<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>135(21)</volume><submitter>Tang X</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Abnormal 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.&lt;h4>Methods&lt;/h4>A 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.&lt;h4>Results&lt;/h4>High 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 &lt;0.001) in T1DM and is associated with an elevated risk of high TG and low HDL-C (all P for trend &lt;0.01) in T2DM. Low BCF was not associated with risks of dyslipidemia in patients with T1DM or T2DM after adjustment for potential confounders.&lt;h4>Conclusion&lt;/h4>High 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.</pubmed_abstract><journal>Chinese medical journal</journal><pagination>2554-2562</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9944004</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Associations of insulin resistance and beta-cell function with abnormal lipid profile in newly diagnosed diabetes.</pubmed_title><pmcid>PMC9944004</pmcid><pubmed_authors>Yang X</pubmed_authors><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Huang G</pubmed_authors><pubmed_authors>Jiang H</pubmed_authors><pubmed_authors>Yan X</pubmed_authors><pubmed_authors>Zhou H</pubmed_authors><pubmed_authors>Su H</pubmed_authors><pubmed_authors>Niu X</pubmed_authors><pubmed_authors>Tang X</pubmed_authors><pubmed_authors>Zhou Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>Associations of insulin resistance and beta-cell function with abnormal lipid profile in newly diagnosed diabetes.</name><description>&lt;h4>Background&lt;/h4>Abnormal 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.&lt;h4>Methods&lt;/h4>A 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.&lt;h4>Results&lt;/h4>High 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 &lt;0.001) in T1DM and is associated with an elevated risk of high TG and low HDL-C (all P for trend &lt;0.01) in T2DM. Low BCF was not associated with risks of dyslipidemia in patients with T1DM or T2DM after adjustment for potential confounders.&lt;h4>Conclusion&lt;/h4>High 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.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Nov</publication><modification>2025-04-04T12:44:35.101Z</modification><creation>2025-04-04T12:44:35.101Z</creation></dates><accession>S-EPMC9944004</accession><cross_references><pubmed>35245924</pubmed><doi>10.1097/CM9.0000000000002075</doi></cross_references></HashMap>