Histological changes in the pancreatic islets of alloxan-treated mice, with comments on β-cell regeneration

Patent, Gregory J.; Alfert, Max

doi:10.1159/000142962

Cited by 40 publications

(11 citation statements)

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“…The average diameters of the A 2-and the B-cell-nuclei were significantly increased (Fig. 8 a and b) which suggests an increased protein-synthetic activity [15,28,26,34]. Orei et al [27] reported an increased number of lysosomal bodies which contain the specific %-granules in A2-cells of streptozotocin-treated diabetic rats.…”

Section: Resultsmentioning

confidence: 87%

“…Whether these single cells secrete insulin remains to be clarified. I t is well known that in certain animal species, such as mice, guinea pigs and rabbits, but also in infants of diabetic mothers [14,20,21,22,3,5,28] hyperglycaemia seems to be a stimulus for B-cell proliferation and neoformation. To our knowledge only Arison et al [1] mention a slight regenerative activity in mild streptozotocin diabetic rats ; Logothetopoulos et al [23] found no indications for a sustained regeneration of B-cells in streptozotocin-diabetic mice.…”

Section: Resultsmentioning

confidence: 99%

“…The still controversial reports on regenerative activity and neoformation of B-cells in diabetes [14,20,21,22,23,28] and the discussions about the function of the glueagonoeytes (A2-eells) in hyperglyeaemia have encouraged us to study these phenomena morphologically and bioehemieally in rats rendered chronically diabetic by streptozotocin. Streptozotoein is a * Reported in part at the annual meeting of the Schweiz.…”

Section: Key-wordsmentioning

confidence: 99%

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Untersuchungen zur Inselzell-Regeneration, Hyperplasie und zu intrainsul�ren zellul�ren Beziehungen wahrend eines Langzeit-Streptozotocin-Diabetes bei Ratten

et al. 1970

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Studies on islet cell regeneration, hyperplasia and intrainsular cellular interrelations in long.lasting streptozotocin diabetes in ratsSummary. Diabetes was induced in rats with various single i.v. doses of streptozotocin. The rats were killed 4--10 months thereafter. Marked hyperglycaemia, ketonaemia and a rise of plasma free fatty acids resulted. The weight increase was markedly reduced. There was a clear reciprocal correlation between the injected dose of the diabetogenic agent and plasma IRI. The same was true for the B-cell counts. There was a marked B-cell hypertrophy, whereas we found only slight indication for B-cell regeneration. In one animal a functioning B-cell adenoma developed and almost all the parameters tested were normalized. In the diabetic animals the Ae-eells were predominant in the islets of Langerhans and their mean nuclear diameters were increased. In the duodenal nmeosa no increase in the number of glucagonoeytes was found.We interpret this activity of the glueagonoeytes as a consequence of permanent and long-lasting hyperglyeaemia. Investigations sur la regdndration et l'hyperplasie des cellules dans les ilots de Langerhans et sur les interrelations cellulaires intrainsulaires dans le diab~te de longue durde provoqud par la streptozotocine chez le ratRdsumd. Par des doses diffgrentes de Streptozotocine i.v. on provoque chez des rats un diab6te d'une durde de 4 ~ 10 tools. On note une hyperglyc6mie sdv~re, une ac6ton@mie et une augmentation moddr6e des acides gras. La prise de poids est diminude de fagon marqude. --I1 existe une nette eorrdlation rdeiproque entre la quantitd d'agent diab@tog~ne injeetd et l'insuline immunordactive plasmatique (IRI). On trouve le m@me rapport entre le nombre des cellules Bet Ia quantitd de Streptozotocine. On note unc eorrdlation direete entre le nombre des eellules Bet I'IRI. --L'hypertrophie des eellules B est importante alors qu'on ne trouve que pea de signes de r@gdndration des ilots et des eellules B. --Chez un des rats on note l'apparition d'un addnome ~ cellules B fonctionnant, provoquant une normalisation du m6tabolisme glueidique. --Chez les animaux diabdtiques, les cellules A 2 prgdominent et le diam~tre moyen des noyaux est augment6. On ne note pas d'augmentation signifieative des glueagonoeytes de la muqueuse duod6nale.Nous consid@rons que eette augmentation de l'aetivit@ des glucagonoeytes est fonction de l'hyperglyedmie perm~nente et de longue durge.

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Section: Resultsmentioning

confidence: 87%

Section: Resultsmentioning

confidence: 99%

Section: Key-wordsmentioning

confidence: 99%

See 1 more Smart Citation

Untersuchungen zur Inselzell-Regeneration, Hyperplasie und zu intrainsul�ren zellul�ren Beziehungen wahrend eines Langzeit-Streptozotocin-Diabetes bei Ratten

et al. 1970

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“…In mice the islets of Langerhans occur as discrete pancreatic substructures devoid of acinar cells; the islet tissue is comprised almost entirely of relatively few glucagon-containing az-cells and many insulin containing fl-cells, the latter being by far the major population (see (Patent & Alfert, 1967; Hellerstr6m, Hellman, Petersson & Alm, 1964). In view of this anatomical arrangement, impalement of cells towards the periphery of islets was avoided as far as possible.…”

Section: Resultsmentioning

confidence: 99%

Glucose‐induced electrical activity in pancreatic islet cells

Dean¹,

Matthews²

1970

The Journal of Physiology

356

181

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SUMMARY1. Intracellular recording of the transmembrane potential in mouse pancreatic cells revealed a membrane potential of -20-1 + 0-8 mV for islet cells and -41-2 + 1P4 mV for acinar cells.2. The membrane potential of islet cells was glucose dependent and in the absence of glucose the cells hyperpolarized to -32-7 mV; with glucose 27-7 mm they depolarized to -16-1 mV.3. Above a threshold concentration of glucose (4 mM) small action potentials of amplitude 1-4 mV were induced in islet cells. The percentage of cells impaled exhibiting action potentials reached a maximum of 80 % at 27-7 mm glucose.4. Mannose 16-6 mm was similar to glucose in its ability to induce action potential discharge in islet cells.5. 2,4-Dinitrophenol (0.25 mM) hyperpolarized islet cells and blocked electrical activity induced by glucose 11 1 mM.6. Adrenaline (1,uM) completely blocked glucose-induced electrical activity but without altering the membrance potential. 7. The origin and functional significance of glucose-induced electrical activity in islet cells is discussed in relation to insulin secretion.

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“…1992 randomly distributed within the islets, nor throughout the pancreas [1][2][3]. Individual is lets present a typical topographical distribu tion of different cell types with a central bulk of insulin-containing P-cells, a peripheral rim of glucagon (a), pancreatic polypeptide (PP), and intermediate placed somatostatin (8) cells. Moreover, islets located in the body and tail of the pancreas contain relatively abun dant glucagon cells and few PP cells.…”

Section: Introductionmentioning

confidence: 99%

Factors Controlling Pancreatic Islet Neogenesis

Vinik¹,

Pittenger²,

Rafaeloff³

et al. 1993

Tumor Biol

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We have established a model in which cellophane wrapping induces reiteration of the normal ontogeny of β-cell differentiation from ductal tissue. The secretion of insulin is physiologic and coordinated to the needs of the animal. Streptozotocin-induced diabetes in hamsters can be ‘cured’ at least half the time. There appears to be activation of growth factor(s) within the pancreas acting in an autocrine, paracrine or juxtacrine manner to induce ductal cell proliferation and differentiation into functioning β-cells. Given the results of our studies to date, it does not seem premature to envisage new approaches to the treatment of diabetes mellitus. Identification of the factory) which regulates islet cell proliferation and differentiation in our model may permit proto-undifferentiated cells and islets to be grown in culture. This concept could be extended to induce endocrine cell differentiation in vitro as well. Furthermore, islet cell growth factors could be used to provide ‘trophic support’ to islet transplants as a means of maintaining graft viability. There may also be greater scope for gene therapy when the growth factor(s) has been isolated, purified, sequenced and cloned.

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Histological changes in the pancreatic islets of alloxan-treated mice, with comments on β-cell regeneration

Cited by 40 publications

References 2 publications

Untersuchungen zur Inselzell-Regeneration, Hyperplasie und zu intrainsul�ren zellul�ren Beziehungen wahrend eines Langzeit-Streptozotocin-Diabetes bei Ratten

Untersuchungen zur Inselzell-Regeneration, Hyperplasie und zu intrainsul�ren zellul�ren Beziehungen wahrend eines Langzeit-Streptozotocin-Diabetes bei Ratten

Glucose‐induced electrical activity in pancreatic islet cells

Factors Controlling Pancreatic Islet Neogenesis

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