Over the previous few decades, despite the concomitant rise in obesity and TC incidence, few studies focusing on the connection between lipid levels and PTC[8]. Here, for the first time, a cross-sectional study was conducted. Data demonstrated that elevated TG and declined HDL-C were linked to increased PTC risk among Chinese of both sexes. Multivariate analysis also demonstrated that FBG, TG, and HDL-C were risk factors for PTC both in males and females.
TG is one of the significant components of body fat. According to recent studies, TG is a potential risk factor for prostate cancer [13] and ovarian cancer [14]. The results of this study suggested that patients with PTC had significantly higher TG levels than controls (P < 0.05) in each age and gender group. In addition, TG was shown as a risk factor for PTC both in male and female groups. Meanwhile, higher levels of TG in PTC patients indicated a deficiency of immunity and tumor proliferation [15–16]. Previous experimental studies using in vivo and in vitro models revealed that TG might cause prostate cancer by altering signaling pathways that support carcinogenic processes, including cell growth and proliferation, oxidative stress, inflammation, and cell migration [17–18]. Zhao et al. investigated the effects of palmitic acid stimulation on thyroid cell function using in vitro tests. Thyroglobulin, sodium iodide transporter, and thyroid peroxidase have lower mRNA and protein levels when palmitic acid, the most prevalent form of palmitic acid, is stimulated. This might be due to the damage to the synthesis of thyroid hormones [19]. However, the underlying mechanisms of how TG mediated progress in PTC still need further illustration.
By encouraging cell migration, proliferation, and invasion, TCH contributes significantly to cancer development [20]. The TCH level was significantly lower in female PTC patients of the youth group (P < 0.05). Another retrospective study of TC patients supported this data and showed lower serum cholesterol levels in TC patients, especially in PTC and FTC patients [21]. Lower TCH in malignancies may be due to the increased need for cholesterol by tumor cells, which is similar to what has been observed in the acute phase responses of various acute and chronic diseases [22]. Lipid dysregulation in cancer may be a response in the acute phase brought on by the transmission of cytokines by inflammation-related cells surrounding tumor cells or by the tumor cells themselves [23].
Interestingly, the results of this study showed that HDL-C could operate as a preventative measure for PTC. In contrast with the controls, patients with PTC had declined HDL-C levels (P < 0.05) in all age and gender groups. HDL-C was shown as an independent PTC biomarker in both male and female groups. A recent study showed that MHR (monocyte / HDL-C) was higher in subjects with PTC, which is an independent PTC risk factor [24]. According to a German primary care provider database with over 60,000 additional patients, lower HDL cholesterol levels positively correlate with cancer [25]. Sterols and lipids have an excellent affinity for cancer cells, and lipid metabolism has been identified to be essential for cancer signaling [26–27]. It was hypothesized that HDL has immunomodulatory, anti-oxidative, anti-apoptotic, and anti-inflammatory properties that may impact the proliferative and inflammatory pathways involved in cancer development [28]. However, two recent studies revealed that subjects with metabolic disease had a greater risk of TC when their HDL-C levels were lower [29–30]. Decreased HDL-C is often accompanied by insulin resistance and diabetes [31]. Although insulin resistance has been identified as a potential contributing factor, the exact mechanism behind the link between HDL-C and TC is yet unknown.
LDL-C is a complex particle made up of a variety of proteins and lipids. The LDL receptor is crucial in endocrine-related tumor cells by improving circulating LDL-C uptake and controlling tumorigenic signaling [32]. Regarding serum cholesterol, only restricted studies have focused on the relationship between LDL-C and TC risk. A retrospective study revealed lower LDL-C levels in a large cohort of female TC patients and women with metastases in the PTC group [33]. However, this study found no noticeable difference in LDL-C between PTC patients and controls in all age groups.
Glucose is the primary source of energy for cells [34]. Numerous studies have linked hyperglycemia to an enhanced risk of developing cancer [35–36]. According to current knowledge, hyperglycemia has a role in the development and spread of tumors via transcription regulators, kinases, growth factors, proteases, oxidoreductases, receptors, developmental proteins, cytokines, and other molecules [37]. In this study, in contrast with the control group, patients with PTC held higher FBG levels (P < 0.05), and an increased OR of PTC was associated with FBG both in the univariate and multivariate analysis (P < 0.001). It has been reported that hyperglycemia induces an increase in intranuclear nuclear factor (NF)-κB, whose ability to regulate proliferative and anti-apoptotic signaling pathways in thyroid neoplastic cells has been found to play a significant role in TC [38].
The high number of participants is the strength of this study. Retrospective big data analysis revealed the correlation between serum lipid and PTC, providing evidence for clinical diagnosis and healthcare. The current study still had several restrictions. First, the study’s single-center retrospective case-control design made it unable to demonstrate whether the link between lipid and PTC is causal or time-dependent. Second, only the first serum lipid levels after admission were collected since they were obtained before surgery and had the fewest influencing factors. However, they cannot represent the daily condition of the patients. Finally, because only Chinese PTC patients were studied, it is difficult to extrapolate these results to other populations.