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Biomedical subjects

W Gepts

Publications and source records attributed to W Gepts.

At least 55 records · Page 3Linked to original sources
PubMed1981

The pancreatic islets in diabetes.

Despite the fact that heterogeneity of diabetes in man has become more and more evident in recent years, its pancreatic pathology is still represented by two distinct entities, roughly corresponding to the classic juvenile-onset and maturity-onset types of the disease. In juvenile-onset, insulin-dependent diabetes, the pancreatic islets show severe and pathognomonic changes. B cells are greatly reduced in number already at clinical onset. Contrary to classic opinion they do not always disappear in the years to follow. Insulitis, a common finding in the pancreas of recent onset juvenile diabetic subjects, is compatible with a viral infection as well as with an autoimmune reaction as the cause of B cell destruction. In the pancreas of juvenile-onset diabetic subjects the islets, which in the past have been regarded as atrophic and inactive, are actually composed of cells containing glucagon and somatostatin. There is also a profound distortion of islet organization, and many endocrine cells are scattered as single cells in the exocrine tissue. These findings may well account for the abnormal secretory behavior of the glucagon-secreting A cells in insulin-dependent juvenile-onset diabetes. In maturity-onset, noninsulin-dependent diabetes, the pancreatic pathology is extremely variable and not pathognomonic. A numeric reduction of the B cells can be demonstrated in many maturity-onset diabetic subjects, but this reduction is much more moderate than in insulin-dependent juvenile-onset diabetic subjects and does not account for the disease. The same amount of B cell reduction can be found in many elderly subjects without clinical evidence of diabetes. In many maturity-onset diabetic subjects, the cytologic characteristics of the B cells suggest a decreased responsiveness to the stimulus of hyperglycemia. Islet fibrosis and hyalinosis (amyloidosis), although common, cannot explain this secretory dysfunction. The exact site of the defect in the B cells of maturity-onset diabetic subjects remains to be defined. Further investigations are necessary to assess the role of disturbed intraislet intercellular relationships in the pathogenesis of late-onset diabetes. The dual pattern of islet pathology in diabetes in man does not preclude a more profound heterogeneity in the etiology and pathogenesis of the disease.

Amyloidosis↗
PubMed1980

Immunocytochemical study of the endocrine pancreas in the rat during normal pregnancy and during experimental diabetic pregnancy.

The distribution of different celltypes (A, B, D and PP cells) of the endocrine pancreas was studied in both the normal and in the experimental diabetic non-pregnant and pregnant rat. In the normal rat the head (juxta duodenal part) of the pancreas contained more PP cells than the tail (12.5 +/- 1.1 versus 5.2 +/- 2.2) but fewer glucagon cells (19.0 +/- 3.5 versus 14.3 +/- 3.6). This difference disappeared during pregnancy, when the total B cell mass increased (2.05 versus 0.82). In the diabetic rat no difference was found in the number of endocrine cells between the tail and the juxta duodenal part of the pancreas. Unlike the non-diabetic rat, the number of B cells did not increase in the pancreas of the pregnant diabetic rat. An absolute increase in the number of glucagon (A) cells was demonstrated in the islets of the pregnant diabetic rat as compared to the non-diabetic rat (35 versus 21.2).

Animals↗
PubMed1980

Ultrastructural aspects of asthenospermia.

In fifty cases of proven asthenospermia semen samples were examined for ultrastructural abnormalities. In 32 of the cases the sperm cells appeared either completely normal, or presented only minor abnormalities. In 15 cases severe teratospermia was observed. In the 3 remaining cases, specific and hitherto undescribed tail abnormalities were detected.

Humans↗
PubMed1979

Localization of pancreatic polypeptide cells in a limited lobe of the human neonate pancreas: remnant of the ventral primordium?

The localization of pancreatic polypeptide (PP) cells was studied in the pancreas of four human neonates by specific immunocytochemical techniques. PP cells were detected in all parts of the pancreas. However, examination at low magnification showed that they were considerably more numerous in a small lobe, located at the posterior-inferior part of the head region. It is suggested that this lobe corresponds to the part of the pancreas that is derived from the ventral primordium. Both in the lobe rich in PP cells and in the remainder of the pancreas, approximately 75% of PP cells were present in the islets and 25% distributed among acini and ducts.

Histocytochemistry↗
PubMed1979

Plasma pancreatic hormone levels in a case of somatostatinoma: diagnostic and therapeutic implications.

Plasma somatostatin immunoreactivity (SIR) was elevated 40-fold in an insulin-treated diabetic with disseminated pancreatic carcinoma. The diagnosis of somatostatinoma was supported by histological and ultrastructural similarities between metastatic cells and pancreatic D cells. Under acid conditions, 75% of the plasma SIR eluted as a 6000- to 7000-dalton protein and 25% as synthetic somatostatin (mol wt 1600), whereas the 20-fold elevated urine SIR consisted almost exclusively of the higher molecular weight fraction. The hypersomatostatinemia was associated with reduced basal and stimulated pancreatic hormone levels, which might reflect its involvement in the steatorrhea and diabetes, and its protection against ketoacidosis. Plasma SIR rose 50% upon insulin withdrawal and 10-fold after tolbutamide injection and fell 30% after diazoxide. It is concluded that an increase in plasma and urine SIR, the presence of a 6000- to 7000-dalton SIR fraction in plasma and urine, a reduction in basal and stimulated pancreatic hormone levels, and tolbutamide-induced somatostatin release can be diagnostic for a somatostatinoma. Streptozotocin reduced tumor volume, hypersomatostatinemia, and tolbutamide-induced somatostatin release, suggesting that this drug may be useful in the treatment of disseminated somatostatinoma.

C-Peptide↗
PubMed1979

Morphological changes in the endocrine pancreas in pregnant rats with experimental diabetes.

This present study has demonstrated that during normal pregnancy in the rat the number of beta-cells is increased (hyperplasia) and the volume of the individual beta-cells is increased (hypertrophy). During experimental diabetes, however, the endocrine pancreas has an impaired capacity to compensate during pregnancy. In the experimental diabetic pregnant rat the beta-cells cannot replicate due to the unfavourable metabolic environment. This could reflect the complications caused by diabetes during human pregnancy.

Animals↗
PubMed1978

[Pancreatic polypeptide (author's transl)].

Pancreatic Polypeptide (PP) was first described in birds by Kimmel et al. (1968). It was later isolated from the pancreas of several mammalian species by Chance and Jones (1974). It has been demonstrated in the islets of many animal species by immunocytochemical methods. PP levels are assayable in plasma and rise sharply after food intake. The pharmacological properties and physiological role of PP are still ill defined. It appears to have a spectrum of actions peculiar to each species. Recent research on this subject is reviewed in this article. High levels of circulating PP have been demonstrated in juvenile and maturity-onset diabetics, as well as in some patients with islet cell tumors. However no definite clinical syndrome due to hypersecretion of PP as been identified as yet. It remains a matter of speculation that a deficiency of PP might be responsible for some types of obesity. PP-cells are rare in the pancreas of healthy young individuals. Hyperplasia of PP-cells has been observed in a wide variety of pathological conditions, but is most prominent in the pancreas of chronic insulin dependent diabetics. Histologic evidence strongly suggests that PP-cell hyperplasia represents an atypical form of islet regeneration. It is always focal in distribution and is most remarkable in those lobules that have lost the capacity to reproduce islets of normal cytologic composition.

Adenoma, Islet Cell↗
PubMed1977

Immunohistochemical and ultrastructural identification of the pancreatic polypeptide-producing cell (PP-cell) in the human pancreas.

The consecutive semithin--thin section method was employed to identify pancreatic-polypeptide-containing cells in the human pancreas. The immunocytochemical staining of semithin sections with the peroxidase-antiperoxidase complex allowed a precise ultrastructural description of the immunoreactive cells on the adjacent thin section. Two populations of small granulated cells could be distinguished with this technique: one group is formed by cells whose secretory granules with a mean diameter of 141 nm show specific immunoperoxidase staining with anti-PP serum, while the other group consists of cells whose secretory granules measuring 118 nm in diameter show no immunoreactivity to anti-PP serum. The former cells which will be designated as PP-cells, are not identical with the D1-cells of the revised Wiesbaden classification of endocrine cells.

Cytoplasmic Granules↗
PubMed1977

alpha-1-Antitrypsin immunoreactivity in islet cells of adult human pancreas.

alpha-1-antitrypsin immunoreactivity was demonstrated by immunofluorescence technique in the peripheral islet cells of all ten normal adult human pancreata examined; normal adult human liver was negative. The specificity of the reactions was confirmed by applying various control tests including absorption of the specific antisera with purified alpha-1-antitrypsin, inhibition and blocking tests and by ensuring the monospecificity of the antisera used. The findings suggest that the pancreatic islet may be an additional source of alpha-1-antitrypsin.

Adult↗