Endocrine Abstracts

Background: Glycated albumin (GA) and glycated haemoglobin (HbA1c) measurements have been used to track the long-term glycemic management of diabetic patients. Other than glycemia, there are known influences on both glycated proteins. In obese, non-diabetic children, GA levels have been found to be low, while in adult diabetic patients, GA levels have been found to be adversely correlated with body mass index (BMI). The causes of the link between obesity and GA are still unknown, though.

Objectives: This research aimed to see if GA and HbA1c were independently correlated with BMI and the inflammation-related inflammatory marker plasma high-sensitivity C-reactive protein (hs-CRP), which is related to obesity.

Material and Methods: This study included 215 non-diabetic participants, of which 150 had normal glucose tolerance and 65 had impaired glucose tolerance. Age, BMI, 2-hour glucose, fasting plasma glucose (FPG), oral glucose tolerance test (OGTT), and hs-CRP impacts on HbA1c and GA were examined. Unpaired Student’s t tests or Fisher’s exact tests, if applicable, were utilised in statistical analyses to compare two groups. With the help of the StatView software, stepwise multivariate regression analysis as well as univariate regression analysis were carried out to examine the impact of explanatory variables on HbA1c, GA, and the GA to HbA1c ratio (for correction). The F-value for the variables’ inclusion in the stepwise multiple regression analysis was set at 2.0, and a P value of less than 0.04 was regarded as statistically significant.

Results: Significant correlations were found between FPG and HbA1c as well as between GA and FPG. While BMI and HbA1c exhibited a substantial positive connection, GA and BMI showed a negative correlation. Plasma hs-CRP was inversely correlated with GA while weakly positively correlated with HbA1c. BMI and hs-CRP were found to be negatively linked with GA but not with HbA1c by stepwise multivariate regression analysis.

Conclusion: This research indicate that in nondiabetic patients, BMI and hs-CRP were independent unfavorable hazards for GA but not for HbA1c. Lower blood GA levels in proportion to glycemia are caused by obesity and the associated chronic inflammation, but not by HbA1c levels.