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

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.

1996 ◽  
Vol 148 (2) ◽  
pp. 223-232 ◽  
Author(s):  
P-M Bourlon ◽  
A Faure-Dussert ◽  
B Billaudel ◽  
B Ch J Sutter ◽  
G Tramu ◽  
...  

Abstract The pancreatic B cell is equipped with specific receptors for 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) and contains vitamin D-dependent calcium binding proteins (calbindin-D). Insulin secretion is impaired by vitamin D deficiency and is restored by 1,25-(OH)2D3 (concomitantly with an improved calcium handling within B cells) but the effect of 1,25-(OH)2D3 on the pancreatic B cell via calbindin-D is unclear. Therefore we examined the relationship between calbindin-D28K or calbindin-D9K and the activity of the endocrine pancreas in normal (N), four week vitamin D-deficient (−D) and one week 1,25-(OH)2D3-replete (+D) rats. Calbindin-D9K was not found in the pancreas, neither in the islets nor in the exocrine part, of any of the groups of rats (N, −D, or +D). Surprisingly, total islet calbindin-D28K content was increased by vitamin D deficiency and partly restored by 1,25-(OH)2D3. Calbindin-D28K immunostaining was observed only on A and B cells in the endocrine part of the pancreas, the greatest staining being found in A cells. This difference in staining density was increased by vitamin D deficiency and decreased by 1,25-(OH)2D3 treatment. In vitro, 1,25-(OH)2D3 also produced a negative influence on calbindin-D28K staining in A cells, as demonstrated using pieces of pancreas incubated with the steroid for 2 h. No significant influence on labeling intensity of B cell calbindin-D28K could be shown. Plasma insulin and islet insulin release in response to 10 mm arginine stimulation were decreased in −D rats and enhanced in +D rats towards N values. In contrast, plasma glucagon and the amount of glucagon secretion, stimulated in vitro by 10 mm arginine or by low (1·7 mm) glucose concentration, was increased in −D rats and attenuated by 1,25-(OH)2D3. Thus there appears to be no relationship between the steady state level of B cell calbindin-D28K and the regulation of insulin secretion by 1,25-(OH)2D3 in vitamin D-deficient rats. However there is a correlation between A cell calbindin-D28K and glucagon secretion, which are both negatively regulated by 1,25-(OH)2D3. The predominance of calbindin-D28K in A cells raises the question as to how A and B cells interact and the role of calbindin-D28K in calcium handling. Journal of Endocrinology (1996) 148, 223–232


Endocrinology ◽  
2003 ◽  
Vol 144 (9) ◽  
pp. 4123-4133 ◽  
Author(s):  
Malgorzata Bielinska ◽  
Helka Parviainen ◽  
Susan B. Porter-Tinge ◽  
Sanne Kiiveri ◽  
Elena Genova ◽  
...  

Abstract Certain inbred strains of mice, including DBA/2J, develop adrenocortical tumors in response to gonadectomy. Spindle-shaped cells with limited steroidogenic capacity, termed A cells, appear in the subcapsular region of the adrenal gland, followed by sex steroid-producing cells known as B cells. These changes result from unopposed gonadotropin production by the pituitary, but the adrenocortical factors involved in tumorigenesis have not been characterized. GATA-4, a transcription factor normally expressed in fetal, but not adult, adrenocortical cells, was found in neoplastic cells that proliferate in the adrenal cortex of gonadectomized DBA/2J mice. GATA-4 mRNA was detected in the adrenal glands of female mice 0.5 months after ovariectomy and reached a maximum by 4 months. Castrated male mice developed adrenocortical tumors more slowly than gonadectomized females, and the onset of GATA-4 expression in the adrenal was delayed. In situ hybridization and immunohistochemistry revealed GATA-4 mRNA and protein in A and B cells, but not in normal adrenocortical cells. mRNA encoding another factor associated with adrenocortical tumorigenesis, LH receptor (LHR), was detected in A and B cells. In addition, transcripts for P450 17α-hydroxylase/C17-C20 lyase, an enzyme essential for the production of sex steroids, and inhibin-α were found in B cells. Unilateral ovarian regeneration, a phenomenon known to occur in gonadectomized mice, was observed in a subset of DBA/2J mice undergoing complete ovariectomy. In these animals, adrenocortical tumor progression was arrested; A cells and GATA-4 expression were evident, but there was no expression of LHR or P450 17α-hydroxylase/C17-C20 lyase. Strain susceptibility to adrenocortical tumorigenesis (DBA/2J ≫ FVB/N) correlated with the expression of GATA-4 and LHR, implicating these factors in the process of adrenocortical neoplasia in response to continuous gonadotropin stimulation.


1998 ◽  
Vol 22 (1) ◽  
pp. 1-6
Author(s):  
Kh. A. Hussain

Pancreatic islets of Turkey were different from those of mammals. It is divided into alpha, beta and mixed types according to the ground of cellular composition. The alpha islets are composed of A-cells and D-cells. Whereas the beta islets are composed of B-cells and D-cells. The mixed islets were composed mainly of B-cells, a few D-cells and A-cells. APP cells were not obvious.


Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1204
Author(s):  
Heike Wanka ◽  
Philipp Lutze ◽  
Alexander Albers ◽  
Janine Golchert ◽  
Doreen Staar ◽  
...  

A stimulated renin-angiotensin system is known to promote oxidative stress, apoptosis, necrosis and fibrosis. Renin transcripts (renin-b; renin-c) encoding a cytosolic renin isoform have been discovered that may in contrast to the commonly known secretory renin (renin-a) exert protective effects Here, we analyzed the effect of renin-a and renin-b overexpression in H9c2 cardiomyoblasts on apoptosis and necrosis as well as on potential mechanisms involved in cell death processes. To mimic ischemic conditions, cells were exposed to glucose starvation, anoxia or combined oxygen–glucose deprivation (OGD) for 24 h. Under OGD, control cells exhibited markedly increased necrotic and apoptotic cell death accompanied by enhanced ROS accumulation, loss of mitochondrial membrane potential and decreased ATP levels. The effects of OGD on necrosis were exaggerated in renin-a cells, but markedly diminished in renin-b cells. However, with respect to apoptosis, the effects of OGD were almost completely abolished in renin-b cells but interestingly also moderately diminished in renin-a cells. Under glucose depletion we found opposing responses between renin-a and renin-b cells; while the rate of necrosis and apoptosis was aggravated in renin-a cells, it was attenuated in renin-b cells. Based on our results, strategies targeting the regulation of cytosolic renin-b as well as the identification of pathways involved in the protective effects of renin-b may be helpful to improve the treatment of ischemia-relevant diseases.


2006 ◽  
Vol 572 (3) ◽  
pp. 691-706 ◽  
Author(s):  
Sheila Vignali ◽  
Veronika Leiss ◽  
Rosi Karl ◽  
Franz Hofmann ◽  
Andrea Welling

1972 ◽  
Vol 20 (11) ◽  
pp. 873-879 ◽  
Author(s):  
S. L. HOWELL ◽  
MARGARET WHITFIELD

A cytochemical method has been used to investigate the localization of adenyl cyclase activity in A and B cells of isolated rat islets of Langerhans. Adenosine triphosphate was initially utilized as substrate, the pyrophosphate liberated being precipitated by lead ions at its site of production. The specificity of the method was increased by the use of adenylyl-imidodiphosphate as an alternative substrate; this adenosine triphosphate analogue was not hydrolyzed by adenosine triphosphatase but provided an effective substrate for adenyl cyclase. Adenyl cyclase activity, which was found to retain its glucagon and fluoride sensitivity in glutaraldehyde-fixed tissue, was found exclusively and almost uniformly in the plasma membranes of A and B cells. Storage granule membrane, incorporated into the plasma membrane during secretion of the granule content by exocytosis, appeared to be devoid of adenyl cyclase activity.


1962 ◽  
Vol 48 (1-2) ◽  
pp. 137-141 ◽  
Author(s):  
Arne Wallgren ◽  
Bo Hellman

Sign in / Sign up

Export Citation Format

Share Document