Arim Choi; Kyung-Soo Kim

doi:10.4093/dmj.2024.0515

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Editorial The Importance of Treating Hyperglycemia in β-Cell Dysfunction of Type 2 Diabetes Mellitus: Arim Choi, Kyung-Soo Kim; Diabetes & Metabolism Journal 2024;48(6):1056-1057.
DOI: https://doi.org/10.4093/dmj.2024.0515
Published online: November 1, 2024

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Department of Internal Medicine, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam, Korea

Corresponding author: Kyung-Soo Kim

Department of Internal Medicine, CHA Bundang Medical Center, CHA University School of Medicine, 59 Yatap-ro, Bundang-gu, Seongnam 13496, Korea E-mail: kks982@hanmail.net

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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The pathogenesis of type 2 diabetes mellitus (T2DM) has been studied for a long time. It is well established that T2DM is characterized by insulin resistance and a progressive decline in pancreatic β-cell function [1]. A prospective cohort study of 4,106 Korean people with normal glucose tolerance followed for 10 years showed that decreased β-cell function, which might be determined partly by genetic factors, and impaired β-cell compensation for progressive decline in insulin sensitivity are crucial factors in the deterioration of glucose tolerance [2]. Furthermore, interaction of a subject’s genetic makeup and their environment, the increasing prevalence of obesity, and insulin resistance and consequent increased islet amyloid polypeptide and specific types of antidiabetic agents are known to affect β-cell functions [3]. However, it is important that each individual’s β-cell function is not fixed but can continuously change.

Kim et al. [4] examined the progressive decline in β-cell function in a cohort of patients with T2DM and compared the relative importance of factors affecting insulin secretion and pancreatic β-cell function. In this study, β-cell function declined steadily over time; however, large differences in β-cell function between individuals have been reported. The β-cell function is flexible depending on the glycemic status at the time of measurement; the amount of accumulated glycosylated hemoglobin (HbA1c), variability in HbA1c levels, and type of treatment were not significantly associated with β-cell function. This study suggested that recent glycemia is a major determinant of β-cell function with a greater impact than other clinical factors, including duration of diabetes or types of antidiabetic agents in patients with T2DM.

The β-cell function and β-cell mass are associated with β-cell dysfunction and seem to be correlated with each other [5]. However, since the endogenous β-cell regenerative capacity of humans may be limited [6], preserving β-cell function is important. The β-cell function started to decline with higher plasma glucose levels, even within the range of normal plasma glucose levels, which suggested that β-cell function is already impaired prior to the development of impaired glucose tolerance (IGT) [7]. DeFronzo et al. [7] have shown that β-cell function is decreased by 80% in patients with IGT and is even lower in patients with T2DM. In the UK Prospective Diabetes Study and A Diabetes Outcome Progression Trial, treatment failure was associated with a progressive decline in β-cell function [8,9]. Thus, poor β-cell function is associated with poor glycemic control and treatment failure, indicating the important role of β-cell function in the treatment of T2DM.

Many attempts have been made to maintain β-cell function. Lifestyle modification appears to have some preservative properties on β-cell function [10]. Early intensive insulin treatment in patients with newly recognized T2DM may be effective in retarding the progressive dysfunction of β-cells [11]. Several antidiabetic agents including glucagon-like peptide-1 agonists, dipeptidyl-peptidase-4 inhibitors, and thiazolidinediones result in maintenance and often improvement of β-cell function [12]. However, no uniformly effective therapy for β-cell preservation has been found. It is especially important that the β-cell function in an individual is not fixed but constantly changes depending on the recent glycemic status. As shown in the results of Kim et al. [4], regardless of duration of diabetes or type of antidiabetic agents, recent glycemic status was most highly related to β-cell function, indicating the importance of as close as possible euglycemic control to improve β-cell function.

As patients with T2DM are increasing worldwide and the average life expectancy is also increasing, it is important to preserve beta cell function for those with T2DM to live a long and healthy life. It will be also important in reducing the pandemic burden of T2DM as a society. Appropriate glycemic control in patients with T2DM not only prevents various comorbidities and complications, but also helps preserve beta cell function, so we should make efforts to provide good glycemic control to all patients.

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No potential conflict of interest relevant to this article was reported.

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The Importance of Treating Hyperglycemia in β-Cell Dysfunction of Type 2 Diabetes Mellitus

Diabetes Metab J. 2024;48(6):1056-1057. Published online November 1, 2024

DOI: https://doi.org/10.4093/dmj.2024.0515

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The Importance of Treating Hyperglycemia in β-Cell Dysfunction of Type 2 Diabetes Mellitus

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Choi A, Kim KS. The Importance of Treating Hyperglycemia in β-Cell Dysfunction of Type 2 Diabetes Mellitus. Diabetes Metab J. 2024;48(6):1056-1057.

DOI: https://doi.org/10.4093/dmj.2024.0515.

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