THE OCCURRENCE OF ARGYROPHIL CELLS IN THE ISLETS OF LANGERHANS OF AMERICAN OBESE-HYPERGLYCAEMIC MICE

1961 ◽  
Vol 36 (4) ◽  
pp. 596-602 ◽  
Author(s):  
Bo Hellman
Keyword(s):  
Islets Of Langerhans ◽  
Islet Cells ◽  
Relative Proportion ◽  
Paraffin Sections ◽  
Argyrophil Cells ◽  
American Variety ◽  
A Cells ◽  
Excessive Secretion ◽  
Obese Hyperglycaemic Syndrome

ABSTRACT Distinct argyrophil islet cells were found in thin paraffin sections of pancreas both from normal mice and from those with the American variety of the obese-hyperglycaemic syndrome. In the obese animals the relative proportion of argyrophil cells was only about half as great as in their thin litter mates. In both groups the argyrophil cells were mainly localized to the periphery in the larger islets. The results are discussed in the light of the hypothesis put forward by Mayer et al. (1953), that hyperglycaemia in the obese strain results from excessive secretion of glucagon from the A cells.

THE SPECIFICITY OF THE ARGYROPHIL REACTION IN THE ISLETS OF LANGERHANS IN MAN

1961 ◽  
Vol 36 (1) ◽  
pp. 22-30 ◽  
Author(s):  
Bo Hellman ◽  
Claes Hellerström
Keyword(s):  
B Cells ◽  
Islets Of Langerhans ◽  
The Other ◽  
Human Pancreas ◽  
Paraffin Sections ◽  
Cell Counts ◽  
A Cells ◽  
Aldehyde Fuchsin ◽  
Differential Cell ◽  
Argyrophil Reaction

ABSTRACT By studying the Islets of Langerhans in man in thin Bouin fixed paraffin sections, first after impregnation with silver, and subsequently after removal of the silver, stained with Gomori's chrome-haematoxylin or aldehyde-fuchsin, it was possible to assess the specificity of the argyrophil reaction. Reports in the literature that some of the B cells were also silver impregnated could not be confirmed. On the other hand, the argyrophil reaction was not characteristic for all the A cells, since a minority of them were not blackened. In agreement with these observations, the considerably higher frequency of silver cells over A cells, previously reported in connection with comparative differential cell counts on the same human pancreas material, was shown to be only apparent.

SOME ASPECTS OF SILVER IMPREGNATION OF THE ISLETS OF LANGERHANS IN THE RAT

1960 ◽  
Vol XXXV (IV) ◽  
pp. 518-532 ◽  
Author(s):  
Claes Hellerström ◽  
Bo Hellman
Keyword(s):  
Islet Cells ◽  
Paraffin Sections ◽  
Treatment Results ◽  
A Cells ◽  
Separate Fraction ◽  
Optimal Period ◽  
Impregnation Time ◽  
Short Time ◽  
Argyrophil Reaction ◽  
Essential Prerequisite

ABSTRACT By using a modification of Davenport's alcoholic silver nitrate method for impregnating nerves, it was possible to obtain a distinct argyrophil reaction on thin paraffin sections from rat pancreas which had been fixed either in formalin or Bouin's solution. Since this was followed by a removal of silver with subsequent granule staining according to Gomori, it became clear that the distinctly blackened cells comprised only some of the A cells. Some post-mortem change seemed to be an essential prerequisite of the argyrophil reaction, since this almost completely failed to appear after fixation in an ice-cold Bouin's solution. The reducing material was considerably resistent to acids; strongly blackened islet cells could be observed even after refixation in hydrochloric acid at a pH of 0.5. Although a preoxidation, e. g. with an acid solution of potassium permanganate, is essential for the differentiation of the islet cells with the modern granule stains, such treatment results in the argyrophil reaction becoming weaker or not appearing at all. Actual blackening, except in the case of those A cells, which could be distinguished as silver cells even after a short time, could not be produced by lengthening the impregnation time, but instead, the argyrophil reaction tended to decrease after a certain optimal period. The observation that among those cells, which by granule staining were classified as A cells, a separate fraction with distinctly blackened cytoplasm could be distinguished, led to the suggestion that the blackened cells should be called A1 cells and the remaining ones, A2 cells.

Distribution of alloxan-C14 in islet and other tissues of the toadfish (Opsanus tau)

1964 ◽  
Vol 207 (2) ◽  
pp. 423-430 ◽  
Author(s):  
S. J. Cooperstein ◽  
Arnold Lazarow
Keyword(s):  
Cell Membrane ◽  
Islets Of Langerhans ◽  
Intravenous Injection ◽  
Islet Cells ◽  
Primary Site ◽  
Opsanus Tau ◽  
Extracellular Compartment ◽  
Islet Tissue ◽  
Acinar Tissue ◽  
Discrete Mass

These studies on the mechanism by which alloxan selectively destroys the ß cells in the islets of Langerhans have been carried out in the toadfish because the islet tissue in this species is segregated into a discrete mass, separated from the acinar tissue. We have measured the C14 content of several tissues at various times after intravenous injection of tracer doses of alloxan-2-C14. The islet C14 content never exceeded 50% of that of blood and was no greater than that found in many other tissues. Thus the selectivity of alloxan is not due to selective concentration by islet tissue. The distribution of alloxan-2-C14 was compared with that of d-mannitol-1-H3. A mixture of both isotopic substances was injected and the C14 and H3 in each tissue determined. The distribution of alloxan-2-C14 was very similar to that of d-mannitol-1-H3. This suggests that tracer doses of injected alloxan do not enter islet cells but remain in the extracellular compartment, and that the ß-cell membrane may be a primary site of alloxan action.

scholarly journals Studies on the role of inositol trisphosphate in the regulation of insulin secretion from isolated rat islets of Langerhans

1985 ◽  
Vol 228 (3) ◽  
pp. 713-718 ◽  
Author(s):  
N G Morgan ◽  
G M Rumford ◽  
W Montague
Keyword(s):  
Insulin Secretion ◽  
Islets Of Langerhans ◽  
Islet Cells ◽  
Inositol Trisphosphate ◽  
Rat Islets ◽  
Isolated Rat Islets ◽  
Rat Islets Of Langerhans ◽  
Isolated Rat ◽  
Stimulation Of

Glucose (20 mM) and carbachol (1 mM) produced a rapid increase in [3H]inositol trisphosphate (InsP3) formation in isolated rat islets of Langerhans prelabelled with myo-[3H]inositol. The magnitude of the increase in InsP3 formation was similar when either agent was used alone and was additive when they were used together. In islets prelabelled with 45Ca2+ and treated with carbachol (1 mM), the rise in InsP3 correlated with a rapid, transient, release of 45Ca2+ from the cells, consistent with mobilization of 45Ca2+ from an intracellular pool. Under these conditions, however, insulin secretion was not increased. In contrast, islets prelabelled with 45Ca2+ and exposed to 20mM-glucose exhibited a delayed and decreased 45Ca2+ efflux, but released 7-8-fold more insulin than did those exposed to carbachol. Depletion of extracellular Ca2+ failed to modify the increase in InsP3 elicited by either glucose or carbachol, whereas it selectively inhibited the efflux of 45Ca2+ induced by glucose in preloaded islets. Under these conditions, however, glucose was still able to induce a small stimulation of the first phase of insulin secretion. These results demonstrate that polyphosphoinositide metabolism, Ca2+ mobilization and insulin release can all be dissociated in islet cells, and suggest that glucose and carbachol regulate these parameters by different mechanisms.

scholarly journals Insulin and Glucagon Impairments in Relation with Islet Cells Morphological Modifications Following Long Term Pancreatic Duct Ligation in the Rabbit – A Model of Non-insulin-dependent Diabete

2001 ◽  
Vol 2 (2) ◽  
pp. 101-112 ◽  
Author(s):  
J. Catala ◽  
M. Daumas ◽  
A. Pham Huu Chanh ◽  
B. Lasserre ◽  
E Hollande
Keyword(s):  
Pancreatic Duct ◽  
Islet Cells ◽  
Rabbit Model ◽  
Fold Increase ◽  
Pancreatic Duct Ligation ◽  
A Cells ◽  
Duct Ligation ◽  
Insulin Dependent

Plasma levels of glucose, insulin and glucagon were measured at various time intervals after pancreatic duct ligation (PDL) in rabbits. Two hyperglycemic periods were observed: one between 15–90 days (peak at 30 days of 15.1 ± 1.2mmol/l, p < 0.01), and the other at 450 days (11.2 ± 0.5 mmol/l, p < 0.02). The first hyperglycemic episode was significantly correlated with both hypoinsulinemia (41.8 ± 8pmol/l, r= –0.94, p < 0.01) and hyperglucagonemia (232 ± 21ng/l, r=0.95, p < 0.01). However, the late hyperglycemic phase (450 days), which was not accompanied by hypoinsulinemia, was observed after the hyperglucagonemia (390 days) produced by abundant immunostained A-cells giving rise to a 3-fold increase in pancreatic glucagon stores. The insulin and glucagon responses to glucose loading at 180, 270 and 450 days reflected the insensitivity of B- and A-cells to glucose. The PDL rabbit model with chronic and severe glycemic disorders due to the predominant role of glucagon mimicked key features of the NIDDM syndrome secondary to exocrine disease.

scholarly journals AN APPROACH TO THE QUANTITATIVE HISTOCHEMISTRY OF THE A-CELLS IN THE PANCREATIC ISLETS

1966 ◽  
Vol 14 (1) ◽  
pp. 49-52 ◽  
Author(s):  
SVEN E. BROLIN ◽  
ARNE OHLSSON ◽  
ERIK BORGLUND
Keyword(s):  
B Cells ◽  
Islet Cells ◽  
Lactic Dehydrogenase ◽  
Glutamic Oxaloacetic Transaminase ◽  
Malic Dehydrogenase ◽  
Quantitative Histochemistry ◽  
A Cells ◽  
Fresh Frozen ◽  
Darkfield Microscopy ◽  
A And B Cells

Our present knowledge of the quantitative histochemistry of the pancreas is mainly related to the enzymatic properties of the exocrine parenchyma and the B-cells. Appropriate analyses of A-cells require their isolations, which can be accomplished in animals with different islet cells located in separate groups. In fresh frozen sections of the pancreas from ducks groups of A- and B-cells were recognized by darkfield microscopy combined with ordinary microscopic examination after fixation and staining. Each adjacent section was lyophilized and separate samples of acini, A-and B-cells were dissected by free hand. Using quantitative microchemical techniques malic dehydrogenase, lactic dehydrogenase and glutamic-oxaloacetic transaminase activities were measured. The enzymatic distribution found between samples of B-cells and acini was in accordance with earlier findings in mammals, as B-cells showed higher activities except for lactic dehydrogenase. The A-cells differed from the B-cells by lower activities of malic dehydrogenase and glutamic-oxaloacetic transaminase and from the acini by lower activities of lactic dehydrogenase.

Focal or Diffuse Lesions in Persistent Hyperinsulinemic Hypoglycemia of Infancy: Concerns about Interpretation of Intraoperative Frozen Sections

2001 ◽  
Vol 4 (2) ◽  
pp. 138-143 ◽  
Author(s):  
Virpi V. Smith ◽  
Marian Malone ◽  
R. Anthony Risdon
Keyword(s):  
Islet Cells ◽  
Frozen Section ◽  
Focal Lesion ◽  
Hyperinsulinemic Hypoglycemia ◽  
Frozen Sections ◽  
Paraffin Sections ◽  
Focal Lesions ◽  
Histological Changes ◽  
Diffuse Disease ◽  
Intraoperative Management

Persistent hyperinsulinemic hypoglycemia of infancy (PHHI) results from defects of regulated insulin release from pancreatic (3 cells and is often refractory to medical treatment. Histological changes in the pancreas associated with PHHI may be focal or diffuse, and the intraoperative confirmation and siting of focal lesions would require frozen section diagnosis. The recognition of focal involvement and its distinction from diffuse disease by frozen section depends on the identification and distribution pattern of islet cells with large hyperchromatic nuclei. This study was designed to test the feasibility of using this parameter in PHHI to delineate focal from diffuse diseases prior to the introduction of frozen sections to guide intraoperative management in our institution. A total of 66 coded and randomized paraffin sections (from 18 PHHI and 4 postmortem pancreases) were scored by three independent observers into the following categories: a focal lesion (A), no large endocrine nuclei (B), few large endocrine nuclei (C), and frequent large endocrine nuclei (D). Interobserver concordance was complete in 88%, but there were minor discrepancies in the remaining 12%. When a focal lesion was present in one section no large endocrine nuclei were seen in sections from the rest of the pancreas. In four patients with diffuse PHHI, no or only very scanty large endocrine nuclei were seen. From this finding, and the observation that in other examples of diffuse disease, large endocrine nuclei were sparse even in large paraffin sections, we have reservations about using small frozen sections for reliable diagnosis.

The characteristics of β-adrenergic binding sites on pancreatic islets of Langerhans

1986 ◽  
Vol 111 (2) ◽  
pp. 263-270 ◽  
Author(s):  
J. M. Fyles ◽  
M. A. Cawthorne ◽  
S. L. Howell
Keyword(s):  
Insulin Secretion ◽  
Adenylate Cyclase ◽  
Guinea Pig ◽  
Islets Of Langerhans ◽  
Binding Sites ◽  
Adrenergic Receptors ◽  
Islet Cells ◽  
Pancreatic Islets Of Langerhans ◽  
Β Adrenergic Receptors ◽  
Stimulation Of

ABSTRACT The sympathetic nervous system is believed to play a part in the control of insulin release from the pancreatic islets of Langerhans. Stimulation of α-adrenoceptors is thought to inhibit the release of insulin whereas stimulation of β-adrenoceptors enhances insulin release. The present experiments were conducted to establish the existence of β-adrenergic receptors on guinea-pig and rat islet cells and to quantify them using the selective β-adrenergic ligands [3H]dihydroalprenolol (DHA) and [125I]cyanoiodopindolol (CYP). Guinea-pig islets had 62 fmol β-adrenoceptors/mg protein using [3H]DHA, corresponding to 43 700 binding sites/cell and 25 fmol β-adrenoceptors/mg protein using [125I]CYP, corresponding to 17 400 sites/cell. Rat islet cells were found to have 4·6 fmol β-adrenoceptors/mg protein using [125I]CYP, corresponding to 7200 sites/cell. Adenylate cyclase activation exhibited a positive dose–response relationship when exposed to the β-adrenoceptor agonist isoprenaline, with a maximum response (190 ± 21% above basal) at 10 μmol isoprenaline/l. This response was abolished with 1 μmol/l of the β-adrenergic antagonist 1-alprenolol. Insulin secretion in the presence of 10 mmol glucose/l, but in the absence of the α-adrenoceptor blocker phentolamine, was not affected by 10 μmol isoprenaline/l. However, perifusion experiments showed that secretion of insulin from isolated rat islets in the presence of 10 mmol glucose/l was significantly increased (332%) by 10 μmol isoprenaline/l in the presence of 10 μmol phentolamine/l. These results suggest that binding of selective radio-labelled ligands occurs to β-adrenergic receptors on the B cell surface of the islets of Langerhans, and that these receptors are functionally coupled to insulin secretion through modulation of adenylate cyclase activity. J. Endocr. (1986) 111, 263–270

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