目的:急性胰腺炎(AP)和慢性胰腺炎(CP)通常代表疾病谱的一部分。虽然越来越多的证据表明胰腺内脂肪沉积(IPFD)在胰腺炎的发病机制中起重要作用,没有对活体个体的研究调查AP和CP的IPFD。Further,IPFD与肠道激素之间的关联仍有待阐明。目的是调查IPFD与AP的关联,CP,和健康;并研究肠道激素是否影响这些关联。
方法:在同一3.0特斯拉扫描仪上使用磁共振成像来确定201名研究参与者的IPFD。这些参与者被安排到健康,AP,和CP组。肠道激素(ghrelin,胰高血糖素样肽-1,抑胃肽,肽YY,和胃泌酸调节素)在血液中测量,经过8小时的禁食和摄入标准化的混合餐后。进行了一系列线性回归分析,考虑年龄,性别,种族,身体质量指数,糖化血红蛋白,和甘油三酯。
结果:与健康组相比,AP组和CP组的IPFD均明显更高,在所有模型中一致(在最多调整模型中趋势为0.027的p)。空腹状态下的Ghrelin与AP组(但与CP组或健康组无关)的IPFD呈显著正相关,在所有模型中一致(在调整最多的模型中p=0.019)。所研究的餐后状态的肠道激素均与IPFD没有显着相关。
结论:在AP和CP患者中,胰腺中的脂肪沉积相似。肠-脑轴,更具体地说是生长素释放肽的过表达,可能导致AP患者IPFD增加。
Acute pancreatitis (AP) and chronic pancreatitis (CP) often represent parts of the spectrum of disease. While growing evidence indicates that intra-pancreatic fat deposition (IPFD) plays an important role in the pathogenesis of pancreatitis, no study of living individuals has investigated IPFD in both AP and CP. Further, the associations between IPFD and gut hormones remain to be elucidated. The aims were to investigate the associations of IPFD with AP, CP, and health; and to study whether gut hormones affect these associations.
Magnetic resonance imaging on the same 3.0 Tesla scanner was used to determine IPFD in 201 study participants. These participants were arranged into the health, AP, and CP groups. Gut hormones (ghrelin, glucagon-like peptide-1, gastric inhibitory peptide, peptide YY, and oxyntomodulin) were measured in blood, both after an 8-hour overnight fasting and after ingestion of a standardised mixed meal. A series of linear regression analyses was run, accounting for age, sex, ethnicity, body mass index, glycated haemoglobin, and triglycerides.
Both the AP group and CP group had significantly higher IPFD in comparison with the health group, consistently across all models (p for trend 0.027 in the most adjusted model). Ghrelin in the fasted state had a significant positive association with IPFD in the AP group (but not the CP or health group), consistently across all models (p = 0.019 in the most adjusted model). None of the studied gut hormones in the postprandial state was significantly associated with IPFD.
Fat deposition in the pancreas is similarly high in individuals with AP and those with CP. The gut-brain axis, and more specifically overexpression of ghrelin, may contribute to increased IPFD in individuals with AP.