The influence of subclinical hypothyroidism on serum lipid profile, PCSK9 levels and CD36 expression on monocytes

Abstract

BackgroundProprotein convertase subtilisin/kexin type 9 (PCSK9) is a serine protease and a secreted protein which increases cholesterol levels in plasma via inducing degradation of low-density lipoprotein receptor (LDLR). Cluster of differentiation 36 (CD36) is a member of a family of cell surface proteins in many cells. CD36 is known as fatty acid translocase (FAT) because it imports fatty acids inside cells and participate in triglyceride storage. It has been suggested that PCSK9 regulates CD36 in some tissues. MethodsData and serum levels of TSH, FT4, lipid profile and PCSK9 and the expression of CD36 on monocytes from 40 new untreated patients with subclinical hypothyroidism (SH) and 40 age- sex- and BMI-matched euthyroid controls were analyzed in a cross-sectional study. Then the relationships between these parameters were examined. ResultsPatients with SH had higher TSH, FT4, total cholesterol (TC) and triglyceride (TG) Low-density lipoprotein (LDL) and PCSK9 levels than controls. There were significant and positive correlations between serum TSH levels and lipid parameters except HDL-C. PCSK9 had a significant and negative correlation with FT4. No significant correlation could be found in relation to PCSK9 and CD36. ConclusionsPCSK9 inhibitors are used to reduce blood cholesterol levels as drugs. If it will be proven that PCSK9 can induce CD36 degradation, taking these drugs may have unwanted side effects. This study showed that serum PCSK9 and lipid profile levels increase in patients with subclinical hypothyroidism and there is no relationship between PCSK9 and CD36 in these patients.