Studies on the pancreas of the guinea pig

Bensley, R. R.

doi:10.1002/aja.1000120304

Cited by 403 publications

(77 citation statements)

References 12 publications

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“…It is perhaps not surprising, therefore, that we have observed (Yuan et al 1996) that islets maintained in culture can undergo a phenotypic switch to duct-like epithelial structures by a process known as transdifferentiation, a change from one differentiated cell phenotype to another, where change includes morphological and functional phenotypic markers (Okada 1986). To understand why islet cells are replaced by duct-like cells, one need only recall pancreatic morphogenesis, during which an epithelial-mesenchymal interaction is soon followed by the appearance of a multipotential stem cell that differentiates into either an exocrine or endocrine phenotype (Bensley 1911, Golosow & Grobstein 1962, Orci et al 1979, Dudek & Lawrence 1988. During this early stage, the cells of the endocrine pancreas develop from progenitor cells that migrate out from the embryonic ductal epithelium (Githens 1986).…”

Section: Introductionsupporting

confidence: 43%

Factors mediating the transdifferentiation of islets of Langerhans to duct epithelial-like structures

Wang

Li²,

Rosenberg

2001

Journal of Endocrinology

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We have previously shown that isolated islets embedded in type 1 collagen gel in the presence of a defined medium undergo transdifferentiation within 96 h to duct epithelial structures. The aim of this study was to identify the factors implicated in this process. Freshly isolated canine islets were embedded in type 1 collagen gel, Matrigel or agarose for up to 120 h and cultured in (i) Dulbecco's modified Eagle's medium (DMEM)/F12 plus cholera toxin (CT), (ii) medium CMRL1066 plus CT, (iii) CMRL1066 plus forskolin and (iv) CMRL1066 alone. At 16 h, intracellular levels of cAMP (fmol/10 3 islets) were increased in groups i-iii (642 17, 338 48, 1128 221) compared with group iv (106 19, P<0·01). Epithelial differentiation correlated with the total amount of intracellular cAMP measured over 120 h. Islet-epithelial transformation during the initial 36 h was associated with a wave of apoptosis which was followed by a wave of cell proliferation. During epithelial differentiation there was a progressive loss of all islet hormones and the concomitant expression of cytoskeletal proteins characteristic of duct epithelial cells. Islets in collagen and Matrigel demonstrated high rates of epithelial differentiation (63 2% and 71 4% respectively) compared with those in agarose gel (0 0%, P<0·001). Islets suspended in DMEM/F12 plus CT supplemented with soluble laminin or fibronectin did not undergo transformation. Prior incubation of freshly isolated islets with an integrin-binding arginine-glycineaspartate motif-presenting synthetic peptide also reduced islet transformation. These studies confirm the biological potential of islets of Langerhans to differentiate to duct epithelial structures. cAMP-mediated signal transduction and an appropriate integrin-matrix interaction are necessary for this process to proceed.

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Section: Introductionsupporting

confidence: 43%

Factors mediating the transdifferentiation of islets of Langerhans to duct epithelial-like structures

Wang

Li²,

Rosenberg

2001

Journal of Endocrinology

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“…Originally the B cell (or fl cell as it was called by Lane) was characterized by its content of cytoplas- [10,14] mic granules, which were soluble in alcohol but preserved in tissues fixed in chrome-sublimate and thus bestowed the cell with specific staining characteristics [1,2]. At that time nothing was known of the hormone-producing capability of the B cell, but there was nevertheless morphological evidence that this cell type would somehow be involved in the development of diabetes [3,4].…”

supporting

confidence: 44%

The life story of the pancreatic B cell

Hellerström

1984

Diabetologia

115

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Summary. Most research on the pancreatic B cell has so far focussed on the regulation and molecular biology of insulin biosynthesis and release. The present review draws attention to some additional areas of islet research which have become accessible to investigation by recent methodological progress and which may advance our understanding of the role of the B cell in diabetes. There is now evidence to suggest that B cells arise from a pool of undifferentiated precursor cells in the fetal and newborn pancreas. These ceils may contribute to islet growth and, if inappropriately stimulated, also to early islet hyperplasia. In the postnatal state, B-cell function is finely tuned by a complex set of incoming signals, one of which is the nutrient supply provided by the blood. Recent studies indicate that a disproportionately high fraction of pancreatic blood is diverted to the islets and that the islet blood flow is increased by glucose. An acute stimulus to insulin release may thus be accompanied by a process which enhances the distribution of the hormone to the target cells. Long-term adjustments of B-cell function are made by changes in B-cell number and total mass. Adaptive growth responses to an increased insulin demand occur in a number of hereditary diabetic syndromes in animals, but in some of these there is an inherited restriction on the capacity for B-cell proliferation leading to further deterioration of the glucose tolerance. Some evidence suggests that a similar mechanism may operate also in human non-insulin-dependent diabetes. A critical appraisal of this hypothesis requires, however, that human B cells should be tested for their growth characteristics. Studies of B-cell proliferation in experimental animals have shown that the B cell passes through the cell cycle at a relatively high rate but that the fraction of proliferating cells is low. Regulation of growth of the total B-cell mass seems to take place by changes in the number of B cells passing through the cell cycle rather than by changes in the rate of the cycle. The number of proliferating B cells also shows a marked decrease with age. It is at present uncertain to what extent these regulatory mechanisms apply also to the human B cell but it can be anticipated that further technical developments will elucidate this problem.

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“…The A and B cells were described by Lane in 1907, the C cell by Bensley in 1911, and the D cell by Bloom in 1931. Thomas (1937) reported I) cells to be present in all the 41 mammalian species which he had examined, but stated that C cells are present only in the guinea pig.…”

Section: Introductionmentioning

confidence: 99%

The ultrastructure of the human pancreatic islets

1971

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Summary. The ultrastructure of the pancreatic islets was studied in seven surgical specimens of human pancreas. The effects of two different fixation methods were compared: osmium tetroxide alone and glutaraldehyde followed by osmium. On the basis of their ultrastructural characteristics, four main types of islet cells were identified: 1. B cells, with polymorphous, often crystalline granules contained in wide sacs. 2. A cells with rounded granules enclosed in tight fitting sacs and composed of an electron-dense core surrounded by a clearer halo. 3. Type III cells, with rounded, large homogeneous granules of varying sizes and electron densities. They presumably secrete gastrin. Comparable cells were found in samples of human gastric and duodenal mucosae. 4. Type IV cells, with rounded, small, homogeneous granules of low electron density. Comparable cells were found in human gastrie and duodenal mucosae. The nature of their secretion remains obscure. A fifth cell type was observed in the pancreas but was not restricted to the islets. Ceils of type V have small, polymorphous and very electron-dense granules. They offer a certain resemblance with the serotonin secreting cells which are found in the digestive tract. L'ultrastructure des ~tots de Langerhans de pancrgas humains. I. Lee ~lots des aduttesRdsumd. L'ultrastrueture des riots de Langerhans a 6t6 6tudi6e sur des pr616vements chirurgicaux de sept pancr6as humains. Les effets de la fixation par le t6troxyde d'osmium seulet par la glutarald6hyde suivie d'osmium ont 6t6 eompar6s. Quatre types eellulaires ont pu 6tre identifi6s: 1. Cellules B, ~ granulation polymorphe, de structure fr6quemment eristalline, incluses dans de larges v6sieules. 2. Cellules A k granules arrondis, eompos6s d'un noyau dense entour6 par un halo clair et inelus ~ l'6troit dans une enveloppe membranaire. 3. Cellules du type III grosses granulations arrondies, de structure homog6ne, de densit6 et de forme variables. Ces cellules s6cr6tent peut-6tre de la gastrine. Des 616ments similaires ont 6t6 rencontr6s dans les muqueuses gastrique et duod6nale. 4. Cellules du type IV, k petites granulations homog6nes et p&les. Des 616ments similaires ont 6t6 aper~us dans les muqueuses gastrique et duod6nale; leur fonetion reste inconnue. Des eellules d'un einqui6me type se voient dans le paner6as, m~me en dehors des ilots. Elles sont caract6-ris6es par de petits granules, tr6s denses et polymorphes: elles offrent une eertaine ressemblance avec les cellules s6rotonine que l'on trouve dans le tube digestif. Die Ultrastruletur der Inseln des menschlichen Pankreas. I. Die Inseln yon ErwachsenenZusamrnenfassung. Die Ultrastruktur der Langerhansschen Inseln wurde an Hand yon chirurgischen Probeexzisionen an 7 menschliehen Pankreata studiert. Die Ergebnisse der Fixierung durch Osmium-Tetraoxyd einerseits und dureh Glutaraldehyd gefolgt yon Osmium anderseits wurden vergliehen. So konnten vier Zelltypen identifiziert werden: 1. B-Zellen mit polymorphen, und oft kristallinen Granulationen, die in breiten S/~ekche...

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Studies on the pancreas of the guinea pig

Cited by 403 publications

References 12 publications

Factors mediating the transdifferentiation of islets of Langerhans to duct epithelial-like structures

Factors mediating the transdifferentiation of islets of Langerhans to duct epithelial-like structures

The life story of the pancreatic B cell

The ultrastructure of the human pancreatic islets

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