Department of Surgery, Indiana University School of Medicine, 535 Barnhill Drive, RT 130, Indianapolis, IN 46202, USA.
Dig Dis Sci. 2011 Aug;56(8):2318-25. doi: 10.1007/s10620-011-1626-x. Epub 2011 Feb 24.
Acute pancreatitis is a substantial clinical problem accounting for 240,000 hospital admissions yearly in the United States. Obesity is epidemic and is clearly an independent risk factor for increased severity of acute pancreatitis (AP). Adipose tissue is an endocrine organ that secretes a variety of metabolically active substances termed adipokines. However, the role of adipokines in modulating acute pancreatitis severity remains incompletely understood. Dietary fish oil is rich in omega-3 free fatty acids and attenuates adipose tissue-induced inflammation. Therefore, we hypothesized that feeding obese mice diets rich in fish oil would alter the adipokine milieu and attenuate the severity of pancreatitis.
Lean (C57BL/6 J) and obese (LepDb) mice were fed either a soybean oil- or fish oil-rich diet for 4 weeks. AP was induced by six hourly intraperitoneal injections of cerulein (50 μg/kg). Serum adipokine levels were measured, and pancreatitis severity was assessed histologically and by measuring pancreatic concentrations of interleukin-1 beta (IL-1β), interleukin-6 (IL-6), myleoperoxidase (MPO), and monocyte chemoattractant protein-1 (MCP-1).
Obese mice developed more severe pancreatitis than lean mice. Fish oil significantly decreased serum leptin (lean and obese) and increased serum adiponectin (lean only). Fish oil did not alter the baseline pancreatic inflammatory milieu, nor did it change histologic or biochemical pancreatitis severity.
These data demonstrate that a diet rich in fish oil altered the adipokine milieu in lean and congenitally obese mice; however, fish oil did not improve pancreatitis severity induced with cerulein hyperstimulation.
在美国，每年有 24 万例急性胰腺炎住院，这是一个严重的临床问题。肥胖是一种流行疾病，显然是急性胰腺炎（AP）严重程度增加的独立危险因素。脂肪组织是一种内分泌器官，它分泌多种代谢活跃的物质，称为脂肪因子。然而，脂肪因子在调节急性胰腺炎严重程度方面的作用仍不完全清楚。饮食中的鱼油富含 ω-3 游离脂肪酸，可减轻脂肪组织诱导的炎症。因此，我们假设肥胖小鼠食用富含鱼油的饮食会改变脂肪因子环境，并减轻胰腺炎的严重程度。
瘦（C57BL/6 J）和肥胖（LepDb）小鼠分别用富含大豆油或鱼油的饮食喂养 4 周。通过每 6 小时腹腔注射鹅膏蕈碱（50μg/kg）诱导 AP。测量血清脂肪因子水平，并通过测量胰腺白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）、髓过氧化物酶（MPO）和单核细胞趋化蛋白-1（MCP-1）的浓度来评估胰腺炎的严重程度。
肥胖小鼠比瘦小鼠发生更严重的胰腺炎。鱼油显著降低瘦（瘦和肥胖）和增加血清脂联素（仅瘦）。鱼油并未改变基础胰腺炎症环境，也未改变组织学或生化胰腺炎严重程度。
这些数据表明，富含鱼油的饮食改变了瘦和先天性肥胖小鼠的脂肪因子环境；然而，鱼油并没有改善鹅膏蕈碱过度刺激引起的胰腺炎严重程度。
