The prediabetic stages of fasting glycaemia (i-IFG), isolated glucose tolerance (i-IGT), or mixed IFG/IGT are reached when blood sugar levels rise. Improved knowledge of the pathophysiology and aetiology of prediabetic conditions may serve as a foundation for the creation of personalised prevention/treatment plans for type 2 diabetes (Philips, 2012).
Glucose screening test is the first requirement for the measurement of blood glucose level. The glucose level measurement in the blood is the initial measure for the screening of prediabetic and diabetic conditions. Internationally accepted cut points for identifying intermediate Hyper glycemia (prediabetes) using fasting plasma glucose (FPG), 2-hour post-load glucose (2-h PG), and/or HbA1c have been a topic of discussion in recent years. To characterise Dysglycemic situations during the OGTT, the 2-h PG has nevertheless been the subject of a continuous global consensus. (Jagannathan et al., 2020).
A standard dose of glucose is consumed orally during the most popular test variant, the oral glucose tolerance test (OGTT), and blood levels are assessed two hours later. With varied standard doses of glucose, additional administration methods, variable sample intervals, and different chemicals monitored in addition to blood glucose, numerous GTT versions have been developed over time for diverse objectives (Philips, 2012).
Two abnormalities that distinguish the transition between normal glucose tolerance to type 2 diabetes are insulin resistance and an insulin secretory insufficiency brought on by beta cell malfunction. Insulin resistance manifests as decreased tissue sensitivity to insulin and significant compensatory hyperinsulinemia. The initial range of plasma glucose levels is maintained. The beta cell secretory capacity decreases in persons who will later acquire diabetes. A rise in postprandial glucose levels brought on by decreased first-phase insulin production is the first anomaly of glucose found. As beta cell activity declines over time, the fasting glucose levels increase. A further decrease in insulin production eventually leads to diabetes (Brunton, 2016).
Owing to the role of glucose tolerance test in the screening of the diabetic conditions, the present report aim to provide an overview on how blood glucose level is regulated in the blood.
From the result of the glucose tolerance test conducted for patient’s blood sample, it is evident that there is no variation in the blood glucose level for control (water) group with the increase in time (from 0 minutes-120 minutes). However, variation in the blood glucose level was observed in the treated (glucose) group with increase in time (from 0 minutes-120 minutes). From figure 1, it is observed that after 30 minutes, the blood glucose level increased from 5 mmol/L to 8.9 mmol/L. This value further reduced to 7 mmol/L after 60 minutes. The drastic increase in the value indicates the presence of diabetes condition in the patient.
Table 1: Blood Glucose reading after completion of the Glucose Tolerance Test
Time |
Water (Blue) |
Glucose (Red) |
0 minutes |
5.5 |
5.5 |
30 minutes |
5.4 |
8.9 |
60 minutes |
5.0 |
7.0 |
90 minutes |
5.0 |
6.5 |
120 minutes |
4.9 |
6.4 |
It has long been difficult to accurately quantify glycemia with valid and practical tools for screening and early detection. There are many reasons to conduct the OGTT (Table 1). The OGTT has changed significantly over the past century, including the amount of glucose solution used for the tests, the use of plasma glucose instead of whole blood, the timing of sample collection (from to 120 minutes), the number of samples needed for diagnosis, and the criteria and terminology for diagnosing dysglycemia. For more than a century, the primary method for diagnosing T2DM has been plasma glucose concentrations, evaluated either after an overnight fast or glucose loading.
The appropriate glucose load for the OGTT was suggested by the American Diabetes Association (ADA) based on estimation of body surface area.9 The World Health Organisation (WHO), however, advocated global standardisation of the OGTT with a 75-g glucose load in 1980, and this recommendation is still in use today. The US National Diabetes Data Group (NDDG) and the WHO have both endorsed a protocol for the diagnosis of diabetes (FPG 7.8 mmol/L and 2-h PG 11.1 mmol/L), which was prompted by data from cross-sectional studies that showed a strong linear association between FPG and 2-h PG values with diabetic retinopathy. These cut-points were obtained from epidemiological studies that looked at retinopathy across a range of glucose levels and were cross-sectional in nature (Faerch et al., 2009).
These thresholds were designed to simplify the diagnostic process (FPG versus OGTT) and to represent the difference between the 2-h PG and FPG (since many patients may have a 2-h PG 11.1 mmol/L and/or an FPG 7.8 mmol/L).12 The WHO therefore changed the 2-hour PG threshold for diagnosing T2DM while maintaining the FPG cut-off point of 7.0 mmol/L. In 2009, the ADA13 and the WHO both approved the use of glycated haemoglobin (HbA1c) for the diagnosis of diabetes. According to Bogdanet et al. (2020), glucose levels frequently increase to the prediabetic phases of isolated impaired fasting glycemia (i-IFG), isolated impaired glucose tolerance (i-IGT), or combined glucose intolerance (IFG+IGT).
Therefore, it is concluded that switching from current screening methods to earlier diagnosis of diabetic individuals offers the potential possibilities to further decrease the progression to diabetes, the development of microvascular complications, and death from the disease, thus contributing advantages above and beyond those already shown in international diabetes prevention programmes. The FPG, 2-h PG, and HbA1c are three contemporary diagnostic techniques that have limitations in their ability to detect high-risk people. The result that 1-h PG>8.6 mmol/L seems to be a superior option for detecting high-risk patients at the point when pancreatic ß-cell function is significantly more robust is supported by epidemiologic data that is consistent across a number of populations.
Bogdanet, D., O’Shea, P., Lyons, C., Shafat, A. and Dunne, F., 2020. The oral glucose tolerance test—Is it time for a change?—A literature review with an emphasis on pregnancy. Journal of clinical medicine , 9 (11), p.3451.
Brunton, S., 2016. Pathophysiology of type 2 diabetes: the evolution of our understanding. J Fam Pract , 65 (4 Suppl), p.supp_az_0416.
Faerch, K., Borch-Johnsen, K., Holst, J.J. and Vaag, A., 2009. Pathophysiology and aetiology of impaired fasting glycaemia and impaired glucose tolerance: does it matter for prevention and treatment of type 2 diabetes?. Diabetologia , 52 , pp.1714-1723.
Jagannathan, R., Neves, J.S., Dorcely, B., Chung, S.T., Tamura, K., Rhee, M. and Bergman, M., 2020. The oral glucose tolerance test: 100 years later. Diabetes, Metabolic Syndrome and Obesity , pp.3787-3805.
Phillips, P.J., 2012. Oral glucose tolerance testing. Australian Family Physician, 41 (6), pp.391-393.
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