Seymour N E, Brunicardi F C, Chaiken R L, Lebovitz H E, Chance R E, Gingerich R L, Elahi D, Andersen D K
Department of Surgery, State University of New York Health Science Center, Brooklyn 11203.
Surgery. 1988 Aug;104(2):119-29.
Pancreatic polypeptide (PP) deficiency has been associated with impaired hepatic sensitivity to insulin and pancreatogenic diabetes in chronic pancreatitis. Since pancreatic resection might also result in PP deficiency, hepatic responses to insulin infusion (0.25 mU/kg/min) were determined by the euglycemic glucose clamp technique in 10 patients who had previously undergone pancreatic resection for trauma and in eight healthy control subjects. Six resection patients (RES-PP) demonstrated deficient PP levels, with a mean increase of plasma immunoreactive PP of 20 +/- 7 pg/ml above basal rate after a test meal compared with 232 +/- 82 pg/ml in control subjects (p less than 0.01) and 353 +/- 133 pg/ml in four other patients undergoing resection with normal levels of immunoreactive PP (RES + PP) (p less than 0.03). Three identical insulin infusion studies were performed in each subject, the second of which was performed during the final 2 hours of an 8-hour infusion of bovine PP (2.0 pmol/kg/min). Whereas hepatic glucose production (HGP) in control subjects fell 74% +/- 4% from a basal rate of 2.0 +/- 0.1 mg/kg/min to a 60- to 120-minute value of 0.5 +/- 0.1 mg/kg/min during insulin infusion, HGP was suppressed only 58% +/- 5% in RES-PP subjects, from 1.9 +/- 0.1 to 0.8 +/- 0.1 mg/kg/min (p less than 0.05 vs controls). Intravenous infusion of PP corrected the hepatic resistance to insulin seen in the PP-deficient group. During PP infusion, HGP was suppressed 74% +/- 5% in RES-PP subjects, from 2.1 +/- 0.2 to 0.5 +/- 0.1 mg/kg/min (p less than 0.04 compared with initial study). PP infusion produced no significant change in glucose metabolism in control and RES + PP subjects. Overall glucose disposal rates were not altered by PP infusion in any group. These findings support a role of PP as a glucoregulatory hormone and suggest that PP deficiency may serve as a reversible pathophysiologic factor in the abnormal glucose metabolism seen after pancreatic resection.
胰多肽（PP）缺乏与慢性胰腺炎患者肝脏对胰岛素的敏感性受损及胰源性糖尿病有关。由于胰腺切除也可能导致PP缺乏，我们采用正常血糖葡萄糖钳夹技术，对10例因外伤曾接受胰腺切除的患者及8名健康对照者进行了研究，以测定肝脏对胰岛素输注（0.25 mU/kg/分钟）的反应。6例切除患者（RES-PP）PP水平不足，试餐后血浆免疫反应性PP平均较基础值升高20±7 pg/ml，而对照者为232±82 pg/ml（p<0.01），另外4例免疫反应性PP水平正常的切除患者（RES+PP）为353±133 pg/ml（p<0.03）。对每位受试者进行了3次相同的胰岛素输注研究，第二次研究在8小时输注牛PP（2.0 pmol/kg/分钟）的最后2小时进行。胰岛素输注期间，对照者肝脏葡萄糖生成（HGP）从基础值2.0±0.1 mg/kg/分钟下降74%±4%，至60至120分钟时为0.5±0.1 mg/kg/分钟，而RES-PP受试者HGP仅被抑制58%±5%，从1.9±0.1降至0.8±0.1 mg/kg/分钟（与对照者相比，p<0.05）。静脉输注PP纠正了PP缺乏组所见的肝脏对胰岛素的抵抗。在PP输注期间，RES-PP受试者HGP被抑制74%±5%，从2.1±0.2降至0.5±0.1 mg/kg/分钟（与初始研究相比，p<0.04）。PP输注在对照者和RES+PP受试者中未引起葡萄糖代谢的显著变化。PP输注在任何组中均未改变总体葡萄糖处置率。这些发现支持了PP作为一种葡萄糖调节激素的作用，并提示PP缺乏可能是胰腺切除后所见异常葡萄糖代谢中一个可逆的病理生理因素。
