostudies-other
Project description:BackgroundHyperuricemia has been proposed to be a risk factor for cardiovascular disease and chronic kidney disease. Since diabetes is often complicated by hypertension and hyperuricemia, efficient therapeutic strategy against these two complications is very important in diabetic treatment. It has been reported that the antihypertensive drug, irbesartan, inhibits the renal uric acid reabsorptive transporters, URAT1 and GLUT9; this result suggests that irbesartan decreases serum uric acid level (SUA).Subjects and methodsA retrospective study of 107 patients with hypertension and diabetes was performed to analyze the effects of irbesartan on blood pressure, estimated glomerular filtration rate (eGFR), and SUA. The follow-up period was 6-12 months. Seventy percent of the patients were diagnosed with diabetic nephropathy stage II-IV. We excluded patients treated with drugs that influenced SUA. The multiple logistic regression analysis was introduced to identify the relative factors for SUA decline. The time-dependent SUA changes were examined in a mixed-linear model.ResultsIrbesartan reduced blood pressure significantly after 1, 6, and 12 months' treatment. No subject showed significant change in eGFR from baseline level throughout the period. The multiple logistic regression analysis revealed that SUA baseline significantly influenced SUA decline after 6-12 months. In patients whose SUA baseline was ?5.9 mg/dL, the SUA was significantly decreased from 6.6±0.16 mg/dL to 6.2±0.16 mg/dL (P=0.010), after 12 months' irbesartan treatment. In the SUA baseline <5.9 mg/dL group, the SUA did not show significant change over the monitoring period.ConclusionOur results demonstrate that irbesartan reduces the risk of hyperuricemia. No decline in renal function was observed after the initiation of irbesartan treatment. The present report determines the criteria of SUA baseline for introducing an antihyperuricemic effect using irbesartan. Its antihypertensive effect coupled with SUA decline would be effective for the treatment of hypertension complicated by hyperuricemia.
| S-EPMC4014383 | biostudies-literature
Project description:Background. Leprosy reactions are acute inflammatory episodes that occur mainly in the multibacillary forms of the disease. The reactions are classified as type 1 (reverse reaction) or type 2 (erythema nodosum leprosum). Leprosy-associated oxidative stress has been widely demonstrated. Several recent studies have shown uric acid (UA) to have antioxidative effects under pathologic conditions. The objective of this study was to assess serum levels of UA in patients with leprosy reactions, with the aim of monitoring their levels before and after treatment, compared with levels in leprosy patients without reactions. Methods. The study included patients aged 18-69 years assisted at a leprosy treatment reference center in the Central Region of Brazil. Patients who were pregnant; were using immunosuppressant drugs or immunobiologicals; or had an autoimmune disease, human immunodeficiency virus infection, acquired immune deficiency syndrome, or tuberculosis were excluded. Upon recruitment, all individuals were clinically assessed for skin lesions and neural or systemic impairment. Some patients had already completed treatment for leprosy, while others were still undergoing treatment or had initiated treatment after being admitted. The treatment of the reactional episode was started only after the initial evaluation. Laboratory assessments were performed upon admission (baseline) and at approximately 30 and 60 days (time points 1 and 2, respectively). Results. A total of 123 leprosy patients were recruited between June 2012 and June 2015; among them, 56, 42, and 25 presented with type 1, type 2, and no reactions, respectively. Serum UA levels were significantly reduced in patients with type 2 leprosy reactions compared with patients in the control group and remained lower in the two subsequent assessments, after initiation of anti-reaction treatments, with similar values to those recorded before the treatment. Discussion. The decreased serum UA levels in patients with type 2 leprosy reactions might be due to the consumption of UA to neutralize the enhanced production of oxygen- and nitrogen-reactive species that occurs during type 2 reactions. The maintenance of the reduced levels in the follow-up assessments may indicate persistence of oxidative stress in the initial post-treatment stages, despite improved clinical conditions. The results of this study suggest that serum UA may play an antioxidative role during type 2 leprosy reactions.
| S-EPMC4793330 | biostudies-literature
Project description:Despite advances in diabetes technology and treatment, a majority of children and adolescents with type 1 diabetes (T1D) fail to meet hemoglobin A1c (HbA1c) targets. Among high-income nations, the United States has one of the highest mean HbA1c values. We tracked the HbA1c values of 261 patients diagnosed with T1D in our practice over a 2.5-year period to identify inflection points in the HbA1c trajectory. The HbA1c declined until 5 months postdiagnosis. There was a rise in the HbA1c between the fifth and sixth month postdiagnosis. The HbA1c continued to steadily rise and by 18 months postdiagnosis, the mean HbA1c was 8.2%, which is also our clinic mean. Understanding the HbA1c trajectory early in the course of diabetes has helped to identify opportunities for intensification of diabetes management to flatten the trajectory of HbA1c and improve clinical outcomes.
| S-EPMC7001422 | biostudies-literature
Project description:BackgroundWe aimed to evaluate the effects of short-term therapy with dapagliflozin on serum uric acid (SUA) and urinary uric acid (UUA) levels in patients with type 2 diabetes.MethodsIn this prospective pilot trial, 8 patients with type 2 diabetes mellitus were assigned to the treatment group with dapagliflozin 10 mg once daily for one week, and 7 subjects with normal glucose tolerance were recruited into the control group. Data of anthropometric measurements, SUA, 24-h UUA, fractional excretion of UA (FEUA), serum lipid parameters and 3-h oral glucose tolerance test (OGTT) were collected in both treatment and control groups; all examinations were repeated after treatment. The area under the curve of glucose (AUCGlu) was calculated to reflect the general glucose levels, while insulin resistance and islet β-cell function were reflected by indexes calculated according to the data obtained from the OGTT.ResultsThe weight and serum lipid parameters showed no differences before and after treatment with dapagliflozin for one week. We found SUA levels decreased from 347.75 ± 7.75 μmol/L before treatment to 273.25 ± 43.18 μmol/L after treatment, with a statistically significant difference (P = 0.001) and was accompanied by a significant increase in FEUA from 0.009 to 0.029 (P = 0.035); there was a linear correlation between SUA and FEUA levels. Glucose control, insulin sensitivity and islet β-cell function were improved to a certain extent. We also found a positive correlation between the decrease in glucose levels and the improvement in islet β-cell function.ConclusionsThe SUA-lowering effect of dapagliflozin could be driven by increasing UA excretion within one week of treatment, and a certain degree of improvement in glucose levels and islet β-cell function were observed.Trial registration ClinicalTrials.gov identifier, NCT04014192. Registered 12 July 2019, https://www.clinicaltrials.gov/ct2/show/NCT04014192:term=NCT04014192&draw=2&rank=1. Yes.
| S-EPMC7590796 | biostudies-literature
Project description:IntroductionNational data suggest tobacco smoke is positively associated with higher glycated hemoglobin (HbA1c) among adults. Our objective was to examine the association between serum cotinine and HbA1c among adolescents without known diabetes.MethodsWe assessed adolescents 12-19 years old (N = 11550) who participated in the 1999-2012 National Health and Nutrition Examination Survey. We applied sampling weights while performing multiple linear regression analyses.ResultsThe prevalence of serum cotinine indicative of no tobacco smoke exposure (TSE, <0.05 ng/mL) was 43.2%, passive TSE (0.05-2.99 ng/mL) was 38.9%, and active TSE (>3 ng/mL) was 17.9% in our sample. Mean (± standard error) HbA1c in participants with no TSE was 5.16% (±0.01), passive TSE was 5.16% (±0.01), and active TSE was 5.14% (±0.01). No differences in HbA1c were found between TSE groups including sex, age, race/ethnicity, education, income, and physical activity or the fully adjusted model with waist circumference. We found cotinine × sex (p = .01) and cotinine × age (p = .02) interactions. There was an association between cotinine and HbA1c for males but not females. Within males, participants with cotinine ?3 ng/mL (5.26 ± 0.02) had higher mean HbA1c than those with cotinine 0.05-2.99 ng/mL and <0.05 ng/mL (both 5.20 ± 0.01, p ? .02). The negative association between age and HbA1c was stronger for participants with cotinine ?3 ng/mL than participants with cotinine <0.05 ng/mL.ConclusionNo linear association was found between HbA1c and serum cotinine in adolescents overall after adjusting for potential confounders. Differences between TSE groups were found in males. Future research in adolescents should examine chronic TSE over time to examine the potential for development of type 2 diabetes.ImplicationsTSE has been associated with increased risk for the development of type 2 diabetes among adults. It is unclear if this relationship holds in adolescents. We examined the association between serum cotinine and HbA1c in adolescents without known diabetes who completed the 1999-2012 National Health and Nutrition Examination Survey. Although no association was found between serum cotinine and HbA1c overall while controlling for potential confounding factors, we observed interaction effects that are indicative of TSE influencing HbA1c differentially by sex and age. Reducing TSE in adolescents should be a priority for future tobacco control efforts.
| S-EPMC5896452 | biostudies-literature