Wade Terence E, Mathur Abhishek, Lu Debao, Swartz-Basile Deborah A, Pitt Henry A, Zyromski Nicholas J
Department of Surgery, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.
J Surg Res. 2009 Jun 1;154(1):78-84. doi: 10.1016/j.jss.2008.05.006. Epub 2008 Jun 2.
Obesity is epidemic in the 21st century and has been shown to be a risk factor for developing severe acute pancreatitis. Adipose tissue produces small molecules called adipokines, which are important in modulating metabolism and inflammation. The anti-inflammatory adipokine adiponectin is decreased in obesity and inversely mirrors the severity of pancreatitis in a murine experimental model. Adiponectin acts through two receptors, AdipoR1 and AdipoR2; no data are currently available regarding adiponection receptor expression in the obese murine pancreas.
Immunohistochemical and reverse transcription-polymerase chain reaction analysis were undertaken to determine expression of adiponectin receptors AdipoR1 and AdipoR2 in the pancreas and liver of lean (C57BL/6J) and congenitally obese (Lep(Ob) and Lep(Db)) mice.
Immunohistochemistry confirmed expression of both AdipoR1 and AdipoR2 in the pancreas of all three murine strains. Staining was positive in acinar cells and to a lesser extent in islet cells. Pancreatic gene expression of AdipoR2 was similar among lean and obese mice. AdipoR1 gene expression, however, was significantly (P < 0.001) decreased in the pancreas of both Lep(Ob) and Lep(Db) mice compared to wild-type lean animals. Gene expression of both AdipoR1 and AdipoR2 was significantly less in the liver of obese (Lep(Ob) and Lep(Db)) mice compared to wild-type lean animals (P < 0.001).
These data show for the first time that the adiponectin receptors AdipoR1 and AdipoR2 are expressed in the obese murine pancreas. The paucity of AdipoR1 receptors may be important when considering the role played by adipokines in the genesis of severe pancreatitis in obesity.
肥胖在21世纪呈流行趋势，并且已被证明是发生重症急性胰腺炎的一个危险因素。脂肪组织产生称为脂肪因子的小分子，这些小分子在调节代谢和炎症方面很重要。抗炎性脂肪因子脂联素在肥胖中减少，并且在小鼠实验模型中与胰腺炎的严重程度呈负相关。脂联素通过两种受体AdipoR1和AdipoR2发挥作用；目前尚无关于肥胖小鼠胰腺中脂联素受体表达的数据。
采用免疫组织化学和逆转录聚合酶链反应分析来确定脂联素受体AdipoR1和AdipoR2在瘦型（C57BL/6J）和先天性肥胖（Lep(Ob)和Lep(Db)）小鼠的胰腺和肝脏中的表达。
免疫组织化学证实所有三种小鼠品系的胰腺中均有AdipoR1和AdipoR2的表达。腺泡细胞染色呈阳性，胰岛细胞染色程度较轻。瘦型和肥胖小鼠胰腺中AdipoR2的基因表达相似。然而，与野生型瘦型动物相比，Lep(Ob)和Lep(Db)小鼠胰腺中AdipoR1的基因表达显著降低（P < 0.001）。与野生型瘦型动物相比，肥胖（Lep(Ob)和Lep(Db)）小鼠肝脏中AdipoR1和AdipoR2的基因表达均显著降低（P < 0.001）。
这些数据首次表明脂联素受体AdipoR1和AdipoR2在肥胖小鼠胰腺中表达。在考虑脂肪因子在肥胖相关性重症胰腺炎发生中所起的作用时，AdipoR1受体的缺乏可能很重要。
