Kaya, AysemOnat, AltanYuksel, HusniyeCan, GunayYuksel, MuratAdemoglu, Evin2024-04-242024-04-2420170032-54811941-9260https://doi.org/10.1080/00325481.2017.1342508https://hdl.handle.net/11468/16654Objectives: Some evidence suggests that serum lipoprotein[Lp](a) may be inversely linked to type-2 diabetes. We aimed to determine in nondiabetic people the relationship of serum [Lp](a) with insulin resistance and new-onset diabetes (NOD). Materials and methods: Population-based middle-aged adults (n = 1685) were categorized by fasting glucose and stratified to gender, having excluded prevalent diabetic subjects. NOD (n = 90) occurred over a median 5 years' follow-up. Results: Subjects that subsequently developed NOD, derived both from the normoglycemia and impaired fasting glucose (IFG) groups,were distinguished, among others, primarily by significantly elevated serum gamma glutamyltransferase, reduced Lp(a) (by 31%) and, compared to IFG, by low total cholesterol levels. Partial correlation of Lp(a) with homeostatic model assessment (HOMA) was inverse in normoglycemic men; such correlation, neutral in normoglycemic women, proved inverse in IFG (r = -0.17). Circulating Lp(a) in individuals with paired measures increased significantly (1.55-fold) in the period from baseline up to NOD. Multivariable-adjusted logistic regression analysis for NOD in combined sexes indicated independent and additive prediction by serum Lp(a), albeit inverse in direction (RR 0.84, [95%CI 0.72; 0.97]). Conclusion: Lp(a) is significantly reduced in the period preceding NOD and is inversely associated with HOMA index, observations consistent with underlying autoimmune activation.eninfo:eu-repo/semantics/closedAccessAutoimmune ActivationDiabetesType-2Impaired Fasting GlucoseInsulin ResistanceLipoprotein(A)Article1296611618WOS:0004067647000082-s2.0-850210754612863358510.1080/00325481.2017.1342508Q1Q2