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28 records · Page 2Linked to original sources
PubMed1978

Fine structural studies of the islets of langerhans in the Djungarian hamster (Phodopus sungorus).

A study of the pancreatic islets of Langerhans in the Djungarian hamster (Phodopus sungorus) was initiated by the observation that 98 percent of the animals of a recently established colony showed ketoacidosis soon after birth, about ten percent of which later developed persistent hyperglycemia. The islets are made up of a centrally located mass of insulin-producing B-cells surrounded by a peripheral rim of A- and D-cells. Most islets are richly supplied by unmyelinated nerve fibers which terminate on all three cell types with cholinergic synaptic endings. Early changes in islet fine structure due to ketosis comprise degranulation of A-cells combined with signs of crinophagia of alpha-granules. After the manifestation of hyperglycemia, degranulation of B-cells is followed by deposition of glycogen which in the late phase of the diabetic syndrome forms large masses obscuring the regular cellular organelles. In six- to nine-month hyperglycemic animals degenerative changes are also observed in D-cells in the form of autophagic vacuoles.

Animals↗
PubMed1978

[Malignant insuloma. Evaluation of the response to treatment with streptozotocin, using selective arteriography of the celiac axis].

A patients with metastatic insulin-producing islet-cell carcinoma has been treated with Streptozotocin intravenously and studied by selective celiac angiography during treatment. A 50% decrease of the tumor's size has been demonstrated by this technique after a total dose of 19 grams of the drug together with return to normal of the serum-insulin and blood-glucose values. The usefulness of angiography in evaluating the tumor response to Streptozotocin and in managing chemotherapy is discussed.

Adenoma, Islet Cell↗
PubMed1975

The ultrastructure of focal islet cell adenomatosis in the newborn with hypoglycemia and hyperinsulinism.

In a newborn severe persistent hypoglycemia due to an insulin-producing tumorous proliferation of pancreatic islet cells (insulinoma) was observed. The insulinoma showed the histologic pattern of focal adenomatosis of islet cells. According to the present literature the focal proliferation of islet cell complexes seems to be a frequent and particular feature of insulinomas in the newborn. Differential islet cell staining identified 80%-90% of the proliferated islet cells as B cells. 10%-20% of the cells were found to be A or D cells. Ultrastructurally the majority of the proliferated islet cells were well differentiated B cells. The remaining cells represented either A or D cells or a fourth islet cell type with small spheric granules. Electronmicrscopic evidence of transitions between differentiated islet cells, particularly B cells, and the fourth islet cell type suggests that the fourth islet cell type might represent a precursor cell within the APUD-cell system.

Adenoma, Islet Cell↗
PubMed1978

Localization of insulinomas and islet cell hyperplasias by pancreatic vein catheterization and insulin assay.

Percutaneous transhepatic portal vein catheterization and transfemoral portal and caval catheterizations were performed under local anesthesia in five patients with symptoms of organic hypoglycemia. During the investigation, results of pancreatic phlebography revealed the pancreatic venous anatomy. Blood obtained from the celiac artery, caval branches and pancreatic veins was assayed for insulin by two different radioimmunoassay methods. Pathologically high, pancreatic arteriovenous insulin differences in two patients with insulinomas and in two patients with islet cell hyperplasia. In one of the patients with an insulinoma, one of the assays failed to detect the tumor insulin. This inconsistency still remains unexplained. Angiography revealed a pancreatic abnormality in only two patients. During operation, two of the tumors were found upon palpation and inspection. Pancreatic resections were performed according to the findings of pathologic hormone differences in all five patients. Immunocytochemistry revealed that three of the patients had insulin-producing tumors and two had local islet cell hyperplasia. Catheterizations performed two months postoperatively confirmed the radicality of the operation in all patients, with the possible exception of one patient. In one patient, a recurrance was detected by catheterization ten months postoperatively.

Adenoma, Islet Cell↗
PubMed1975

Failure of somatostatin to inhibit tolbutamide-induced insulin secretion in patients with insulinomas: a possible diagnostic tool.

The effects of somatostatin on tolbutamide-stimulated insulin release were studied in 4 patients with insulin-producing tumors of the pancreas and in 6 normal subjects. In contrast to its effective inhibition of insulin release in normal subjects, somatostatin, without exception, failed to inhibit tolbutamide-induced insulin release in the patients with pancreatic beta-cell tumors. This differential effect of somatostatin may prove useful in the diagnosis of insulin-producing tumors of the pancreas.

Adenoma, Islet Cell↗
PubMed1976

Insulinoma in a pregnant woman.

The case of a 37-year-old primigravida suffering from severe hypoglycemia due to insulinoma is reported. Diagnosis was established on clinical grounds by assessment of inappropriate insulin release. Laparotomy was performed by the 12th gestational week. A wide distal pancreatectomy was carried out, and histopathologic study proved the existence of multiple islet cell adenomatosis. Glycemic levels and insulin secretion returned to normal immediately after surgery. The course of pregnancy was unhampered, judged by clinical criteria and by serial estimations of human chorionic somatomammotropin levels before and after removal of the insulin-producing tumor. A normal female infant was delivered at term, and no histopatholgic changes were detected in the placenta. After 1 year, clinical and analytical evaluation of both mother and child was normal.

Adenoma, Islet Cell↗
PubMed1976

The neural crest and the origin of the insulin-producing and other gastrointestinal hormone-producing cells.

It has been proposed that the endocrine cells of the digestive tract derive from the neuroectoderm (neural crest). To test this hypothesis we removed the entire ectoderm, the precursor of the neural crest, of embryonic rats prior to the formation of the neural crest and cultured the mesoendoderm for 11 days. In every case where a pancreas developed, insulin was detected or B cells were observed. Thus, a neural crest origin for these cells is eiliminated.

Amines↗
PubMed1976

Histochemistry, ultrastructure and hormone content of human insulinomas.

Forty human insulin-producing tumors were investigated with histochemical, immunohistological and ultrastructural methods and extracted for insulin and proinsulin. These studies resulted in the following findings: 1) A variable number of tumor cells contained only a few or often no beta granules. 2) The insulin concentration was lower and the proinsulin percentage higher in insulinoma cells compared with normal beta-cells. 3) According to the ultrastructural appearance of the secretory granules four types of insulinoma were established. 4) Insulinomas frequently contained cells with atypical secretory granules which were Grimelius silver-positive. Their similarity to the Type IV islet cell and to cells regularly found in gastrinomas, Verner-Morrison tumors and glucagonomas suggests that all endocrine pancreatic tumors originate from a common precursor cell. 5) The morphological and biochemical findings support the theory that uncontrolled hormone release and/or decreased storage capacity are responsible for fasting hyperinsulinism in insulinoma patients. 6) The severity of hypoglycemia symptoms and the result of stimulatory tests were not related to the size, the insulin concentration and the total insulin content of the tumor.

Adenoma, Islet Cell↗