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Corrigendum
- Contributions of Hepatic Insulin Resistance and Islet β-Cell Dysfunction to the Blood Glucose Spectrum in Newly Diagnosed Type 2 Diabetes Mellitus
- Mengge Yang, Ying Wei, Jia Liu, Ying Wang, Guang Wang
- Diabetes Metab J. 2026;50(2):432-433. Published online February 5, 2026
- DOI: https://doi.org/10.4093/dmj.2024.0537.c1
- Corrects: Diabetes Metab J 2025;49(4):883
- 425 View
- 34 Download
Original Article
- Others
- Contributions of Hepatic Insulin Resistance and Islet β-Cell Dysfunction to the Blood Glucose Spectrum in Newly Diagnosed Type 2 Diabetes Mellitus
- Mengge Yang, Ying Wei, Jia Liu, Ying Wang, Guang Wang
- Diabetes Metab J. 2025;49(4):883-892. Published online February 13, 2025
- DOI: https://doi.org/10.4093/dmj.2024.0537
- Correction in: Diabetes Metab J 2026;50(2):432
- 7,379 View
- 288 Download
- 9 Web of Science
- 13 Crossref
-
Abstract
PDF
Supplementary Material
PubReader 
ePub - Background
Our previous studies have investigated the role of hepatic insulin resistance (hepatic IR) and islet β-cell function in the pathogenesis of diabetes. This study aimed to explore the contributions of hepatic IR and islet β-cell dysfunction to the blood glucose spectrum in patients with newly diagnosed type 2 diabetes mellitus.
Methods
Hepatic IR was assessed by the hepatic insulin resistance index (HIRI). Islet β-cell function was assessed by insulin secretion- sensitivity index-2 (ISSI2). The associations between blood glucose spectrum and hepatic IR and ISSI2 were analyzed.
Results
A total of 707 patients with new-onset diabetes were included. The fasting blood glucose (FBG) and 30 minutes postload blood glucose elevated with rising HIRI (both P for trend <0.001). The FBG, 30 minutes, 2 hours, and 3 hours post-load blood glucose elevated with decreasing ISSI2 quartiles (all P for trend <0.001). There was a negative correlation between ISSI2 and HIRI after adjusting blood glucose levels (r=–0.199, P<0.001).
Conclusion
Hepatic IR mainly contributed to FBG and early-phase postprandial plasma glucose, whereas β-cell dysfunction contributed to fasting and postprandial plasma glucose at each phase. -
Citations
Citations to this article as recorded by
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