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Background. To determine the extent of dissection in curative resection for cancer of the pancreatic head, the mode of recurrence was determined at autopsy and by radiographic examinations. Materials and Methods. Records of 45 patients who had undergone macroscopically curative resection of carcinoma of the head of pancreas were analyzed to determined the mode of recurrence. The mode of recurrence was divided into four types: hepatic metastasis, peritoneal dissemination, retroperitoneal recurrence, and distant metastasis. Retroperitoneal recurrence was subdivided into lymph node metastasis and local recurrence, primarily neural invasion and lymphatic invasion. Results. Thirty patients experienced disease recurrence. Patients with Stage I or II disease experienced recurrence significantly less often than did patients with Stage III or IV disease (P < 0.05). Local retroperitoneal recurrence was discovered in 12 of 15 (80%) postmortem examinations, hepatic metastasis in 10 (66%), peritoneal dissemination in 8 (53%), and lymph node recurrence in 7 (47%). In 15 antemortem studies, retroperitoneal recurrence occurred most frequently (87%), followed by hepatic metastasis (53%). Almost all patients with liver metastasis also had local retroperitoneal recurrence. Conclusions. The frequency of retroperitoneal recurrence of carcinoma of the head of the pancreas suggests that retroperitoneal resection, including nerve plexi and lymph nodes, should be included in curative resections for patients with Stage I or II pancreatic cancer.

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The number of patients with diabetes mellitus, who exhibit insulin resistance, is increasing recently all over the world. 1) The major causes have been suggested to be functional disorders in insulin secreting capacity and in carbohydrate metabolism deterioration with aging. 2,3) In the type 2 diabetic patients without obesity, who have been frequently found in Japanese, Chinese and Korean, the reduction in insulin secretion seems to be more important than the increase in insulin resistance. 4) These defects may be caused by long term hypersecretion of insulin in response to the intake of high calorie food owing to westernized food habits. The hypersecretion of insulin leads to depletion of the insulin stock and hence to the decline in insulin secretion from the pancreatic beta cells.Several kinds of knock-out mice have been recently developed as animal models for diabetes. Although these models express several important molecular pathological features of diabetes, they carry some disadvantages in that they do not exactly express some of the symptoms of type 2 diabetes. Moreover, maintenance of these genetically-modified mice requires intensive managements in large-scaled facilities so that it needs so much cost. In order to overwhelm these disadvantages of genetically-modified model mice, we attempted to establish a type 2 diabetic model with non-obese features mouse by a non-genetic way.Streptozotocin (STZ) is a widely used chemical inducer for type 1 diabetes. 5) STZ has been shown to produce free radicals in the body which specifically cut DNA chains in the pancreatic beta cells, resulting in disorder of the function of pancreatic beta cell and, at a later phase, destruction of the beta cells by necrosis. 6) These processes evoke activation of the poly ADP ribose synthase to repair the damaged DNA, 7) and a large amount of nicotinamide dinucleotide 8) is consumed for this restoration. 9) Here, consumption of NAD is effectively supplemented by intake of nicotinamide (NA). Meanwhile, in some clinical practice, a high dose of NA is occasionally administered to diabetic patients to prevent the progress of insulin-dependent diabetes (IDDM). 10) Type 2 diabetic model in rats with combined application of STZ and NA has been already reported. 11) Thus it was considered that the similar procedures would be applicable for the prevention from STZ-induced excessive destruction of beta cells in mice. We report here the establishment of a novel method for producing non-obese type 2 diabetic mouse model with a non-genetic way, as well as its pathophysiological characterization. We also show that the present mouse model is useful for searching drugs that are beneficial to treatment of the non-obese type 2 diabetes. MATERIALS AND METHODS Animals and DrugsAll animal experiments were carried out according to the "Principles of Laboratory Animal Care" (NIH publication number 85-23, revised 1985) and the Guidelines of the Animal Investigation Committee, Chiba University, Japan.Male C57BL/6J mice of 5-6 week old age were purchas...