Could SCGF-Beta Levels Be Associated with Inflammation Markers and Insulin Resistance in Male Patients Suffering from Obesity-Related NAFLD?

Could SCGF-Beta Levels Be Associated with Inflammation Markers and Insulin Resistance in Male Patients Suffering from Obesity-Related NAFLD?
复制标题

DOI:
10.3390/diagnostics10060395
复制
发表时间:
2020-06-01
期刊:
影响因子:
3.6
通讯作者:
Capone, Domenico
Capone, Domenico
中科院分区:
医学3区
文献类型:
--
作者:
Tarantino, Giovanni;Citro, Vincenzo;Capone, Domenico

文献摘要

被引文献

相似文献

肥胖的病理标志之一是脂肪组织的巨噬细胞浸润,其已被证实为多能成体干细胞的来源。干细胞生长因子-β(SCGF-β)与粒细胞巨噬细胞集落刺激因子(GM-CSF)和巨噬细胞集落刺激因子(M-CSF)组合显示对粒细胞/巨噬细胞祖细胞的活性。肥胖相关炎症诱导胰岛素抵抗(IR),这是非酒精性脂肪肝病(NAFLD)或肝性脂肪变性(HS)的核心。我们研究了肥胖HS患者SCGF-β水平与C反应蛋白(CRP)、白细胞介素-6(IL-6)、肿瘤坏死因子-β(TNF-β)、白细胞介素-12 p40(IL-12 p40)、白细胞介素-10(IL-10)、铁蛋白、GM-CSF和M-CSF水平之间的关系,以及SCGF-β浓度与IR之间的关系。对80例肥胖患者进行回顾性研究。血清细胞因子水平通过基于磁珠的多重免疫测定法进行评估。采用稳态模型评估法(HOMA)、HOMA-B %(HOMA-B%)、定量胰岛素敏感性检查指数(QUICKI)和单点胰岛素敏感性评估法(SPISE)评价IR。通过超声(US)评估HS和脾脏体积。仅在男性中,SCGF-β和IL-6水平预测HOMA值(分别为p= 0.032和0.041)。在男性患者中,CRP和IL-6水平(p= 0.007)预测SCGF-β浓度(分别为p= 0.03和0.007),进而预测US时的HS,p= 0.037。SCGF-β水平与IR和HS严重程度相关,CRP起中介作用。IL-10水平与SCGF-β浓度呈负相关(p= 0.033)。M-CSF水平可预测TNF-β和IL-12 p40的血清浓度(p= 0.00),但不能预测血清IL-10(p= 0.30)。通过SCGF-β水平预测HOMA值,可能由炎症标志物介导,是本研究的特征,揭示了肥胖相关NAFLD男性患者IR诱导/恶化的机制。
One of the pathologic hallmarks of obesity is macrophage infiltration of adipose tissue that has been confirmed as source of multipotent adult stem cells. Stem cell growth factor-beta (SCGF-beta) shows activity on granulocyte/macrophage progenitor cells in combination with granulocyte macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF). Obesity-associated inflammation induces insulin resistance (IR), which is central to nonalcoholic fatty liver disease (NAFLD) or hepatic steatosis (HS). We searched for relationship between levels of SCGF-beta and those of C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-beta (TNF-beta), interleukin-12p40 (IL-12p40), interleukin-10 (IL-10), ferritin, GM-CSF and M-CSF and between SCGF-beta concentrations and IR in obese patients with HS. Eighty obese patients were retrospectively studied. Serum cytokines levels were appreciated by magnetic bead-based multiplex immunoassays. IR was evaluated by homeostatic model assessment (HOMA), HOMA-derived beta-cell function (HOMA-B%), quantitative insulin sensitivity check Index (QUICKI) and single point insulin sensitivity estimator (SPISE). HS and spleen volume were assessed by ultrasonography (US). SCGF-beta and IL-6 levels predicted HOMA values (p= 0.032 and 0.041, respectively) only in males. In male patients, CRP and IL-6 levels (p= 0.007) predicted SCGF-beta concentrations (p= 0.03 and 0.007, respectively), which in turn predicted HS at US,p= 0.037. SCGF-beta levels were linked to IR and HS severity with the mediation role of CRP. IL-10 levels negatively predicted SCGF-beta concentrations (p= 0.033). M-CSF levels predicted serum concentration of both TNF-beta and IL-12p40 (p= 0.00), but did not predict serum IL-10 (p= 0.30). Prediction of HOMA values by SCGF-beta levels, likely mediated by markers of inflammation, characterizes this study, shedding some light on mechanisms inducing/worsening IR of male patients with obesity-related NAFLD.