{"title":"正常和糖尿病鸭胰腺A、B、D细胞的超微结构。","authors":"F Laurent, C Hindelang, M T Strosser, P Mialhe","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Ultrastructurally and immunocytochemically identified A, B and D cells are highly concentrated in the splenic bulb of the duck pancreas. Ultrastructural features of normal A, B and D cells are similar in the duck and in other species so far studied. However, normal D cells present a striking characteristic, i.e. apical accumulation of dense bodies, which seem to derive from multivesicular bodies and are probably involved in a catabolic regulatory process. Subtotal pancreatectomy in the duck, leaving the splenic bulb and inducing transient diabetes, produces strong secretory stimulation of A and B cells, as indicated by the development of the rough endoplasmic reticulum and the Golgi apparatus and transient degranulation, more marked in B cells. Numerous B cells with degenerative aspects, observed after 12 days, seem to be exhausted following prolonged hyperstimulation: this could explain why diabetes reappears in some cases. In contrast, in D cells, functional inhibition after surgery is suggested by a dramatic increase in the number and size of the dense bodies, associated with a marked decrease in secretory vesicle storage. The morphological data correlate well with the previously reported evolution of plasma and pancreatic hormone concentration after surgery, and suggest that the normal inhibitory control of glucagon and insulin secretion by the local release of somatostatin might be reduced or suppressed during transient diabetes in subtotally depancreatized ducks.</p>","PeriodicalId":77037,"journal":{"name":"Biological structures and morphogenesis","volume":"1 1","pages":"34-42"},"PeriodicalIF":0.0000,"publicationDate":"1988-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The ultrastructure of A, B and D pancreatic cells in normal and in diabetic ducks.\",\"authors\":\"F Laurent, C Hindelang, M T Strosser, P Mialhe\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Ultrastructurally and immunocytochemically identified A, B and D cells are highly concentrated in the splenic bulb of the duck pancreas. Ultrastructural features of normal A, B and D cells are similar in the duck and in other species so far studied. However, normal D cells present a striking characteristic, i.e. apical accumulation of dense bodies, which seem to derive from multivesicular bodies and are probably involved in a catabolic regulatory process. Subtotal pancreatectomy in the duck, leaving the splenic bulb and inducing transient diabetes, produces strong secretory stimulation of A and B cells, as indicated by the development of the rough endoplasmic reticulum and the Golgi apparatus and transient degranulation, more marked in B cells. Numerous B cells with degenerative aspects, observed after 12 days, seem to be exhausted following prolonged hyperstimulation: this could explain why diabetes reappears in some cases. In contrast, in D cells, functional inhibition after surgery is suggested by a dramatic increase in the number and size of the dense bodies, associated with a marked decrease in secretory vesicle storage. The morphological data correlate well with the previously reported evolution of plasma and pancreatic hormone concentration after surgery, and suggest that the normal inhibitory control of glucagon and insulin secretion by the local release of somatostatin might be reduced or suppressed during transient diabetes in subtotally depancreatized ducks.</p>\",\"PeriodicalId\":77037,\"journal\":{\"name\":\"Biological structures and morphogenesis\",\"volume\":\"1 1\",\"pages\":\"34-42\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1988-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biological structures and morphogenesis\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biological structures and morphogenesis","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
The ultrastructure of A, B and D pancreatic cells in normal and in diabetic ducks.
Ultrastructurally and immunocytochemically identified A, B and D cells are highly concentrated in the splenic bulb of the duck pancreas. Ultrastructural features of normal A, B and D cells are similar in the duck and in other species so far studied. However, normal D cells present a striking characteristic, i.e. apical accumulation of dense bodies, which seem to derive from multivesicular bodies and are probably involved in a catabolic regulatory process. Subtotal pancreatectomy in the duck, leaving the splenic bulb and inducing transient diabetes, produces strong secretory stimulation of A and B cells, as indicated by the development of the rough endoplasmic reticulum and the Golgi apparatus and transient degranulation, more marked in B cells. Numerous B cells with degenerative aspects, observed after 12 days, seem to be exhausted following prolonged hyperstimulation: this could explain why diabetes reappears in some cases. In contrast, in D cells, functional inhibition after surgery is suggested by a dramatic increase in the number and size of the dense bodies, associated with a marked decrease in secretory vesicle storage. The morphological data correlate well with the previously reported evolution of plasma and pancreatic hormone concentration after surgery, and suggest that the normal inhibitory control of glucagon and insulin secretion by the local release of somatostatin might be reduced or suppressed during transient diabetes in subtotally depancreatized ducks.