We report a rare case of minute (5 mm x 4 mm) mixed ductal-endocrine carcinoma of the pancreas with predominant intraductal growth. A 34-year-old Japanese man was admitted because of elevated serum pancreatic enzymes. Endoscopic retrograde pancreatography revealed an unidentified material of 18 mm within the main pancreatic duct. Stone or parasite with acute pancreatitis was suspected clinically, and the biopsy revealed malignant cells positive for CA19-9, carcinoembryonic antigen (CEA) and synaptophysin. No apparent tumor was identified in the pancreas by various imaging techniques. Resection of pancreatic body and tail was performed. Grossly, the main pancreatic duct in the pancreatic body was occluded by as much as 20 mm. The pancreas had minute carcinoma of 5 mm x 4 mm just around the occluded main pancreatic duct. The tumor cells invaded the main pancreatic duct and spread within it as long as 20 mm. Histologically, the carcinoma had biphasic pattern; one was ductal carcinoma with tubular formations and another was carcinoma with neuroendocrine features. These two elements were admixed, and the ductal element comprised 30% while the endocrine element comprised 70%. The ductal element was immunoreactive for cytokeratins, CEA and CA19-9, while the endocrine element was immunoreactive for chromogranin A and synaptophysin. No immunoreactivity for pancreatic enzymes was noted. Ultrastructural observations showed dense core granules and no zymogen granules. Our case is unique clinically in that the tumor manifested as an intraductal material and no apparent tumor was found by imaging modalities, and pathologically in that the tumor was rare mixed ductal-endocrine carcinoma and the tumor was very small and mainly grew within the main pancreatic duct.

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Food intake is intricately regulated by glucose, amino acids, hormones, neuropeptides, and trophic factors through a neural circuit in the hypothalamus. Brain-derived neurotrophic factor (BDNF), the most prominent neurotrophic factor in the brain, regulates differentiation, maturation, and synaptic plasticity throughout life. Among its many roles, BDNF exerts an anorexigenic function in the brain. However, the intracellular signaling induced by BDNF to control food intake is not fully understood. One candidate for the molecule involved in transducing the anorexigenic activity of BDNF is the mammalian target of rapamycin (mTOR). mTOR senses extracellular amino acids, glucose, growth factors, and neurotransmitters, and regulates anabolic reactions response to these signals. Activated mTOR increases protein and lipid synthesis and inhibits protein degradation. In the hypothalamus, mTOR activation is thought to reduce food intake. Here we summarize recent findings regarding BDNF- and mTOR-mediated feeding control, and propose a link between these molecules in eating behavior.

Background: Study has shown no significant differences in basal and postprandial plasma active glucagon-like peptide-1 (p-active GLP-1) levels following test meal (TM) between complication-and treatment-naïve non-obese Japanese patients with type 2 diabetes (T2DM) and controls. Methods:In non-obese Japanese patients with T2DM (n=23, group 1) and healthy individuals as control (n=13, group 2), blood levels of plasma glucose (PG), serum insulin (s-IRI), serum C-peptide (s-CPR) and p-active GLP-1 like substances (p-active GLP-1-S) were measured 0, 30, and 60 min after TM (520-560 kcal. 23% fat, 60% carbohydrate and 17% protein). HbA1c levels were also measured in the groups. Patients with mean of 9.2 years disease had various complications and treatment with diet, exercise and/or oral medical drugs except incretin-related drugs for hyperglycemia. Results:There was no significant difference in mean of sex, age, or BMI between groups. Means of HbA1c and basal and postprandial PG with area under curve (AUC), and HOMA-R were significantly higher in group 1 than in group 2. Means of HOMA-β and insulinogenic index after ingestion of TM were significantly lower in group 1 than in group 2. However, there were no significant differences in means of basal and postprandial with AUC levels of s-IRI, s-CPR and p-active GLP-1-S levels between groups.