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胰腺癌与葡萄糖代谢。

Pancreatic cancer and glucose metabolism.

作者信息

Saruç Murat, Karaarslan Mehmet, Rasa Kemal, Saygili Ozlem, Ince Umit, Baysal Cağlar, Pour Parviz M, Cakmakçi Metin, Tözün Nurdan

机构信息

Division of Gastroenterology, School of Medicine and Acibadem Hospital, Istanbul.

出版信息

Turk J Gastroenterol. 2009 Dec;20(4):257-60. doi: 10.4318/tjg.2009.0022.

Abstract

BACKGROUND/AIMS: The mechanism of impaired glucose metabolism that develops in most patients with pancreatic cancer is obscure. The association between pancreatic cancer and diabetes is controversial. Impaired glucose tolerance or diabetes mellitus may develop as a clinical manifestation of pancreatic cancer; however, diabetes may be a predisposing risk factor for pancreatic cancer. We aimed to investigate the relationship between diabetes and pancreatic cancer, and also the impact of tumor removal on glucose metabolism.

METHODS

Eighteen pancreatic cancer patients with resectable tumors and without previous diabetes history were enrolled. All patients underwent oral glucose tolerance test and measurement of insulin levels before and after Whipple procedure.

RESULTS

Eight of 18 (44.4%) patients were diabetic before surgery whereas 4 (22.2%) had impaired glucose tolerance. Only 6 (33.3%) patients had normal glucose metabolism at the first clinical admission. After pancreatectomy, only 4 (22.2%) patients were diabetic and 1 (5%) had impaired glucose tolerance. Thirteen patients (72%) had normal glucose metabolism after tumor removal. In 8 patients, impaired glucose metabolism improved after surgery. Only 1 patient out of 6 (16%) with normal glucose metabolism initially developed impaired glucose tolerance after surgery. All patients with diabetes and impaired glucose tolerance had hyperinsulinemia before and after surgery. Insulin levels were lower after surgery than before surgery, and glucose metabolism was improved postoperatively.

CONCLUSIONS

Our results showed that tumor removal in pancreatic cancer patients improved glucose metabolism. This occurred despite a postoperative reduction in endocrine pancreas mass, which may suggest the presence of insulin resistance and diabetogenic effect of pancreatic cancer. The elucidation of the mechanism is of immense importance for providing an early tumor marker and preventative and therapeutic modalities.

摘要

背景/目的:大多数胰腺癌患者发生糖代谢受损的机制尚不清楚。胰腺癌与糖尿病之间的关联存在争议。糖耐量受损或糖尿病可能作为胰腺癌的临床表现出现;然而,糖尿病也可能是胰腺癌的一个易感危险因素。我们旨在研究糖尿病与胰腺癌之间的关系,以及肿瘤切除对糖代谢的影响。

方法

纳入18例可切除肿瘤且既往无糖尿病史的胰腺癌患者。所有患者在Whipple手术前后均接受口服葡萄糖耐量试验及胰岛素水平测定。

结果

18例患者中,8例(44.4%)术前患有糖尿病,4例(22.2%)糖耐量受损。首次临床入院时仅有6例(33.3%)患者糖代谢正常。胰腺切除术后,仅有4例(22.2%)患者患有糖尿病,1例(5%)糖耐量受损。13例患者(72%)肿瘤切除后糖代谢正常。8例患者糖代谢受损在术后得到改善。最初糖代谢正常的6例患者中只有1例(16%)术后出现糖耐量受损。所有糖尿病和糖耐量受损患者术前及术后均有高胰岛素血症。术后胰岛素水平低于术前,糖代谢术后得到改善。

结论

我们的结果表明,胰腺癌患者肿瘤切除后糖代谢得到改善。尽管术后内分泌胰腺质量减少,但仍出现这种情况,这可能提示存在胰岛素抵抗及胰腺癌的致糖尿病作用。阐明其机制对于提供早期肿瘤标志物以及预防和治疗方法具有极其重要的意义。

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