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PubMed2000

Alteration of the Langerhans islets in pancreatic cancer patients.

An abnormal glucose metabolism occurs in up to 80% of pancreatic cancer patients shortly or a few months before the first clinical admission. Reasons for this abnormality are obscure. We investigated immunohistochemically the pattern of islets in 14 pancreatic cancer specimens and used 14 chronic pancreatitis samples and 10 normal pancreata as controls. To study the topographical relationship of these islets to the cancer, islets in four different arbitrary zones within and around the cancer were evaluated. Ten out of 14 cancer specimens showed a significant loss of beta cells (p < 0.005) and eight of them also showed a significant increase of alpha cells (p < 0.005), all of them from hyperglycemic patients. Most affected islets were found within zone 1 (intratumoral) and zone 2 (peritumoral), to a lesser extent in zone 3 (acini close to tumor) and none in zone 4 (acini remote from tumor). No comparable changes were found in chronic pancreatitis patients. The incidence of 72% with alteration of islets in our material correlates with the frequency of abnormal glucose levels in human pancreatic cancer patients. Our findings support the notion that islet cell abnormalities is likely caused by substances released from cancer cells.

Adult↗
PubMed1999

[Transplantation of porcine Langerhans islets for therapy of type I diabetes. The way to clinical application].

Transplantation of isolated pancreatic islets provides an interesting alternative to the present cure for diabetes: insulin injections and pumps. These are characterized by an insufficient glucose haemostasis and in the long run can induce kidney failure, blindness, heart failure, and amputations. Up to now more than 293 allogeneic islet transplantations have been performed in diabetics with chronical kidney failure. Despite some success, no real breakthrough has been yet achieved, though great efforts are being made to improve the various methodological steps on the way to clinical transplantation. The use of animal (xenogeneic) organs could be a solution to overcome the shortage of allogeneic donors. The current experimental and clinical research focuses on the use of pigs as organ donors, which have a number of advantages over the immunologically more compatible primates. This article reports on success and open questions concerning the efforts to isolate porcine islets for future clinical transplantation: the search for a suitable pig breed, the various isolation steps, purification and in vitro culture, transplantation models using-small and large animals, first clinical trials, and immunological reactions against the xenogeneic tissue. In addition, strategies to circumvent tissue rejection and future perspectives are discussed.

Alginates↗
PubMed1978

[The immunhistochemical investigation of trypsin and trypsin-like-activity in the small intestine, pancreas and isolated Langerhans islets. A light-, fluorescent- and electron microscopic study (author's transl)].

By means of the indirect immunofluorescence and immunenzyme technique trypsin and trypsin-like activity in fixed cryostate sections of pancreas and gut and pellets of isolated pancreatic islets respectively were investigated using specific antiserum against trypsin. The enzyme was demonstrated in the cytoplasma of the acinus cells, the epithel cell of the intercalated ducts and the excretory (interlobular) ducts of the exocrine pancreas. By light and fluorescence microscopy we could also localize a high activity in pancreatic islets. Results taken from electron microscope show the enzyme in the region of the peripheral endoplasmatic reticulum, the surface of the mitochondria, the zymogen granules of the acinus cells and in the region of the membranes of the endoplasmatic reticulum and in the granules of the B-cells of the pancreatic islets. These results are discussed in correlation with biochemical data concerning the importance of trypsin/trypsin-like activity in the specific conversion of prohormones into hormones.

Animals↗