该研究的目的是系统地探讨各种脂肪因子与子宫内膜非典型增生(EAH)风险之间的关系。I型子宫内膜癌(EC),和II型EC。我们在这项研究中招募了219名患者,包括39EAH,87I型EC,38个II型EC和55个对照个体。我们随后探讨了脂肪因子水平和瘦素与脂联素(L/A)比率与EAH的关系,I型EC,和II型EC。EAH组的血浆瘦素水平和L/A比值明显高于对照组(p=0.012)。瘦素,抵抗素,vaspin,I型EC组的内脂素水平明显更高;然而,I型EC的脂联素水平较低,这导致较高的L/A比。值得注意的是,II型EC组的L/A比值和内脂素水平显著升高.多因素logistic回归分析显示,较高的瘦素水平与较高的EAH风险显著相关(p=0.012)。较高的瘦素水平(p=0.042)和L/A比(p=0.027)与I型EC风险增加显着相关。相比之下,较高的瘦素(p=0.059)和内脂素(p=0.003)水平,较高的L/A比(p=0.033),较低的脂联素水平(p=0.042)与II型EC风险增加相关.我们认为脂肪因子可能与EAH和EC风险相关。
关于这个主题已经知道什么?EAH和EC被认为与肥胖和相关的胰岛素抵抗显著相关。研究报道,一些脂肪因子介导肥胖相关的EC风险。这项研究的结果补充了什么?我们系统地探索了从脂肪组织产生的脂肪因子,包括瘦素,脂联素,抵抗素,vaspin,内脂素和L/A比值与EAH增加有关,I型EC,和II型EC风险;它们是否为EAH和EC的独立风险因素。此外,我们分析了这些脂肪因子在EC肿瘤发生和发展中的潜在作用。这些发现对临床实践和/或进一步研究有什么意义?本研究旨在系统地探索各种脂肪因子与EAH风险之间的关系,I型EC,和II型EC,表明脂肪因子水平与EAH和EC风险相关,并分析脂肪因子与子宫内膜癌变的潜在分子机制。这有助于提高我们对EC肿瘤发生和发展的认识。
The aim of the study was to systematically explore the relationships between various adipokines and risks of endometrial atypical hyperplasia (EAH), type I endometrial cancer (EC), and type II EC. We enrolled 219 patients in this study, including 39 EAH, 87 type I EC, 38 type II EC and 55 control individuals. We subsequently explored the association of adipokine levels and the leptin-to-adiponectin (L/A) ratio with EAH, type I EC, and type II EC. The plasma leptin level and L/A ratio were significantly higher in the EAH group than in the control group (p = 0.012). Leptin, resistin, vaspin, and visfatin levels were significantly higher in the type I EC group; however, the adiponectin level was lower in the type I EC, which resulted in a higher L/A ratio. Notably, the L/A ratio and visfatin level in the type II EC group were significantly higher. Multiple logistic regression analysis revealed that a higher leptin level was significantly associated with a higher EAH risk (p = 0.012). Higher leptin level (p = 0.042) and L/A ratio (p = 0.027) were significantly associated with an increased type I EC risk. By contrast, higher leptin (p = 0.059) and visfatin (p = 0.003) levels, higher L/A ratio (p = 0.033), and lower adiponectin level (p = 0.042) were associated with an increased type II EC risk. We suggested that adipokines are potentially correlated with EAH and EC risks.
What is already known on this subject? EAH and EC are considered significantly correlated with obesity and the related insulin resistance. Studies reported that some of the adipokines mediate obesity-related EC risk.What do the results of this study add? We systematically explored whether the adipokines produced from adipose tissue, including leptin, adiponectin, resistin, vaspin, and visfatin as well as the L/A ratio were associated with increased EAH, type I EC, and type II EC risks; whether they are independent risk factors for EAH and EC. Moreover, we analysed the underlying roles of these adipokines in EC tumorigenesis and development.What are the implications of these findings for clinical practice and/or further research? This study aimed to systematically explore the relationships between various adipokines and risks of EAH, type I EC, and type II EC, to suggest that adipokine levels correlated with EAH and EC risks, and to analyse the underlying molecular mechanisms linking adipokines with endometrial carcinogenesis. It is helpful to improve our understanding of EC tumorigenesis and development.