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Chinese medical journal · Nov 2022
Associations of insulin resistance and beta-cell function with abnormal lipid profile in newly diagnosed diabetes.
- Xiaohan Tang, Xiang Yan, Houde Zhou, Gan Huang, Xiaohong Niu, Hongwei Jiang, Heng Su, Xilin Yang, Xia Li, and Zhiguang Zhou.
- Department of Metabolism and Endocrinology, National Clinical Research Center for Metabolic Diseases, Key Laboratory of Diabetes Immunology (Central South University), Ministry of Education, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, China.
- Chin. Med. J. 2022 Nov 5; 135 (21): 255425622554-2562.
BackgroundAbnormal lipids are strong predictors of cardiovascular disease in type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM). However, the potential associations of insulin resistance (IR) and beta-cell function (BCF) with abnormal lipids in newly diagnosed T1DM or T2DM patients are not fully understood.MethodsA cross-sectional survey of 15,928 participants was conducted. Homeostasis model assessment and postprandial C-peptide levels were used to estimate IR and BCF. A restricted cubic spline (RCS) nested in binary logistic regression was used to examine the associations of IR and BCF with abnormal lipids.ResultsHigh triglyceride (TG), low high-density lipoprotein cholesterol, and high low-density lipoprotein cholesterol (LDL-C) accounted for 49.7%, 47.8%, and 59.2% of the participants, respectively. In multivariable analysis, high IR was associated with an increased risk of high TGs ( P for trend <0.001) in T1DM and is associated with an elevated risk of high TG and low HDL-C (all P for trend <0.01) in T2DM. Low BCF was not associated with risks of dyslipidemia in patients with T1DM or T2DM after adjustment for potential confounders.ConclusionHigh IR had different associations with the risk of dyslipidemia in newly diagnosed T1DM and T2DM patients, suggesting that early treatment that improves IR may benefit abnormal lipid metabolism.Copyright © 2022 The Chinese Medical Association, produced by Wolters Kluwer, Inc. under the CC-BY-NC-ND license.
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