As shown in the previous studies, hypothyroidism (HT) is identified to be closely associated with the elevated plasma levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), triglyceride (TG), and with the decreased plasma levels of high density lipoprotein cholesterol (HDL-C). On the other hand, the thyroid hormone (TH), which has been considered as a vital hormone produced and released by the thyroid gland, are well-established to regulate the metabolism of plasma TC; whereas other evidence proposed that the thyroid-stimulating hormone (TSH) also regulated the plasma cholesterol metabolism independently of the TH, which further promotes the progression of hyperlipidemia. Nevertheless, the potential mechanism is still not illustrated. It is worth noting that several studies has found that the progression of HT-induced hyperlipidemia might be associated with the down-regulated plasma levels of TH and the up-regulated plasma levels of TSH, revealing that HT could promote hyperlipidemia and its related cardio-metabolic disorders. Otherwise, multiple novel identified plasma proteins, such as proprotein convertase subtilisin/kexin type 9 (PCSK9), angiopoietin-like protein (ANGPTLs), and fibroblast growth factors (FGFs), have also been demonstrated to embrace a vital function in modulating the progression of hyperlipidemia induced by HT. In the present comprehensive review, the recent findings which elucidated the association of HT and the progression of hyperlipidemia were summarized. Furthermore, other results which illustrated the underlying mechanisms by which HT facilitates the progression of hyperlipidemia and its cardio-metabolic disorders are also listed in the current review.
Read full abstract