By P. J. Lefèbvre (auth.), Professor Dr. Pierre J. Lefèbvre, Professor Dr. Daniel G. Pipeleers (eds.)
Diabetes mellitus represents essentially the most widespread and severe scientific syn dromes in modern drugs. because the finish of the 19th century, the endocrine pancreas has been implicated within the pathogenesis of this affliction. numerous pathologists of the 20th century detected quite a few lesions and mor phologic adjustments within the pancreatic islets of diabetic sufferers, however the patho physiologic foundation in their findings remained lengthy vague. The systematic mi croscopic paintings of WILLY GEPTS clarified the perspectives and similar the diversity in histopathology to variations in foundation, length and scientific expression of the illness. over the last 20 years, the concept that of a multifactorial starting place of diabetes has develop into commonly approved. numerous brokers and mechanisms were pointed out which can result in a quantitative or qualitative deficit in pancre atic B-cells. the aim of this publication is to deliver an replace at the many course methods that may result in an absolute or relative insufficiency in insulin liberate and accordingly a diabetic country. instead of bringing a whole account on all re seek proper to the knowledge of the pathology of the diabetic pancreas, the authors of a few of the chapters of this quantity have focussed on chosen techniques that can impair B-cell functionality, survival or regeneration.
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Additional resources for The Pathology of the Endocrine Pancreas in Diabetes
References 1. Adler G, Kern HF (1975) Regulation of exocrine pancreatic secretory process by insulin in vivo. Horm Metabol Res 7: 290-296 2. Alumets J, Hakanson R, Lundqvist G, Sundler F, Thorell J (1980) Ontogeny and ultrastructure of somatostatin and calcitonin cells in the thyroid gland of the rat. Cell Tissue Res 206: 193-201 3. Banting FG, Best CH (1922) The internal secretion of the pancreas. J Lab Clin Med 7: 251-266 4. Bartow SA, Mukai K, Rosai J (1981) Pseudoneoplastic proliferation of endocrine cells in pancreatic fibrosis.
However, the ratio of D to A does not change, suggesting that the disappearance of B-cells has no preferential influence on either of these two cell types. * • A Cells • • 600 +• 400 • •• 200 () c co a.. c en 0 () Q) c '- () 0 "0 c w ..... 200 0 en en co ~ co 100 0 l- • • t •• o Cells 0 ...... • 200 ~ 8 0 Controls Type I ~ A t 0 § I PP Cells 400 0 • • 0 a Q) • • • Type II • • • • t 0 • 1 8 0 I I 0 Controls Type I Type II Fig. 5. Estimated total mass of each endocrine cell type in the pancreas of control and diabetic subjects [From 82] _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ The Diabetic Pancreas: A Pathologist's View 27 be inferred that the interrelationship between A- and D-cells is insensitive to the architectural modification resulting from the loss of B-cells: it is for example noteworthy to mention that the proportion of D-cells which are scattered throughout the exocrine pancreas increases three- to fourfold in chronic type 1 diabetic patients [S2].
1. Percentage of each endocrine cell type in the various regions of the pancreas of neonates, infants, and adults. [From 79] 32%, and PP-cells less than 1%. In adults, these proportions are respectively 66%, 20%, 10%, and 2%. The proportion of B-cells is thus lower in the normal neonate than in adults, whereas that of D-cells is much higher at birth than in adults. It tends to decrease in the early months of extrauterine life. The presence of a large number of somatostatin cells at birth may suggest that this hormone plays a particular and still undiscovered role during fetal or early extrauterine life.