Xiao Yang, Han Lina, Wang Han, Ke Helin, Xu Shaodan, Huang Zhibin, Lyu Guorong, Li Shilin
Department of Ultrasonography, Second Affiliated Hospital of Fujian Medical University, Quanzhou 362002, China.
Department of Medicine, Quanzhou Medical College, Quanzhou 362002, China.
ACS Omega. 2024 May 10;9(20):21829-21837. doi: 10.1021/acsomega.3c08874. eCollection 2024 May 21.
: despite evidence for mutually reinforcing effects of serum uric acid (SUA) and lipids, the effects of uric levels on pancreatic steatosis are not well-established. In this study, the relationship between low concentrations of uric acid and pancreatic steatosis was evaluated. : forty C57BL/6J mice were fed a diet of high uric acid (HU), high fat (HF), high uric acid and high fat (HUHF), and normal control (NC) (10 mice in each group). Weight was measured weekly. Ultrasonography was performed to observe the pancreatic echo intensity of all mice before the end of feeding. Subsequently, peripheral blood was taken for biochemical examination. Intact pancreatic tissues were taken, part of which was used for pathological examination, part of which was used for PCR experiments and Western Blot experiments to obtain glycerophospholipid-associated mRNA data and protein levels. : body weight was significantly higher in the HF group than in the other three groups. Higher uric acid matched lower total cholesterol and triglyceride, matched higher low-density lipoprotein, and matched equal high-density lipoprotein. Ultrasound images and HE staining of pancreatic tissues of mice showed that higher uric acid matched lower fat content. The mRNA levels of phospholipase A2 group IB were highest in high uric acid group, while relative protein expression levels were lowest in high uric acid and control groups. Phospholipase A2 group IIA showed the opposite patterns. : elevated serum uric acid at low concentrations can inhibit pancreatic steatosis, which is modulated via the glycerophospholipid metabolic pathway.
尽管有证据表明血清尿酸(SUA)和脂质之间存在相互增强的作用,但尿酸水平对胰腺脂肪变性的影响尚未明确。在本研究中,评估了低浓度尿酸与胰腺脂肪变性之间的关系。40只C57BL/6J小鼠被给予高尿酸(HU)、高脂肪(HF)、高尿酸高脂肪(HUHF)饮食以及正常对照(NC)饮食(每组10只小鼠)。每周测量体重。在喂食结束前对所有小鼠进行超声检查以观察胰腺回声强度。随后,采集外周血进行生化检查。取完整的胰腺组织,一部分用于病理检查,一部分用于PCR实验和蛋白质印迹实验,以获取甘油磷脂相关的mRNA数据和蛋白质水平。HF组的体重显著高于其他三组。较高的尿酸水平与较低的总胆固醇和甘油三酯、较高的低密度脂蛋白以及相等的高密度脂蛋白水平相匹配。小鼠胰腺组织的超声图像和HE染色显示,较高的尿酸水平与较低的脂肪含量相匹配。磷脂酶A2第IB组的mRNA水平在高尿酸组中最高,而相对蛋白质表达水平在高尿酸组和对照组中最低。磷脂酶A2第IIA组呈现相反的模式。低浓度的血清尿酸升高可抑制胰腺脂肪变性,这是通过甘油磷脂代谢途径调节的。