Intra-uterine growth retardation has been linked to the development of type 2 diabetes in later life. Mitochondrial changes have been suggested as a link between fetal malnutrition and adult insulin resistance. Taurine has been implicated in this process. We investigated whether protein malnutrition in early life alters mitochondria of the pancreatic islets in adulthood, and whether taurine supplementation restores these changes. Male offspring of rats fed a control diet, a low-protein diet or a low-protein diet supplemented with taurine during pregnancy and lactation were weaned onto the control diet. In each group, at 20 weeks of age, intravenous glucose tolerance tests, euglycaemic -hyperinsulinaemic clamp studies, morphometric analysis of the pancreatic islets and ultra-structural analysis of the mitochondria of the b-cells were performed. The expressions of cytochrome c oxidase (COX) I and mitochondrial respiratory chain complex II were also measured. Fetal protein-malnourished rats showed decreased pancreatic islet mass and reduced insulin-secretory responses to a glucose load. These rats also showed reduced mitochondrial DNA-encoded COX I gene expression in the islets. Electron microscopic examination showed abnormal mitochondrial shapes in the b-cells of fetal protein-malnourished rats. Taurine supplementation to the low-protein diet restored all these changes. Our findings indicate that a maternal protein-restriction diet causes long-lasting mitochondrial changes that may contribute to the development of type 2 diabetes later in life. The lack of taurine may be a key causative factor for these dysfunctional mitochondrial changes.

Various honeys from different sources were analyzed using an electronic nose based on a mass spectrometer. Various honeys were separated with different mixing ratios. Wild honey and artificial honey were blended at ratios of 100:0, 95:5, 90:10, 85:15, 80:20, 75:25, and 70:30, respectively. Data obtained from the electronic nose were used for discriminant function analysis (DFA). The DFA plot indicated a significant separation of honey from different sources. As the concentration of artificial honey increased, the first discriminant function score (DF1) moved from positive to negative (DF1: r

-AbstractAcinar cell carcinoma is a rare tumor that represents 1∼2% of all pancreatic cancers.Clinical and radiologic findings are inconclusive in this disease. Acinar cell carcinoma is characterized by rapid progression and early metastasis, which lead to its poor prognosis.A 41-year-old man was admitted to our hospital for abdominal pain. Abdominal computed tomography (CT) and positron emission tomography-computed tomography (PET-CT) showed a splenic mass, which was being invaded by a pancreatic tail mass and which had increased 18 F-fluorodeoxyglucose (FDG) uptake. Primary radical distal pancreatectomy and splenectomy were performed. Pathologic findings revealed an acinar cell carcinoma of the pancreas. The patient underwent a total gastrectomy three months later because of gastric recurrence. Four months later, multiple hepatic metastases were discovered, and the patient underwent a left hepatectomy. During treatment with capecitabine, there was no evidence of tumor progression for 14 months. We report a case of metastatic pancreatic acinar cell carcinoma, which did not progress for an extended period while the patient was being treated with capecitabine.책임저자：이경희, 대구광역시 남구 대명5동 317-1번지, 영남대학교 의과대학 내과학교실