THE SURVIVAL AND GROWTH OF PANCREATIC TISSUE IN THE ANTERIOR CHAMBER OF THE EYE OF THE ALBINO RAT

1960 ◽  
Vol 20 (1) ◽  
pp. 69-77 ◽  
Author(s):  
R. E. COUPLAND

SUMMARY Pieces of foetal rat pancreas obtained from specimens of 18–40 mm c.r. length were implanted into the anterior chamber of the mother's eye. The subsequent changes were followed using histological methods. Acinar tissue degenerates and completely disappears during the first 2 weeks after implantation. Duct epithelium proliferates and large numbers of islets of Langerhans are produced which contain both α and β cells. In grafts of 1 year's duration islets form the main bulk of the graft. Methods of staining the islet tissue of the rat are discussed.

2019 ◽  
Vol 484 (1) ◽  
pp. 117-120
Author(s):  
V. O. Murovets ◽  
E. A. Sozontov ◽  
T. G. Zachepilo

Protein T1R3, the main subunit of sweet, as well as amino acid, taste receptor, is expressed in the epithelium of the tongue and gastro intestinal tract, in β–cells of the pancreas, hypothalamus, and numerous other organs. Recently, convincing witnesses of T1R3 involvement in control of carbohydrate and lipid metabolism, and control of production of incretines and insulin, have been determined. In the study on Tas1r3-gene knockout mouse strain and parent strain C57Bl/6J as control, priority data concerning the effect of T1R3 on the morphological characteristics of Langerhans islets in the pancreas, are obtained. In Tas1r3 knockout animals, it is found that the size of the islets and their density in pancreatic tissue are reduced, as compared to the parent strain. Additionally, a decrease of expression of active caspase-3 in islets of gene-knockouts is demonstrated. The obtained data show that the lack of a functional, gene encoding sweet-taste receptor protein causes a dystrophy of the islet tissue and associates to the development of pathological changes in the pancreas specific to type-2 diabetes and obesity in humans.


2021 ◽  
Author(s):  
Shristi Shrestha ◽  
Diane C. Saunders ◽  
John T. Walker ◽  
Joan Camunas-Soler ◽  
Xiao-Qing Dai ◽  
...  

ABSTRACTIslet-enriched transcription factors (TFs) exert broad control over cellular processes in pancreatic α and β cells and changes in their expression are associated with developmental state and diabetes. However, the implications of heterogeneity in TF expression across islet cell populations are not well understood. To define this TF heterogeneity and its consequences for cellular function, we profiled >40,000 cells from normal human islets by scRNA-seq and stratified α and β cells based on combinatorial TF expression. Subpopulations of islet cells co-expressing ARX/MAFB (α cells) and MAFA/MAFB (β cells) exhibited greater expression of key genes related to glucose sensing and hormone secretion relative to subpopulations expressing only one or neither TF. Moreover, all subpopulations were identified in native pancreatic tissue from multiple donors. By Patch-seq, MAFA/MAFB co-expressing β cells showed enhanced electrophysiological activity. Thus, these results indicate combinatorial TF expression in islet α and β cells predicts highly functional, mature subpopulations.


1978 ◽  
Vol 26 (3) ◽  
pp. 487
Author(s):  
AW White ◽  
CJF Harrop

The development of the endocrine pancreas in kangaroos was examined histologically with tissue from three kangaroo species, the red kangaroo Megaleia rufa, the euro Macropus robustus erubescens, and the grey kangaroo Macropus giganteus. The relative size of the pancreas of the pouch young was found not to differ significantly from that of adults. Stages of pancreatic development were described from the frequency of the occurrence of the pancreatic epithelial ducts and the B or insulin-secreting cells, while the development and distribution of the A2 or glucagon-producing cells was also observed. In pouch young of less than 22 days of age the pancreas is dominated by ductular epithelial and undifferentiated pancreatic cells. From days 42 to 97 of pouch life B endocrine cells tend to be concentrated together and ductular tissue encroaches into areas previously dominated by connective tissue. After 120-135 days the first A2 cells are apparent and are usually located at the periphery of the islets, which now take on a distinctive appearance as the acinar tissue expands and separates them. After 135 days of pouch life A2 cells outnumber B cells; the endocrine tissue assumes an adult appearance after 150-160 days. The major difference between the development of pancreatic tissue in foetal sheep and pouch-young kangaroo is the prolonged dominance of connective tissue and the slow development of endocrine tissue in the former.


1964 ◽  
Vol 207 (2) ◽  
pp. 423-430 ◽  
Author(s):  
S. J. Cooperstein ◽  
Arnold Lazarow

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.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Luke Ternes ◽  
Ge Huang ◽  
Christian Lanciault ◽  
Guillaume Thibault ◽  
Rachelle Riggers ◽  
...  

AbstractMechanistic disease progression studies using animal models require objective and quantifiable assessment of tissue pathology. Currently quantification relies heavily on staining methods which can be expensive, labor/time-intensive, inconsistent across laboratories and batch, and produce uneven staining that is prone to misinterpretation and investigator bias. We developed an automated semantic segmentation tool utilizing deep learning for rapid and objective quantification of histologic features relying solely on hematoxylin and eosin stained pancreatic tissue sections. The tool segments normal acinar structures, the ductal phenotype of acinar-to-ductal metaplasia (ADM), and dysplasia with Dice coefficients of 0.79, 0.70, and 0.79, respectively. To deal with inaccurate pixelwise manual annotations, prediction accuracy was also evaluated against biological truth using immunostaining mean structural similarity indexes (SSIM) of 0.925 and 0.920 for amylase and pan-keratin respectively. Our tool’s disease area quantifications were correlated to the quantifications of immunostaining markers (DAPI, amylase, and cytokeratins; Spearman correlation score = 0.86, 0.97, and 0.92) in unseen dataset (n = 25). Moreover, our tool distinguishes ADM from dysplasia, which are not reliably distinguished with immunostaining, and demonstrates generalizability across murine cohorts with pancreatic disease. We quantified the changes in histologic feature abundance for murine cohorts with oncogenic Kras-driven disease, and the predictions fit biological expectations, showing stromal expansion, a reduction of normal acinar tissue, and an increase in both ADM and dysplasia as disease progresses. Our tool promises to accelerate and improve the quantification of pancreatic disease in animal studies and become a unifying quantification tool across laboratories.


2005 ◽  
Vol 187 (2) ◽  
pp. 217-224 ◽  
Author(s):  
S Morimoto ◽  
C A Mendoza-Rodríguez ◽  
M Hiriart ◽  
M E Larrieta ◽  
P Vital ◽  
...  

Beta-cell apoptosis is responsible for the development of insulin-dependent diabetes mellitus in the streptozotocin (STZ) rat model. It has been demonstrated that steroid hormones possess antioxidant and protective antiapoptotic effects in many tissues. The aim of the present study was to investigate the early apoptotic damage induced by STZ in rat pancreas, and the effect of testosterone in preventing apoptosis of pancreatic β cells. Intact and castrated adult male Wistar rats were subjected to a unique injection of STZ 60 mg/kg (body weight) in citrate buffer, and the kinetics of apoptosis in β cells was assessed. Insulin and glucose were measured by RIA and a glucometer respectively, and in pancreatic tissue by immunohistochemistry. At 6 h after STZ injection, a marked increase in apoptotic β cells was detected; however, glucose and insulin serum levels were not significantly different from the controls. The castrated animals presented higher percentages of apoptotic β cells (65.75 ± 5.42%) than intact males (20.6 ± 4.38%) and castrated, testosterone-substituted males (30.66 ± 1.38%). The decrease in apoptotic β cells induced by testosterone was reversed by the antiandrogen flutamide (67.69 ± 3.45%). The overall results indicate that early apoptotic damage produced by STZ in castrated animals was reversed by testosterone, suggesting that this hormone exerts a natural protective effect in rat pancreas. This effect could help to explain some sexual differences in diabetes mellitus incidence in man, reinforcing the idea that new approaches in steroid hormone therapies should be considered for treatment of this disease.


1999 ◽  
Vol 8 (3) ◽  
pp. 147-151 ◽  
Author(s):  
Max Nyström ◽  
Magnus Bergenfeldt ◽  
Irena Ljungcrantz ◽  
Èsa Lindeheim ◽  
Kjell Ohlsson

Secretory leucocyte protease inhibitor (SLPI) is a potent inhibitor of granulocyte elastase and cathepsin G, and also an inhibitor of pancreatic enzymes like trypsin, chymotrypsin and pancreatic elastase. SLPI has also been shown to inhibit HIV-1 infections by blocking viral DNA synthesis. Since SLPI is an inhibitor of pancreatic proteases we wished to investigate whether SLPI was also actually produced in the pancreas. M-RNA from human pancreatic tissue showed evidence of SLPI production using the reverse transcriptase polymer chain reaction technique (RTPCR). Using immunohistochemical methods SLPI was demonstrated in the β-ce1ls of the islets of Langerhans. The function could be local protease/antiprotease regulation or antiviral/antibacterial defence in the close vicinity of the cell surface, or even inside the β-cell itself.


1967 ◽  
Vol 38 (2) ◽  
pp. 121-143 ◽  
Author(s):  
B. S. PLATT ◽  
R. J. C. STEWART

SUMMARY The endocrine glands of the protein-calorie deficient animals were smaller than those of pigs of the same age normally fed. However, relative to body weight, the adrenals were large, the hypophysis within the normal range, the thymus small and the pancreas and thyroid showed wide variations attributable to different degrees of oedema. In the tissues of the endocrine glands of the protein-calorie deficient animals the cells exhibited a loss of cytoplasm and, when normally present, of secretory granules, the severity of the change varying widely between the different organs of the same animal. Thus the exocrine portion of the pancreas was more severely affected than the islet tissue; within the latter β cells showed greater changes than did α cells. The cells of the thyroid gland were flattened and epithelioid in shape and those of the hypophysis were small, with many partially or wholly degranulated chromophiles. The zona fasciculata of the adrenal cortex was usually less severely affected, with, at some stages, a relatively excessive activity which contributed to the precarious endocrine balance. Since most of the animals were killed before sexual maturity less attention was given to the gonads. Testes, however, appeared to be affected by the deficiency to a greater extent than did ovaries. The relationships between protein-calorie deficiency, hypophysectomy and an excess of corticosteroids are discussed. It is suggested that in protein-calorie deficiency, an adequate supply of protein for anabolic purposes is the primary factor with a subsequent alteration in hormonal secretions playing an important, but secondary, role.


1998 ◽  
Vol 83 (10) ◽  
pp. 3746-3749 ◽  
Author(s):  
J. C. Reubi ◽  
A. Kappeler ◽  
B. Waser ◽  
A. Schonbrunn ◽  
J. Laissue

Somatostatin and octreotide inhibit endocrine pancreatic functions in man, via specific somatostatin receptors. However, the cellular distribution of the different somatostatin receptor subtype proteins has not been determined in the human pancreas. Here, the immunohistochemical distribution of the sst2A receptor was investigated using the sst2A receptor specific anti-peptide antibody R2-88 in cryostat as well as in formalin-fixed paraffin-embedded sections of human pancreatic tissue, and compared with insulin, glucagon and somatostatin immunostaining of adjacent sections. All pancreatic islets were immunostained with R2-88. Most islet cells were labeled: the sst2A receptors were present in insulin as well as glucagon producing cells, but were not detected in intra-islet vessels nor in adjacent acinar tissue. Absorption of the sst2A antibody with 100 nM of the antigen peptide abolished specific staining in tissue sections. Immunohistochemical staining with 125I-Tyr3-octreotide. Therefore, the clinical efficacy of octreotide on glucagon and insulin release can be explained by the presence of sst2A receptors in human A and B pancreatic islet cells. Moreover, absence of sst2A receptors in human acinar tissue suggests that the action of somatostatin on pancreatic exocrine secretion is mediated either indirectly or through a different somatostatin receptor subtype on acinar cells.


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