Contributions of Hepatic Insulin Resistance and Islet β-Cell Dysfunction to the Blood Glucose Spectrum in Newly Diagnosed Type 2 Diabetes Mellitus

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 new...

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Main Authors: Mengge Yang, Ying Wei, Jia Liu, Ying Wang, Guang Wang
Format: Article
Language:English
Published: Korean Diabetes Association 2025-07-01
Series:Diabetes & Metabolism Journal
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Online Access:http://e-dmj.org/upload/pdf/dmj-2024-0537.pdf
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author Mengge Yang
Ying Wei
Jia Liu
Ying Wang
Guang Wang
author_facet Mengge Yang
Ying Wei
Jia Liu
Ying Wang
Guang Wang
author_sort Mengge Yang
collection DOAJ
description 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 post-load 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.
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publishDate 2025-07-01
publisher Korean Diabetes Association
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series Diabetes & Metabolism Journal
spelling doaj-art-44d19e2d35ef4ad2b2dce7d3574d8d662025-07-13T23:39:37ZengKorean Diabetes AssociationDiabetes & Metabolism Journal2233-60792233-60872025-07-0149488389210.4093/dmj.2024.05372919Contributions of Hepatic Insulin Resistance and Islet β-Cell Dysfunction to the Blood Glucose Spectrum in Newly Diagnosed Type 2 Diabetes MellitusMengge Yang0Ying Wei1Jia Liu2Ying Wang3Guang Wang4 Department of Endocrinology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China Department of Endocrinology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China Department of Endocrinology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China Health Management Center, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China Department of Endocrinology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, ChinaBackground 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 post-load 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.http://e-dmj.org/upload/pdf/dmj-2024-0537.pdfdiabetes mellitus, type 2blood glucoseinsulin resistanceinsulin secretion
spellingShingle Mengge Yang
Ying Wei
Jia Liu
Ying Wang
Guang Wang
Contributions of Hepatic Insulin Resistance and Islet β-Cell Dysfunction to the Blood Glucose Spectrum in Newly Diagnosed Type 2 Diabetes Mellitus
Diabetes & Metabolism Journal
diabetes mellitus, type 2
blood glucose
insulin resistance
insulin secretion
title Contributions of Hepatic Insulin Resistance and Islet β-Cell Dysfunction to the Blood Glucose Spectrum in Newly Diagnosed Type 2 Diabetes Mellitus
title_full Contributions of Hepatic Insulin Resistance and Islet β-Cell Dysfunction to the Blood Glucose Spectrum in Newly Diagnosed Type 2 Diabetes Mellitus
title_fullStr Contributions of Hepatic Insulin Resistance and Islet β-Cell Dysfunction to the Blood Glucose Spectrum in Newly Diagnosed Type 2 Diabetes Mellitus
title_full_unstemmed Contributions of Hepatic Insulin Resistance and Islet β-Cell Dysfunction to the Blood Glucose Spectrum in Newly Diagnosed Type 2 Diabetes Mellitus
title_short Contributions of Hepatic Insulin Resistance and Islet β-Cell Dysfunction to the Blood Glucose Spectrum in Newly Diagnosed Type 2 Diabetes Mellitus
title_sort contributions of hepatic insulin resistance and islet β cell dysfunction to the blood glucose spectrum in newly diagnosed type 2 diabetes mellitus
topic diabetes mellitus, type 2
blood glucose
insulin resistance
insulin secretion
url http://e-dmj.org/upload/pdf/dmj-2024-0537.pdf
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