L.A.M. Konings ¹ ², W.W. Xu ³, V.D. de Jong ³ ⁴, M. Alings⁴ ⁵, D.E. Grobbee³ ⁴, R.P. Peeters ², M. Castro Cabezas ¹ ² ⁴
1. Franciscus Gasthuis & Vlietland, Rotterdam, the Netherlands
2. Erasmus MC Medical Center, Rotterdam, the Netherlands
3. Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands
4. Julius Clinical, Zeist, The Netherlands
5. Department of Cardiology, Amphia Hospital, Breda, the Netherlands
Background and aims: Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by liver steatosis and a cardiometabolic condition. Liver fibrosis is a risk factor for cardiovascular disease. Atherogenic dyslipidemia is typical for both MASLD and T2DM. Whether the presence of MASLD exacerbates dyslipidemia in T2DM is not known. The aim of this study was to investigate lipid patterns in T2DM in relation to liver steatosis and fibrosis reflecting different stages of MASLD.
Methods: 428 T2DM patients who did not use lipid lowering medication were included. Liver steatosis (LS) was estimated with HSI and liver fibrosis (LF) with FIB-4. The cohort was divided into groups of LS and LF.
Results: The mean age was 61±10 (x ±SD) years; 29% was female, BMI was 28.4±5.7 kg/m², 75% had LS and 29% LF. Patients with LS had increased BMI, waist circumference and HOMA-IR compared to those without LS. Patients with LS also had lower HDL-C and higher triglycerides.
Patients with LF were older than those without LF. There was no difference in BMI, waist circumference or HOMA-IR with respect to LF estimations. Patients with LF had significantly lower LDL-C, apoB, total cholesterol and triglycerides than those without LF.
Conclusion: Paradoxically, patients with LS have a more atherogenic dyslipidemia as opposed to patients with LF. This may be explained by a more pronounced insulin resistance associated with LS. Liver fibrosis may lead to less VLDL synthesis resulting in an apparently better lipid profile than in the steatotic, non-fibrotic situation. The increased cardiovascular risk seen in LF cannot be explained by the lipid profile.