Ultrastructural changes in A-cells exposed to diabetic hyperglycaemia. Observations made on pancreas of chinese hamsters
Autor: | W. Stauffacher, Ch. Rouiller, William E. Dulin, Lelio Orci, Albert E. Renold |
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Rok vydání: | 1970 |
Předmět: |
Blood Glucose
Male medicine.medical_specialty Endocrinology Diabetes and Metabolism Cell Golgi Apparatus Cytoplasmic Granules Endoplasmic Reticulum Glucagon Chinese hamster Islets of Langerhans symbols.namesake Cricetinae Internal medicine Diabetes mellitus Diabetes Mellitus Internal Medicine medicine Animals Insulin Cell Nucleus biology Golgi apparatus medicine.disease biology.organism_classification Disease Models Animal Microscopy Electron medicine.anatomical_structure Endocrinology Ultrastructure symbols Acidosis Lysosomes Digestion Pancreas Glycogen |
Zdroj: | Diabetologia. 6:199-206 |
ISSN: | 1432-0428 0012-186X |
DOI: | 10.1007/bf01212230 |
Popis: | Pancreatic A-cells of chinese hamsters with diabetes of varying severity and duration were examined by electron microscopy. Two predominant changes were observed: 1. Lysosomal digestion of secretory granules (“granulolysis”, “crinophagy”) occurred in practically all A-cells of diabetic animals but was rarely observed in those of normoglycemic controls. This is considered a response of A-cells to the cessation of glucagon release secondary to hyperglycemia. 2. In relatively degranulated A-cells of ketotic diabetic animals, dilatation of the cisternae of the RER was seen together with accumulation of pale, flocculent material, possibly reflecting persisting or enhanced glucagon synthesis. In addition, numerous maturing secretory granules were seen in the cisternae of the Golgi complex. Since these apparently contradictory phenomena may be seen in the same cell, it is suggested that “granulolysis” may not only result from decreased hormone release secondary to hyperglycemia but that different and independent stimulatory signals may exist for glucagon synthesis, for glucagon release, and for the initiation of “granulolysis”. |
Databáze: | OpenAIRE |
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