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ORIGINAL RESEARCH article

Front. Endocrinol., 19 January 2026

Sec. Clinical Diabetes

Volume 16 - 2025 | https://doi.org/10.3389/fendo.2025.1731945

This article is part of the Research TopicAdvancements in Biomarker Genetics: Insights from the Genomics EraView all 5 articles

Associations between glycated albumin and current measures of glycaemic control in Saudi adults

Suhad Bahijri,,Suhad Bahijri1,2,3Aliaa Sabban,,Aliaa Sabban1,2,3Sumia Enani,,Sumia Enani2,3,4Maha Saleh AlqahtaniMaha Saleh Alqahtani1Manal Malibary,,*Manal Malibary2,3,4*Mohammad Alhashmi,Mohammad Alhashmi5,6Jaakko Tuomileto,,Jaakko Tuomileto2,7,8
  • 1Department of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia
  • 2Saudi Diabetes Research Group, King Fahd Medical Research Centre, King Abdulaziz University, Jeddah, Saudi Arabia
  • 3Food, Nutrition and Lifestyle Research Unit, King Fahd for Medical Research Centre, King Abdulaziz University, Jeddah, Saudi Arabia
  • 4Department of Food and Nutrition, Faculty of Human Sciences and Design, King Abdulaziz University, Jeddah, Saudi Arabia
  • 5Department of Medical Laboratory Sciences, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia
  • 6Toxicology and Forensic Sciences Unit, King Fahd Medical Research Centre, King Abdulaziz University, Jeddah, Saudi Arabia
  • 7Department of Public Health, University of Helsinki, Helsinki, Finland
  • 8Department of Public Health and Welfare, Finnish Institute for Health and Welfare, Helsinki, Finland

Background: Current dysglycaemia detection methods have limits; glycated albumin (GA), unaffected by conditions that distort HbA1c, is proposed as an alternative. We aimed to estimate the relationship between various glycaemic parameters and their association with GA in Saudi adults to evaluate GA potential utility in screening, detecting, and monitoring diabetes (DM) and intermediate hyperglycaemia (IH).

Method: A total of 132 biobank serum samples (-80°C) representing a wide glycaemia range, using HbA1c, fasting plasma glucose -FPG, and 1 hour plasma glucose- 1h-PG data. Serum GA was measured by ELISA and expressed as %. Correlations with glycaemic markers were assessed, group means (normoglycaemia, IH, DM) were compared, and diagnostic performance evaluated by ROC analysis. Optimal GA cut-offs for dysglycaemia and DM were determined, with significance set at P< 0.05.

Results: Used measures of glycaemia did not consistently classify glycaemic status in the same way. The groups with IH and DM had significantly higher mean GA values compared with the normoglycaemia group (P<0.001). GA values correlated significantly with all glycaemic markers (P<0.001), showing the strongest correlation with HbA1c, and the weakest with 1h-PG. the optimal GA cut-off values for detecting dysglycaemia was 13.9% (Sensitivity= 0.786, specificity= 0.917), and 14.7% (Sensitivity= 0.857, specificity= 0.747) for DM.

Conclusion: GA correlated significantly with other markers and can be suggested as an alternative to detect and monitor glycaemic status among Saudis. Further research is required to determine ranges in our population.

Introduction

The prevalence of dysglycaemia and its components, diabetes mellitus (DM) and intermediate hyperglycaemia (IH- also called prediabetes) - including impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) - are increasing globally (1, 2). DM and dysglycaemia, disorders of glucose homeostasis of different degrees, which, if left undiagnosed and unmanaged, can result in damage to multiple organs (1, 2). Therefore, early detection of all forms of disorders in glucose homeostasis is utmost important to prevent their potential deleterious effects.

DM and IH have been traditionally diagnosed using fasting plasma glucose (FPG) or 2-h plasma glucose (2-h PG) after a 75-g oral glucose tolerance test (OGTT) (3). However, the association between FPG and 2-h PG is affected by various factors resulting in a significant variability in the classification of glycaemic status (4). Both measurements have limitations and disadvantages; the optimal FPG cut-off value for diagnosing is less sensitive than the 2-hPG (59), while the 2-h OGTT is time consuming (10). The American Diabetes Association (ADA) endorsed the use of glycohemoglobin (HbA1c) as a diagnostic criterion for DM in 2010 (11) based on the recommendation of the International Expert Committee (IEC) (12). However, HbA1c also has many disadvantages. It is unreliable in many physiological and clinical conditions due to factors that affect lifespan of the erythrocytes and haemoglobin variants. In addition, HbA1c is a less sensitive biomarker for detecting dysglycaemia than glucose measurement (1315).

To achieve the best possible sensitivity and specificity it was suggested to use a combination method (HbA1c and FPG) for diabetes screening and diagnosis using HbA1c not as an alternative but as an adjunct to FPG (16, 17). The practicability and cost effectiveness of this remains to be evaluated.

Interest in the 1-h post-challenge PG has re-emerged in the early 2000s (18). Studies have confirmed its association with insulin sensitivity and pancreatic β-cell function (1921). In addition, several studies across diverse populations have reported that the 1-h PG is superior to FPG, 2-h PG, and HbA1c in predicting incident DM (19, 2225), and various complications associated with DM, including cardiovascular disease (26) in individuals with normal glucose tolerance (NGT) with current criteria. A petition was published proposing the use of 1-hPG for diagnosing IGT, suggesting a cut-off point of 8.6 mmol/l (27). Recently, a Position Statement by the International Diabetes Federation was published recommending that people with a 1-h PG ≥ 155 mg/dL (8.6 mmol/L) are considered to have IH, while those with a 1-h PG ≥ 209 mg/dL (11.6 mmol/L) are classified as having DM (28).

To avoid glucose loading and the need for fasting, another glycated protein with a shorter half-life than haemoglobin, namely glycated albumin (GA), was proposed as a biomarker of glycaemic status (29). Albumin, which is produced in the liver, is considered the major protein in blood, comprising about 60% of serum proteins (30). It has many important physiological roles including maintenance of colloid-osmotic pressure, acting as a carrier to various hormones, metal ions, fatty acids and bilirubin, as well as having anti-oxidant activities (30). In addition, albumin level has been long used in the assessment of nutritional status with low levels indicating malnutrition (31). Low Albumin level has also been associated with inflammation (32), and various other conditions including liver disease, kidney disease, acute pulmonary embolism and cancer (33, 34). Albumin in plasma is glycated by a non-enzymatical reaction faster than haemoglobin (35). Therefore, it may reflect changes in glycaemic status earlier than HbA1c, and detect any fluctuations following medical therapy faster due to the shorter life of albumin (36). Moreover, unlike HbA1C, GA level is not affected by the presence of various hemoglobinopathies (37) anaemia, or pregnancy (38). Indeed, results of various clinical studies on different populations and age groups have indicated that GA is a promising marker in DM (3942). Moreover, GA was reported to be better than the HbA1c for evaluating short-term changes in plasma glucose and hence may be considered as a suitable measure for the effectiveness of anti-diabetic medication in type 2 diabetic patients (43). Another study found linear associations between serum GA, plasma glucose, and HbA1c, and in cases where HbA1c did not adequately reflect the glycaemic status in the diagnosis of diabetes, serum GA provided a valuable substitute especially that it is more practical and saves more time than performing an OGTT (44). In addition, several studies have indicated that in patients with diabetes and chronic kidney disease, GA was found to be a better marker of glycaemic control (4547), especially that HbA1C is not a reliable marker in these cases (47). Furthermore, studies reported an association of GA with the chronic complications of type 1 (48) and type 2 diabetes (49).

In view of the high prevalence and incidence of diabetes in Saudi Arabia (50) there is an increased need for an effective test to screen, detect, and monitoring DM and IH among Saudis. Apart of a small study to evaluate the association between glycated-albumin and various biochemical parameters in long-standing (>10 years) type-2 diabetic subjects (51), no studies evaluating the value of GA measurements as a marker of glycaemic control among the Saudi adults with a wide range of glycaemic status have been carried out.

Therefore, the aim of this study was to estimate the association between various glycaemic parameters in Saudi adults - including HbA1c, FPG, and 1h-PG and their association with GA to evaluate its potential utility in screening, detecting, and monitoring DM and IH.

Materials and methods

Study design and population

A cross-sectional design was adopted for this study. Ethical approval was obtained from the Committee on Ethics of Human Research at the Faculty of Medicine, King Abdulaziz University (Approval No. 345-22, dated June 30, 2022). All procedures involving human participants and use of stored biological samples were conducted in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Declaration of Helsinki and its later amendments or comparable ethical standards.

A total of 132 serum samples from the biobank stored at -80°C in the Food, Nutrition and Lifestyle Research Unit at King Fahad Medical Research Centre (KFMRC) and collected earlier from different health care centres all over the city of Jeddah as outlined in an earlier study (52) to ensure socioeconomic and ethnic diversity were chosen to represent a wide range of glycaemia, based on HbA1c, FPG, and 1h-PG. In summary, a cross-sectional design was used aiming to recruit 1500 (750 men and 750 women) participants from selected public healthcare centres by employing stratified, 2-stage cluster sampling method (53). A consent form was signed by recruited participants. Demographics, lifestyle variables, dietary habits, and personal medical and family history were obtained using a predesigned questionnaire based on factors associated with dysglycaemia found in other populations (5457).

Participants were instructed to fast overnight for 8 to 14 hours, and fasting blood sample was collected to estimate fasting plasma glucose (FPG) and glycated haemoglobin (HbA1c). Another sample was collected 1 hour after ingestion of 75-g glucose solution (CASCO NERL Diagnostics, East Providence, RI, USA) for estimating plasma glucose (1-hour oral glucose tolerance test; 1 h-OGTT) (58, 59). All samples (whole blood or plasma) were analysed at the Clinical Chemistry Laboratory at National Guard Hospital in Jeddah. HbA1c was measured with HbA1c analyser G8 (TOSOH Corporation, Japan). Plasma glucose was measured by spectrophotometric methods using Architect c8000 autoanalyzer (ABBOTT, USA).

The individuals were classified into three categories: (i) those within normal glycaemic range (normoglycaemia), (ii) those within the intermediate glycaemic range (IH), and (iii) those within the diabetic range (DM) using a combined glycaemic reference, in which, placement into a range was assigned if any of the three measures (HbA1c, FPG or 1-h PG) fell within the corresponding range (28, 60). All samples were collected from volunteers without prior identification of dysglycaemia. Participants samples with HbA1c concentrations of 5.7-6.4%, and/or FPG of 5.6-6.9 mmol/L, and/or 1h-PG of 8.6-11.5 mmol/L were classified as IH, while participants with HbA1c 6.5%, or FPG ≥ 7 mmol/L, or 1h-PG ≥11.6 mmol/L were classifies as having DM. Dysglycaemia was defined as the presence of either IH or DM. Participants with any acute or chronic conditions that may significantly impact blood albumin or glucose metabolism including hemoglobinopathies, kidney and liver diseases were excluded.

As a result, 52 samples reflected DM status, 32 reflected IH, and 48 reflected normoglycaemia.

Demographic and anthropometric data, including age, sex, and BMI, were retrieved from the participants records stored in the unit files. Similarly, results of the medical investigation, including the biochemistry profile - comprising FPG, HbA1c,1h-PG, total serum albumin, and lipid profile - were also collected from the records.

Biochemical assay for GA

GA was measured in samples using an ELISA kit (CUSABIO GA kit, Cusabio Technology LLC, China) to quantitatively determine human GA concentrations in serum and plasma and following the manufacturer’s instructions. The assay is based on competitive inhibition reaction. A microtiter plate, pre-coated with GA, is provided in the kit. standards or samples are added into the designated wells along with a Horseradish Peroxidase (HRP) conjugated antibody specific to GA. A competitive binding interaction occurs between the immobilised GA and GA present in the samples. After incubation, a substrate solution is added, leading to a colorimetric reaction that is inversely proportional to the GA concentration in the samples. Absorbance was measured using a microplate reader (DNM-9602, Drawell International Technology Limited Co., China). The percentage of GA was calculated using the formula: (GA%= serum GA/total albumin x100) (61). Quality assurance was maintained by random incorporation of standard reference materials into the sample plates, ensuring the results consistently met satisfactory criteria.

Statistical analysis

All statistical analyses were performed using g IBM SPSS statistics version 20.0 for Windows (IBM Corporation, Armonk, NY, USA). Data were analysed and descriptive statistics were expressed as frequencies or mean ± standard deviation. Variables with homogeneous variances were compared across glycaemic groups using one-way ANOVA with Bonferroni post-hoc tests, whereas variables with heterogeneous variances were compared using Welch’s ANOVA with Games-Howell post-hoc comparisons. Correlation between markers of glycaemic status (FPG, 1-hPG, and HbA1c) and GA were assessed by the Spearman’s test. The ANOVA test was used to compare normoglycaemic, IH, and DM groups.

The performance of serum GA in identifying dysglycaemia (defined as IH or DM), and specifically DM – based on the three measures of glycaemic status (HbA1c, FPG, and 1h-PG) – was evaluated using the receiver operating characteristic (ROC) curve. As participants were classified into normoglycaemia, IH and DM using a combined glycaemic reference in which placement into a range was assigned if any of the three measures fell within the corresponding range, the combined definition was used as the reference “true status” in the ROC analysis. The optimal cut-off for serum GA was derived from the ROC curve with the shortest distance to the top-left corner in the ROC curve and the Youden index (Y = sensitivity + specificity–1). The diagnostic performance of various GA thresholds (ranging from GA of 10.0% to 23.0%, at 0.1% intervals) for identifying dysglycaemia and DM was calculated, including the sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), false negative rates (FNR), and false positive rates (FPR). A p-value of<0.05 was considered to be statistically significant.

Results

Characteristics of the study participants

Data for all variables were available for all 132 individuals except for 1h-PG. 1h-PG values were available for 96 individuals only. Characteristics of the study participants grouped according to their glycaemic status, are outlined in Table 1. Across the three glycaemic groups, significant differences were observed in several biochemical and clinical variables. HbA1c, fasting glucose, 1-h glucose, and glycated albumin were progressively higher from normoglycaemia to intermediate hyperglycaemia and from intermediate hyperglycaemia to diabetes (all p< 0.001), and pairwise comparisons were significant for all three group contrasts. Triglycaerides was also elevated in the diabetes group compared with normoglycaemia (p< 0.01) and albumin was lower in the diabetes group compared with normoglycaemia (p< 0.01). Age, BMI, systolic blood pressure, and diastolic blood pressure differed significantly among groups, with higher values observed in the diabetes group compared with normoglycaemia (all p ≤ 0.03). Total cholesterol, LDL-c, HDL-c, height, and weight did not differ significantly between groups (all p > 0.05).

Table 1
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Table 1. Baseline characteristics of study participants by glycaemic status.

Correlation between GA with the other glycaemic measurements

A highly significant Spearman correlation coefficient was observed between GA and all glycaemic markers, as presented in Table 2.

Table 2
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Table 2. Correlation of GA with other glycaemic markers.

The strongest correlation coefficient with GA was observed with HbA1c, while the weakest with 1h-PG. HbA1c also showed significant correlations with both FPG and 1h-PG to a similar extent. Additionally, a strong and significant correlation was found between FPG and 1h-PG (r= 0.758). Figure 1 displays the relationships between GA and HbA1c (Figure 1a), GA and FPG (Figure 1b), GA and 1-hPG and (Figure 1c), GA and (Figure 1d), and FPG and HbA1c (Figure 1d).

Figure 1
Four scatter plots display relationships between various blood sugar indicators.   Panel a: Shows GA% versus HbA1c%, indicating a positive correlation.  Panel b: Displays GA% against FBG (mmol/L), with a noticeable positive trend.  Panel c: Illustrates GA% versus 1h-PG (mmol/L), showing a positive relationship.  Panel d: Depicts FBG (mmol/L) versus HbA1c%, indicating positive correlation.   Each plot suggests a positive correlation between the variables.

Figure 1. Correlations between glycaemic measures (a–d): (a) HbA1c vs GA, (b) FPG vs GA, (c) 1h-PG vs GA, and (d) HbA1c vs FPG. HbA1c, glycated haemoglobin A1c; FPG, fasting plasma glucose; 1h-PG, 1-hour plasma glucose; GA, glycated albumin.

The proportion of people identified with hyperglycaemia (IH and diabetes) through HbA1c, FPG and 1h-PG

Different measures of hyperglycaemia classified the samples differently. Based on HbA1c measurements, 36.4% (n=48) were normoglycaemic, 31.8% (n=42) were classified as having IH, and 31.8% (n=42) DM. According to FPG results, 71.2% (n=94) were normoglycaemic, 6.8% (n=9) were classified as having IH, and 22% (n=29) DM. Using 1h-PG values, 28.8% (n=38) were normoglycaemic, 23.5% (n=31) had IH, and 20.5% (n=27) had DM.

A total of 96 samples were tested for all three measures - HbA1c, FPG and 1h-PG. Although significant correlations were observed between HbA1c with both FPG and 1h-PG, the three measures did not consistently classify glycaemic in the same way. The concordance between the three measures in classifying of glycaemic status is illustrated in the Venn diagram (Figure 2).

Figure 2
Venn diagram illustrating the overlap among three glucose measurement methods: HbA1c, FPG, and 1h-PG. HbA1c captures 17 percent of cases, FPG captures 4.2 percent, and 1h-PG captures 8.3 percent. Overlaps include 11.5 percent between all three methods, 37.5 percent between HbA1c and 1h-PG, 1 percent between HbA1c and FPG, and 3.1 percent between FPG and 1h-PG. Percentages represent the proportion of cases captured by each method, with total counts shown.

Figure 2. The percentage of individuals detected as having dysglycaemia through HbA1c, FPG, and 1h-PG. HbA1c, glycated haemoglobin A1c; FPG, fasting plasma glucose; 1h-PG, 1-hour plasma glucose.

Based on HbA1c, 67% (n=64) of the samples showed dysglycaemia (IH or DM), with 17% (n=16) identified by HbA1c alone. Similarly, 60% (n=58) were classified as having dysglycaemia using 1h-PG, with 8.3% (n=8) detected exclusively by 1h-PG alone. Additionally, 20% (n=19) of the samples showed dysglycaemia based on FPG, with 4.2% (n=4) identified only through FPG analysis. Only 11.5% (n=11) of all dysglycaemic samples showed elevated values across all three measures of glycaemia simultaneously.

Prevalence of dysglycaemia at different levels of glycated albumin

The prevalence of dysglycaemia at different levels of GA is presented in Table 3.

Table 3
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Table 3. Prevalence of dysglycaemia, IH and DM across GA categories.

Diagnostic performance of glycated albumin for identifying dysglycemia (IH or DM) and DM

A GA level of 14% can be suggested as a cut-off point for detecting dysglycaemia in Saudi adults. To support this suggestion a ROC curve was constructed (Figure 3) to evaluate the discriminative power of GA in identifying metabolic abnormalities (IH or DM), as well as DM alone. The area under the curve (AUC), most appropriate cut-off point, as well as specificity and sensitivity were calculated for both conditions and presented in Table 4.

Figure 3
Two Receiver Operating Characteristic (ROC) curves comparing sensitivity versus one minus specificity. Chart a shows a highlight at 13.9, and chart b highlights 14.7. Both graphs plot sensitivity from zero to one, demonstrating performance metrics with distinct stepped lines.

Figure 3. The discriminative power of glycated albumin % for detecting dysglycaemia (diabetes or intermediate hyperglycaemia) (a) and DM alone (b). Participants were classified into normal glycaemic range (normoglycaemia), intermediate glycaemic range (IH), diabetic range (DM) using a combined glycaemic reference, in which, placement into a range was assigned if any of the three measures (glycated hemoglobin (HbA1c), fasting plasma glucose (FPG) and 1-hour plasma glucose (1h-PG)) fell within the corresponding range. Dysglycaemia includes IH and DM combined. The combined definition was used as the reference “true status” in the ROC analysis. Panel (a) shows the ROC curve for detecting dysglycaemia (including diabetes and intermediate hyperglycaemia), with an optimal cut-off point of 13.9%. Panel (b) displays the ROC curve for detecting DM alone, with an optimal cut-off of 14.7%. Sensitivity is plotted against 1-specificity to evaluate diagnostic performance.

Table 4
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Table 4. Diagnostic performance of glycated albumin (%) for detecting dysglycaemia and DM.

Discussion

With the increasing prevalence of diabetes in Saudi Arabia (50), alongside the high rates of the medical conditions that limit the reliability of HbA1c as a glycaemic indicator (6266) in the country, there is a growing need to identify an alternative marker of glycaemic status that is more reliable, cost-effective, time-efficient, and does not require fasting (67). Therefore, the aim of this pilot study was to examine how glycated albumin relates to other glycaemic control measurements (namely HbA1c, FPG, and 1h-PG) in order to evaluate its potential usefulness for screening, detection, and monitoring dysglycaemia and diabetes in the Saudi population.

The findings from this study clearly indicate that the currently recommended measures of glycaemia (HbA1c, FPG and 1h-PG) do not consistently classify glycaemic status of the samples in the same manner. Notable, only 11.5% of the samples identified dysglycaemia by all the three measures, highlighting the need for evaluating another, more robust and reliable biomarker of glycaemic status.

In this study, GA was measured and its correlations with HbA1c, FPG, and 1h-PG were investigated using the stored data of 132 serum samples collected from participants without prior diagnosis of disorders of glucose metabolism. The samples represented a broad range of glycaemic status - normoglycaemic, IH, and DM - Based on the currently recommended diagnostic criteria (28, 60). We found that people with IH and DM had significantly higher mean GA levels compared with those with normoglycaemia (P<0.001). Additionally, the mean GA values observed in our study were very similar to those reported in a comparable population sample from China (68) even though their sample size was 1935 subjects, which is much larger than our sample in this pilot study. Other studies from different countries gave similar results also. Large epidemiological cohorts have evaluated GA alongside other nontraditional glycaemic markers at substantially greater scale (e.g., ARIC analyses reporting GA in >10,000 adults) (69). providing narrower confidence intervals and greater power for subgroup analyses than is possible here. Conversely, several diagnostic cut-off studies have used intermediate sample sizes (hundreds to ~1,000); for instance, one Korean ROC analysis referenced an evaluation in 852 individuals (70). Using a different method for estimating GA than ours, and much smaller sample of 32 normoglycemic Italian adults, Paroni et al. estimated the reference interval for GA to be 11.7%-16.9% (71).Taken together, our sample size is smaller than many population cohorts, but it intentionally spans a wide glycaemic range and uses a combined glycaemic reference (HbA1c, FPG and 1h-PG) to strengthen classification; therefore, our findings are best interpreted as a Saudi-specific pilot estimate of GA discrimination that warrants confirmation in a larger, fully phenotyped cohort.

However, we were unable to compare our results for newly identified people with DM with previously published GA levels in a small study on Saudi people with long-standing T2DM (51) Differences between GA levels reported here and those previously published may reflect both biological/clinical differences in the sampled populations and methodological differences in GA measurement. The GA quantification in this previous study used a different commercial immunoassay kit with GA measured from a standard curve as a concentration readout on antigen-precoated plates, whereas the current manuscript used the CUSABIO competitive ELISA (competitive inhibition format) and then expressed GA as GA% (GA/total albumin ×100), which explicitly normalises to albumin concentration and may reduce between-person variability attributable to serum albumin differences (51). In addition, comparison was not appropriate for the following reasons: a) Enrolled subjects had long-standing T2DM, and must have been on various medications, unlike those in our study, b)Stated demographic and biochemical characteristics of enrolled subjects were different to the characteristics in our study, c) No coexisting complications were mentioned, but are expected in view of the reported HbA1c levels and the duration of DM, all of which could affect GA levels.

We also found that GA correlated significantly and strongly with all three measures of glycaemia. The strongest correlation was observed with HbA1c (r=0.701), while the weakest one was with 1h-PG. This pattern of correlations – highest with HbA1c, followed by FPG, and lowest 1-hPG is similar to that reported in a previous study conducted in China (68). Our findings are also in keeping with findings reported in previous studies in other populations on people with diabetes (39, 40, 42). The lower correlation coefficient between GA and FPG compared with that with HbA1c might be attributed to the nature of FPG as a point-in-time measure which can be affected by the duration of fasting and recent food intake. In contrast, both HbA1c like GA reflect average blood glucose levels over a period of several weeks, which may explain their stronger inter-correlation. The relatively weaker correlation between GA and 1h-PG might be partially explained by the smaller number of samples available for 1-hPG analysis. However, a more probable explanation is that the 1-hPG level, like FPG, is a point-in-time measure that depends on the shape of the glucose tolerance curve, which, in turn, depends on whether the studied individuals had impaired fasting glucose (IFG) or impaired glucose tolerance (IGT) (72). People having IFG show a fast increase in plasma glucose concentration with a peak at 1 hour, and a return to normal or near normal values after 2 hours, while people with IGT have a more gradual initial increase in plasma glucose concentration which continues to rise after 1 hour and remains markedly increased at 2 hours (72). In addition, people with NGT commonly present with a biphasic OGTT, while people with IGT usually have a monophasic OGTT (73, 74). Our sample included people with NGT as well as IFG, IGT and even some with diabetes, explaining the slightly lower correlation coefficient compared to GA which reflects average blood glucose levels over the previous weeks.

Nevertheless, the significant correlations observed across all three measures of glycaemia with GA support the potential utility of GA as a biomarker for detecting IH and DM among Saudi adults.

In this study, we identified the optimal GA cut-off values for detecting dysglycaemia and its components - IH and DM- with an excellent AUC, excellent specificity, and very good sensitivity. Previous studies conducted in various populations have reported a range of GA cut-off values (39, 44, 68, 7577). For example, studies on Asian populations for diagnosing DM, have suggested optimal GA cut-off values between 14%-16%, whereas a lower cut-off value of 13.5% has been proposed for Caucasian populations (75).The observed variations in GA cut-off values across populations are likely attributed to study designs, differences in participant selection, laboratory methods, and environmental and genetic factors, highlighting the need to find out whether true population-based differences in GA values exist or whether uniform cut-off points should be adopted, similar to plasma glucose and HbA1c.

To enhance the diagnostic power of GA for diagnosing or excluding DM, it was suggested to use FPG and GA in combination (44). While we did not attempt this in our study due to its pilot nature and a relatively small sample size, this could be a focus of future research, particularly with a larger sample size. A multi-ethnic study using a standardised protocol is needed to find out the optimal cut-off point for GA for detecting IH and DM.

Our study has limitations as well as points of strengths.

The main strength of this study lies in it being the first study in Saudi Arabia to evaluate GA as a new tool for assessing glycaemic status in Saudi adults not previously diagnosed with DM. Additionally, this study compares GA with the currently recommended measures of glycaemia assessment to establish cut-off points for detecting IH and DM. GA has been proposed as offering advantages over other current measures of hyperglycaemia, particularly in the presence of certain medical conditions common among Saudis. The primary limitation of the study is the relatively small sample size. Nevertheless, the sample size was sufficient for this pilot study, providing valuable insights for planning larger future studies. Another limitation is the use of frozen stored samples, which may limit reproducibility in real world setting. However, an earlier study reported that samples frozen at - 70°C and stored for as long as 23 years are suitable for the GA assay (78). Our samples were collected between July 2016 and February 2017, and stored at - 80°C which lends credibility to our methods and findings.

In conclusion, given the high occurrence of DM in Saudi Arabia, there is an urgent need for an effective screening, detection, and monitoring tools suitable for the local population. Additionally, the high rates of conditions affecting erythrocyte integrity pose significant challenges to the reliability of current diagnostic tests used to detect hyperglycaemia in this country. GA emerges as a promising alternative glycaemic test as it is unaffected by medical conditions associated with erythrocyte integrity, thus offering accurate and reliable results essential for early detection of DM and monitoring of its control.

Future research on GA as a diagnostic test for IH and DM should focus on studies with a larger sample size to establish reference values for the diagnosis of IH and DM in the Saudi population and beyond. Longitudinal studies are needed to assess whether GA can serve as a better marker for monitoring DM management and predicting complications associated with hyperglycaemia.

Data availability statement

The original contributions presented in the study are included in the article/supplementary material. Further inquiries can be directed to the corresponding author.

Ethics statement

The studies involving humans were approved by Committee on Ethics of Human Research at the Faculty of Medicine, King Abdulaziz University (Approval No. 345-22, dated June 30, 2022). The studies were conducted in accordance with the local legislation and institutional requirements. The participants provided their written informed consent to participate in this study.

Author contributions

SB: Conceptualization, Formal analysis, Methodology, Project administration, Supervision, Writing – original draft, Writing – review & editing. AS: Conceptualization, Data curation, Investigation, Methodology, Writing – original draft, Writing – review & editing. SE: Data curation, Formal analysis, Investigation, Writing – original draft, Writing – review & editing. MSA: Formal analysis, Investigation, Writing – original draft, Writing – review & editing, Data curation, Methodology. MM: Formal analysis, Investigation, Writing – original draft, Writing – review & editing, Visualization. MA: Formal analysis, Investigation, Writing – original draft, Writing – review & editing. JT: Formal analysis, Investigation, Methodology, Writing – original draft, Writing – review & editing.

Funding

The author(s) declared that financial support was not received for this work and/or its publication.

Conflict of interest

The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Generative AI statement

The author(s) declared that generative AI was not used in the creation of this manuscript.

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References

1. Association AD. 2. Classification and diagnosis of diabetes. Diabetes Care. (2015) 39:S13–22. doi: 10.2337/dc16-S005

PubMed Abstract | Crossref Full Text | Google Scholar

2. Association AD. Erratum. Classification and diagnosis of diabetes. Sec. 2. In Standards of Medical Care in Diabetes–2016. Diabetes Care. (2016) 39:S13–22. doi: 10.2337/dc16-er09

PubMed Abstract | Crossref Full Text | Google Scholar

3. Association AD. Diagnosis and classification of diabetes mellitus. Diabetes Care. (2013) 37:S81–90. doi: 10.2337/dc14-S081

PubMed Abstract | Crossref Full Text | Google Scholar

4. Selvin E, Crainiceanu CM, Brancati FL, and Coresh J. Short-term variability in measures of glycemia and implications for the classification of diabetes. Arch Intern Med. (2007) 167:1545–51. doi: 10.1001/archinte.167.14.1545

PubMed Abstract | Crossref Full Text | Google Scholar

5. Chang CJ, Wu JS, Lu FH, Lee HL, Yang YC, and Wen MJ. Fasting plasma glucose in screening for diabetes in the Taiwanese population. Diabetes Care. (1998) 21:1856–60. doi: 10.2337/diacare.21.11.1856

PubMed Abstract | Crossref Full Text | Google Scholar

6. Doi Y, Kubo M, Yonemoto K, Ninomiya T, Iwase M, Arima H, et al. Fasting plasma glucose cutoff for diagnosis of diabetes in a Japanese population. J Clin Endocrinol Metab. (2008) 93:3425–9. doi: 10.1210/jc.2007-2819

PubMed Abstract | Crossref Full Text | Google Scholar

7. Engelgau MM, Thompson TJ, Herman WH, Boyle JP, Aubert RE, Kenny SJ, et al. Comparison of Fasting and 2-Hour Glucose and HbA1c Levels for Diagnosing Diabetes: Diagnostic criteria and performance revisited. Diabetes Care. (1997) 20:785–91. doi: 10.2337/diacare.20.5.785

PubMed Abstract | Crossref Full Text | Google Scholar

8. Ko GT, Chan JC, Lau E, Woo J, and Cockram CS. Fasting plasma glucose as a screening test for diabetes and its relationship with cardiovascular risk factors in hong kong chinese. Diabetes Care. (1997) 20:170–2. doi: 10.2337/diacare.20.2.170

PubMed Abstract | Crossref Full Text | Google Scholar

9. Ramachandran A, Snehalatha C, Vijay V, and Viswanathan M. Fasting plasma glucose in the diagnosis of diabetes mellitus: a study from southern India. Diabetes Med. (1993) 10:811–3. doi: 10.1111/j.1464-5491.1993.tb00171.x

PubMed Abstract | Crossref Full Text | Google Scholar

10. Jagannathan R, Neves JS, Dorcely B, Chung ST, Tamura K, Rhee M, et al. The oral glucose tolerance test: 100 years later. Diabetes Metab Syndr Obes. (2020) 13:3787–805. doi: 10.2147/dmso.S246062

PubMed Abstract | Crossref Full Text | Google Scholar

11. Association AD. Diagnosis and classification of diabetes mellitus. Diabetes Care. (2010) 33:S62–S9. doi: 10.2337/dc10-S062

PubMed Abstract | Crossref Full Text | Google Scholar

12. Committee TIE. International Expert Committee report on the role of the A1C assay in the diagnosis of diabetes. Diabetes Care. (2009) 32:1327–34. doi: 10.2337/dc09-9033

PubMed Abstract | Crossref Full Text | Google Scholar

13. Mostafa SA, Davies MJ, Webb D, Gray LJ, Srinivasan BT, Jarvis J, et al. The potential impact of using glycated haemoglobin as the preferred diagnostic tool for detecting Type 2 diabetes mellitus. Diabetes Med. (2010) 27:762–9. doi: 10.1111/j.1464-5491.2010.03015.x

PubMed Abstract | Crossref Full Text | Google Scholar

14. Olson DE, Rhee MK, Herrick K, Ziemer DC, Twombly JG, and Phillips LS. Screening for diabetes and pre-diabetes with proposed A1C-based diagnostic criteria. Diabetes Care. (2010) 33:2184–9. doi: 10.2337/dc10-0433

PubMed Abstract | Crossref Full Text | Google Scholar

15. Zhou X, Pang Z, Gao W, Wang S, Zhang L, Ning F, et al. Performance of an A1C and fasting capillary blood glucose test for screening newly diagnosed diabetes and pre-diabetes defined by an oral glucose tolerance test in Qingdao, China. Diabetes Care. (2010) 33:545–50. doi: 10.2337/dc09-1410

PubMed Abstract | Crossref Full Text | Google Scholar

16. Manley SE, Sikaris KA, Lu ZX, Nightingale PG, Stratton IM, Round RA, et al. Validation of an algorithm combining haemoglobin A(1c) and fasting plasma glucose for diagnosis of diabetes mellitus in UK and Australian populations. Diabetes Med. (2009) 26:115–21. doi: 10.1111/j.1464-5491.2008.02652.x

PubMed Abstract | Crossref Full Text | Google Scholar

17. Takahashi Y, Noda M, Tsugane S, Kuzuya T, Ito C, and Kadowaki T. Prevalence of diabetes estimated by plasma glucose criteria combined with standardized measurement of HbA1c among health checkup participants on Miyako Island, Japan. Diabetes Care. (2000) 23:1092–6. doi: 10.2337/diacare.23.8.1092

PubMed Abstract | Crossref Full Text | Google Scholar

18. Abdul-Ghani MA, Williams K, DeFronzo RA, and Stern M. What is the best predictor of future type 2 diabetes? Diabetes Care. (2007) 30:1544–8. doi: 10.2337/dc06-1331

PubMed Abstract | Crossref Full Text | Google Scholar

19. Kuang L, Huang Z, Hong Z, Chen A, and Li Y. Predictability of 1-h postload plasma glucose concentration: A 10-year retrospective cohort study. J Diabetes Investig. (2015) 6:647–54. doi: 10.1111/jdi.12353

PubMed Abstract | Crossref Full Text | Google Scholar

20. Oka R, Aizawa T, Miyamoto S, Yoneda T, and Yamagishi M. One-hour plasma glucose as a predictor of the development of Type 2 diabetes in Japanese adults. Diabetes Med. (2016) 33:1399–405. doi: 10.1111/dme.12994

PubMed Abstract | Crossref Full Text | Google Scholar

21. Tfayli H, Lee SJ, Bacha F, and Arslanian S. One-hour plasma glucose concentration during the OGTT: what does it tell about β-cell function relative to insulin sensitivity in overweight/obese children? Pediatr Diabetes. (2011) 12:572–9. doi: 10.1111/j.1399-5448.2011.00745.x

PubMed Abstract | Crossref Full Text | Google Scholar

22. Abdul-Ghani MA, Abdul-Ghani T, Ali N, and Defronzo RA. One-hour plasma glucose concentration and the metabolic syndrome identify subjects at high risk for future type 2 diabetes. Diabetes Care. (2008) 31:1650–5. doi: 10.2337/dc08-0225

PubMed Abstract | Crossref Full Text | Google Scholar

23. Abdul-Ghani MA, Lyssenko V, Tuomi T, DeFronzo RA, and Groop L. Fasting versus postload plasma glucose concentration and the risk for future type 2 diabetes: results from the Botnia Study. Diabetes Care. (2009) 32:281–6. doi: 10.2337/dc08-1264

PubMed Abstract | Crossref Full Text | Google Scholar

24. Oh TJ, Lim S, Kim KM, Moon JH, Choi SH, Cho YM, et al. One-hour postload plasma glucose concentration in people with normal glucose homeostasis predicts future diabetes mellitus: a 12-year community-based cohort study. Clin Endocrinol (Oxf). (2017) 86:513–9. doi: 10.1111/cen.13280

PubMed Abstract | Crossref Full Text | Google Scholar

25. Pareek M, Almgren P, Jagannathan R, Nielsen ML, Groop L, Nilsson PM, et al. Clinical utility of a 1-hour oral glucose tolerance test for prediction of type 2 diabetes. Diabetologia. (2016) 59:S107–S108.

Google Scholar

26. Bianchi C, Miccoli R, Trombetta M, Giorgino F, Frontoni S, Faloia E, et al. Elevated 1-hour postload plasma glucose levels identify subjects with normal glucose tolerance but impaired β-cell function, insulin resistance, and worse cardiovascular risk profile: the GENFIEV study. J Clin Endocrinol Metab. (2013) 98:2100–5. doi: 10.1210/jc.2012-3971

PubMed Abstract | Crossref Full Text | Google Scholar

27. Bergman M, Manco M, Sesti G, Dankner R, Pareek M, Jagannathan R, et al. Petition to replace current OGTT criteria for diagnosing prediabetes with the 1-hour post-load plasma glucose ≥ 155 mg/dl (8.6 mmol/L). Diabetes Res Clin Pract. (2018) 146:18–33. doi: 10.1016/j.diabres.2018.09.017

PubMed Abstract | Crossref Full Text | Google Scholar

28. Bergman M, Manco M, Satman I, Chan J, Schmidt MI, Sesti G, et al. International Diabetes Federation Position Statement on the 1-hour post-load plasma glucose for the diagnosis of intermediate hyperglycaemia and type 2 diabetes. Diabetes Res Clin Pract. (2024) 209:111589. doi: 10.1016/j.diabres.2024.111589

PubMed Abstract | Crossref Full Text | Google Scholar

29. Kohzuma T, Yamamoto T, Uematsu Y, Shihabi ZK, and Freedman BI. Basic performance of an enzymatic method for glycated albumin and reference range determination. J Diabetes Sci Technol. (2011) 5:1455–62. doi: 10.1177/193229681100500619

PubMed Abstract | Crossref Full Text | Google Scholar

30. Carter DC and Ho JX. Structure of serum albumin. Adv Protein Chem. (1994) 45:153–203. doi: 10.1016/s0065-3233(08)60640-3

PubMed Abstract | Crossref Full Text | Google Scholar

31. Don BR and Kaysen G. Serum albumin: relationship to inflammation and nutrition. Semin Dial. (2004) 17:432–7. doi: 10.1111/j.0894-0959.2004.17603.x

PubMed Abstract | Crossref Full Text | Google Scholar

32. Eckart A, Struja T, Kutz A, Baumgartner A, Baumgartner T, Zurfluh S, et al. Relationship of nutritional status, inflammation, and serum albumin levels during acute illness: A prospective study. Am J Med. (2020) 133:713–22.e7. doi: 10.1016/j.amjmed.2019.10.031

PubMed Abstract | Crossref Full Text | Google Scholar

33. Sheinenzon A, Shehadeh M, Michelis R, Shaoul E, and Ronen O. Serum albumin levels and inflammation. Int J Biol Macromol. (2021) 184:857–62. doi: 10.1016/j.ijbiomac.2021.06.140

PubMed Abstract | Crossref Full Text | Google Scholar

34. Tanık VO, Çınar T, Karabağ Y, Şimşek B, Burak C, Çağdaş M, et al. The prognostic value of the serum albumin level for long-term prognosis in patients with acute pulmonary embolism. Clin Respir J. (2020) 14:578–85. doi: 10.1111/crj.13176

PubMed Abstract | Crossref Full Text | Google Scholar

35. Anguizola J, Matsuda R, Barnaby OS, Hoy KS, Wa C, DeBolt E, et al. Review: Glycation of human serum albumin. Clin Chim Acta. (2013) 425:64–76. doi: 10.1016/j.cca.2013.07.013

PubMed Abstract | Crossref Full Text | Google Scholar

36. Freitas PAC, Ehlert LR, and Camargo JL. Glycated albumin: a potential biomarker in diabetes. Arch Endocrinol Metab. (2017) 61:296–304. doi: 10.1590/2359-3997000000272

PubMed Abstract | Crossref Full Text | Google Scholar

37. Koga M and Kasayama S. Clinical impact of glycated albumin as another glycemic control marker. Endocr J. (2010) 57:751–62. doi: 10.1507/endocrj.k10e-138

PubMed Abstract | Crossref Full Text | Google Scholar

38. Kim C, Bullard KM, Herman WH, and Beckles GL. Association between iron deficiency and A1C Levels among adults without diabetes in the National Health and Nutrition Examination Survey, 1999-2006. Diabetes Care. (2010) 33:780–5. doi: 10.2337/dc09-0836

PubMed Abstract | Crossref Full Text | Google Scholar

39. Furusyo N, Koga T, Ai M, Otokozawa S, Kohzuma T, Ikezaki H, et al. Utility of glycated albumin for the diagnosis of diabetes mellitus in a Japanese population study: results from the Kyushu and Okinawa Population Study (KOPS). Diabetologia. (2011) 54:3028–36. doi: 10.1007/s00125-011-2310-6

PubMed Abstract | Crossref Full Text | Google Scholar

40. Lee JW, Kim HJ, Kwon YS, Jun YH, Kim SK, Choi JW, et al. Serum glycated albumin as a new glycemic marker in pediatric diabetes. Ann Pediatr Endocrinol Metab. (2013) 18:208–13. doi: 10.6065/apem.2013.18.4.208

PubMed Abstract | Crossref Full Text | Google Scholar

41. Suzuki S, Koga M, Amamiya S, Nakao A, Wada K, Okuhara K, et al. Glycated albumin but not HbA1c reflects glycaemic control in patients with neonatal diabetes mellitus. Diabetologia. (2011) 54:2247–53. doi: 10.1007/s00125-011-2211-8

PubMed Abstract | Crossref Full Text | Google Scholar

42. Yang C, Li H, Wang Z, Zhang W, Zhou K, Meng J, et al. Glycated albumin is a potential diagnostic tool for diabetes mellitus. Clin Med (Lond). (2012) 12:568–71. doi: 10.7861/clinmedicine.12-6-568

PubMed Abstract | Crossref Full Text | Google Scholar

43. Shima K, Komatsu M, Noma Y, and Miya K. Glycated albumin (GA) is more advantageous than hemoglobin A1c for evaluating the efficacy of sitagliptin in achieving glycemic control in patients with type 2 diabetes. Intern Med. (2014) 53:829–35. doi: 10.2169/internalmedicine.53.1364

PubMed Abstract | Crossref Full Text | Google Scholar

44. Wu WC, Ma WY, Wei JN, Yu TY, Lin MS, Shih SR, et al. Serum glycated albumin to guide the diagnosis of diabetes mellitus. PloS One. (2016) 11:e0146780. doi: 10.1371/journal.pone.0146780

PubMed Abstract | Crossref Full Text | Google Scholar

45. Freedman BI, Shenoy RN, Planer JA, Clay KD, Shihabi ZK, Burkart JM, et al. Comparison of glycated albumin and hemoglobin A1c concentrations in diabetic subjects on peritoneal and hemodialysis. Perit Dial Int. (2010) 30:72–9. doi: 10.3747/pdi.2008.00243

PubMed Abstract | Crossref Full Text | Google Scholar

46. Sany D, Elshahawy Y, and Anwar W. Glycated albumin versus glycated hemoglobin as glycemic indicator in hemodialysis patients with diabetes mellitus: variables that influence. Saudi J Kidney Dis Transpl. (2013) 24:260–73. doi: 10.4103/1319-2442.109568

PubMed Abstract | Crossref Full Text | Google Scholar

47. Zheng CM, Ma WY, Wu CC, and Lu KC. Glycated albumin in diabetic patients with chronic kidney disease. Clin Chim Acta. (2012) 413:1555–61. doi: 10.1016/j.cca.2012.04.025

PubMed Abstract | Crossref Full Text | Google Scholar

48. Nathan DM, McGee P, Steffes MW, and Lachin JM. Relationship of glycated albumin to blood glucose and HbA1c values and to retinopathy, nephropathy, and cardiovascular outcomes in the DCCT/EDIC study. Diabetes. (2014) 63:282–90. doi: 10.2337/db13-0782

PubMed Abstract | Crossref Full Text | Google Scholar

49. Selvin E, Rawlings AM, Grams M, Klein R, Sharrett AR, Steffes M, et al. Fructosamine and glycated albumin for risk stratification and prediction of incident diabetes and microvascular complications: a prospective cohort analysis of the Atherosclerosis Risk in Communities (ARIC) study. Lancet Diabetes Endocrinol. (2014) 2:279–88. doi: 10.1016/s2213-8587(13)70199-2

PubMed Abstract | Crossref Full Text | Google Scholar

50. Magliano DJ and Boyko EJ. committee IDFDAtes. IDF Diabetes Atlas. Idf diabetes atlas Vol. 2021. . Brussels: International Diabetes Federation (2021).

Google Scholar

51. Abdalla SB and Abelwahab SI. Association of glycated albumin with glycemic markers, lipid profile and liver function tests for the assessment control in saudi patients with long-standing type-2 diabetes mellitus. J Appl Pharm Science. (2016) 6:096–100. doi: 10.7324/JAPS.2016.60316

Crossref Full Text | Google Scholar

52. Bahijri S, Al-Raddadi R, Ajabnoor G, Jambi H, Al Ahmadi J, Borai A, et al. Dysglycemia risk score in Saudi Arabia: A tool to identify people at high future risk of developing type 2 diabetes. J Diabetes Invest. (2020) 11:844–55. doi: 10.1111/jdi.13213

PubMed Abstract | Crossref Full Text | Google Scholar

53. Sedgwick P. Stratified cluster sampling. BMJ: Br Med J. (2013) 347:f7016. doi: 10.1136/bmj.f7016

Crossref Full Text | Google Scholar

54. Eriksson KF and Lindgärde F. Prevention of type 2 (non-insulin-dependent) diabetes mellitus by diet and physical exercise. The 6-year Malmö feasibility study. Diabetologia. (1991) 34:891–8. doi: 10.1007/bf00400196

PubMed Abstract | Crossref Full Text | Google Scholar

55. Saaristo T, Moilanen L, Korpi-Hyövälti E, Vanhala M, Saltevo J, Niskanen L, et al. Lifestyle intervention for prevention of type 2 diabetes in primary health care: one-year follow-up of the Finnish National Diabetes Prevention Program (FIN-D2D). Diabetes Care. (2010) 33:2146–51. doi: 10.2337/dc10-0410

PubMed Abstract | Crossref Full Text | Google Scholar

56. Tuomilehto J, Lindström J, Eriksson JG, Valle TT, Hämäläinen H, Ilanne-Parikka P, et al. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med. (2001) 344:1343–50. doi: 10.1056/nejm200105033441801

PubMed Abstract | Crossref Full Text | Google Scholar

57. Makrilakis K, Liatis S, Grammatikou S, Perrea D, Stathi C, Tsiligros P, et al. Validation of the Finnish diabetes risk score (FINDRISC) questionnaire for screening for undiagnosed type 2 diabetes, dysglycaemia and the metabolic syndrome in Greece. Diabetes Metab. (2011) 37:144–51. doi: 10.1016/j.diabet.2010.09.006

PubMed Abstract | Crossref Full Text | Google Scholar

58. Phillips L, Ziemer D, Kolm P, Weintraub W, Vaccarino V, Rhee M, et al. Glucose challenge test screening for prediabetes and undiagnosed diabetes. Diabetologia. (2009) 52:1798–807. doi: 10.1007/s00125-009-1407-7

PubMed Abstract | Crossref Full Text | Google Scholar

59. Pareek M, Bhatt DL, Nielsen ML, Jagannathan R, Eriksson KF, Nilsson PM, et al. Enhanced predictive capability of a 1-hour oral glucose tolerance test: A prospective population-based cohort study. Diabetes Care. (2018) 41:171–7. doi: 10.2337/dc17-1351

PubMed Abstract | Crossref Full Text | Google Scholar

60. Association AD. 2. Classification and diagnosis of diabetes: standards of medical care in diabetes-2021. Diabetes Care. (2021) 44:S15–s33. doi: 10.2337/dc21-S002

PubMed Abstract | Crossref Full Text | Google Scholar

61. Ciobanu DM, Bogdan F, Pătruţ CI, and Roman G. Glycated albumin is correlated with glycated hemoglobin in type 2 diabetes. Med Pharm Rep. (2019) 92:134–8. doi: 10.15386/mpr-1247

PubMed Abstract | Crossref Full Text | Google Scholar

62. Alsuwaida AO, Farag YM, Al Sayyari AA, Mousa D, Alhejaili F, Al-Harbi A, et al. Epidemiology of chronic kidney disease in the Kingdom of Saudi Arabia (SEEK-Saudi investigators) - a pilot study. Saudi J Kidney Dis Transpl. (2010) 21:1066–72.

PubMed Abstract | Google Scholar

63. Hamali HA. Glucose-6-phosphate dehydrogenase deficiency: an overview of the prevalence and genetic variants in Saudi Arabia. Hemoglobin. (2021) 45:287–95. doi: 10.1080/03630269.2022.2034644

PubMed Abstract | Crossref Full Text | Google Scholar

64. Jastaniah W. Epidemiology of sickle cell disease in Saudi Arabia. Ann Saudi Med. (2011) 31:289–93. doi: 10.4103/0256-4947.81540

PubMed Abstract | Crossref Full Text | Google Scholar

65. Mohammed M, Alqahtani AAA, Asirri SA, Alwuthaynani MT, Ishaq YMA, Hasan ER, et al. Prevalence of thalassemia in Saudi Arabia: a systematic review and meta-analysis. IJMDC. (2024) 8:2903–12. doi: 10.24911/IJMDC.51-1729873974

Crossref Full Text | Google Scholar

66. Owaidah T, Al-Numair N, Al-Suliman A, Zolaly M, Hasanato R, Al Zahrani F, et al. Iron deficiency and iron deficiency anemia are common epidemiological conditions in Saudi Arabia: report of the national epidemiological survey. Anemia. (2020) 2020:6642568. doi: 10.1155/2020/6642568

PubMed Abstract | Crossref Full Text | Google Scholar

67. Webber S. International diabetes federation. J Diabetes Nursing. (2011) 15:118–9. doi: 10.1016/j.diabres.2011.10.040

PubMed Abstract | Crossref Full Text | Google Scholar

68. Li G-Y, Li H-Y, and Li Q. Use of glycated albumin for the identification of diabetes in subjects from northeast China. World J Diabetes. (2021) 12:149. doi: 10.4239/wjd.v12.i2.149

PubMed Abstract | Crossref Full Text | Google Scholar

69. Selvin E, Rawlings AM, Lutsey PL, Pankow JS, Kao L, Steffes MW, et al. Abstract 11: fructosamine and glycated albumin with risk of coronary heart disease and death. Circulation. (2014) 129:A11–A. doi: 10.1161/circ.129.suppl_1.11

Crossref Full Text | Google Scholar

70. Yu H-J, Park C-H, Shin K, Woo H-Y, Park H, Sung E, et al. Cutoff values for glycated albumin, 1,5-anhydroglucitol, and fructosamine as alternative markers for hyperglycemia. J Clin Lab Anal. (2024) 38:e25097. doi: 10.1002/jcla.25097

PubMed Abstract | Crossref Full Text | Google Scholar

71. Paroni R, Ceriotti F, Galanello R, Battista Leoni G, Panico A, Scurati E, et al. Performance characteristics and clinical utility of an enzymatic method for the measurement of glycated albumin in plasma. Clin Biochem. (2007) 40:1398–405. doi: 10.1016/j.clinbiochem.2007.08.001

PubMed Abstract | Crossref Full Text | Google Scholar

72. Abdul-Ghani MA, Jenkinson CP, Richardson DK, Tripathy D, and DeFronzo RA. Insulin secretion and action in subjects with impaired fasting glucose and impaired glucose tolerance: results from the Veterans Administration Genetic Epidemiology Study. Diabetes. (2006) 55:1430–5. doi: 10.2337/db05-1200

PubMed Abstract | Crossref Full Text | Google Scholar

73. Kanauchi M, Kimura K, Kanauchi K, and Saito Y. Beta-cell function and insulin sensitivity contribute to the shape of plasma glucose curve during an oral glucose tolerance test in non-diabetic individuals. Int J Clin Pract. (2005) 59:427–32. doi: 10.1111/j.1368-5031.2005.00422.x

PubMed Abstract | Crossref Full Text | Google Scholar

74. Zhou W, Gu Y, Li H, and Luo M. Assessing 1-h plasma glucose and shape of the glucose curve during oral glucose tolerance test. Eur J Endocrinol. (2006) 155:191–7. doi: 10.1530/eje.1.02188

PubMed Abstract | Crossref Full Text | Google Scholar

75. Bellia C, Zaninotto M, Cosma C, Agnello L, Bivona G, Marinova M, et al. Clinical usefulness of glycated albumin in the diagnosis of diabetes: results from an Italian study. Clin Biochem. (2018) 54:68–72. doi: 10.1016/j.clinbiochem.2018.02.017

PubMed Abstract | Crossref Full Text | Google Scholar

76. Hwang Y-C, Jung CH, Ahn H-Y, Jeon WS, Jin S-M, Woo J-T, et al. Optimal glycated albumin cutoff value to diagnose diabetes in Korean adults: a retrospective study based on the oral glucose tolerance test. Clinica chimica Acta. (2014) 437:1–5. doi: 10.1016/j.cca.2014.06.027

PubMed Abstract | Crossref Full Text | Google Scholar

77. Ma XJ, Pan JM, Bao YQ, Zhou J, Tang JL, Li Q, et al. Combined assessment of glycated albumin and fasting plasma glucose improves the detection of diabetes in Chinese subjects. Clin Exp Pharmacol Physiol. (2010) 37:974–9. doi: 10.1111/j.1440-1681.2010.05417.x

PubMed Abstract | Crossref Full Text | Google Scholar

78. Nathan DM, Steffes MW, Sun W, Rynders GP, and Lachin JM. Determining stability of stored samples retrospectively: the validation of glycated albumin. Clin Chem. (2011) 57:286–90. doi: 10.1373/clinchem.2010.150250

PubMed Abstract | Crossref Full Text | Google Scholar

Keywords: biomarkers/blood, diabetes mellitus/diagnosis, glycated albumin, hyperglycaemia/diagnosis, ROC curve

Citation: Bahijri S, Sabban A, Enani S, Alqahtani MS, Malibary M, Alhashmi M and Tuomileto J (2026) Associations between glycated albumin and current measures of glycaemic control in Saudi adults. Front. Endocrinol. 16:1731945. doi: 10.3389/fendo.2025.1731945

Received: 04 November 2025; Accepted: 29 December 2025; Revised: 22 December 2025;
Published: 19 January 2026.

Edited by:

Simone L. Cree, University of Otago, New Zealand

Reviewed by:

Junjun Liu, Shandong First Medical University, China
Olatunde Olayanju, Babcock University, Nigeria

Copyright © 2026 Bahijri, Sabban, Enani, Alqahtani, Malibary, Alhashmi and Tuomileto. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Manal Malibary, bWFtYWxpYmFyeUBrYXUuZWR1LnNh

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