Localization of inorganic phosphate in the pancreatic B cell and its loss on glucose stimulation

Science ◽  
1978 ◽  
Vol 201 (4361) ◽  
pp. 1124-1126 ◽  
Author(s):  
N Freinkel ◽  
K. Pedley ◽  
P Wooding ◽  
R. Dawson
Keyword(s):  
B Cell ◽  
Inorganic Phosphate ◽  
Glucose Stimulation ◽  
Pancreatic B Cell

Subcutaneous Xenotransplantation of Hybrid Artificial Pancreas Encapsulating Pancreatic B Cell Line (MIN6): Functional and Histological Study

1997 ◽  
Vol 6 (5) ◽  
pp. 541-545 ◽  
Author(s):  
Yoshiyuki Kawakami ◽  
Kazutomo Inoue ◽  
Hiroyuki Hayashi ◽  
W.j. Wang ◽  
Hiroshi Setoyama ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
B Cell ◽  
Cell Line ◽  
Histological Study ◽  
Artificial Pancreas ◽  
Bioartificial Pancreas ◽  
Glucose Stimulation ◽  
Min6 Cells ◽  
Pancreatic B Cell ◽  
Endocrine Tissues

The biohybrid artificial pancreas is designed to enclose pancreatic endocrine tissues with a selectively permeable membrane that immunoisolates the graft from the host immune system, allowing those endocrine tissues to survive and control glucose metabolism for an extended period of time. The pancreatic B cell line MIN6 is established from a pancreas B cell tumor occurring in transgenic mice harboring the human insulin promoter gene connected to the SV40 T-antigen hybrid gene. It has been proven that glucose-stimulated insulin secretion in MIN6 cells retains a concentration-dependent response similar to that of normal islets. In this study, we performed the histological and functional examination of three-layer microbeads employing MIN6 cells after subcutaneous xenotransplantation to evaluate this device as bioartificial pancreas. MIN6 cells were microencapsulated in three-layer microbeads formulated with agarose, polystyrene sulfonic acid, polybrene, and carboxymethyl cellulose. Microbeads were xenogenically implanted in the subcutaneous tissue of the back of Lewis rats with streptozotocin-induced diabetes. One week after implantation, microbeads were retrieved and cultured for 24 h before the static incubation. There was no evidence of adhesion to the graft and the fibrosis in the transplantation site as determined by gross visual inspection. Microscopic examination demonstrated that retrieved microbeads maintained normal shape, containing intact MIN6 cells. Histological study showed that these MIN6 cells in the microbeads appeared to be viable without cellular infiltration within or around the microbeads. Immunohistochemical analysis of the microbeads clearly revealed the intense staining of insulin in the cytoplasm of encapsulated MIN6 cells. Insulin productivity of MIN6 cells in the microbeads is strongly suggested to be preserved. In response to 16.7 mM glucose stimulation, static incubation of microbeads 1 wk after implantation caused the 2.3 times increase in insulin secretion seen after 3.3 mM glucose stimulation (84.3 ± 10.0 vs. 37.4 ± 10.7 μU/3 × 106 cells/hr, n = 5 each, p < 0.01). This study demonstrates that three-layer microbeads encapsulating MIN6 cells retain excellent biocompatibility and maintain good insulin secretion even after subcutaneous xenotransplantation, suggesting the possible future clinical application of this unique bioartificial pancreas to subcutaneous xenotransplantation.

Plasmalemma localisation of inorganic phosphate in B cells pancreas

1978 ◽  
Vol 36 (2) ◽  
pp. 528-529
Author(s):  
F. B. P. Wooding ◽  
K. Pedley ◽  
N. Freinkel ◽  
R. M. C. Dawson
Keyword(s):  
Electron Microscope ◽  
B Cells ◽  
B Cell ◽  
Pancreatic Islets ◽  
High Glucose ◽  
Lead Acetate ◽  
Inorganic Phosphate ◽  
Slight Modification ◽  
Uranyl Acetate ◽  
Lead Phosphate

Freinkel et al (1974) demonstrated that isolated perifused rat pancreatic islets reproduceably release up to 50% of their total inorganic phosphate when the concentration of glucose in the perifusion medium is raised.Using a slight modification of the Libanati and Tandler (1969) method for localising inorganic phosphate by fixation-precipitation with glutaraldehyde-lead acetate we can demonstrate there is a significant deposition of lead phosphate (identified by energy dispersive electron microscope microanalysis) at or on the plasmalemma of the B cell of the islets (Fig 1, 3). Islets after incubation in high glucose show very little precipitate at this or any other site (Fig 2). At higher magnification the precipitate seems to be intracellular (Fig 4) but since any use of osmium or uranyl acetate to increase membrane contrast removes the precipitate of lead phosphate it has not been possible to verify this as yet.

Seasonal changes in pancreatic B-cell function in euthermic yellow-bellied marmots

1985 ◽  
Vol 249 (2) ◽  
pp. R159-R165 ◽  
Author(s):  
G. L. Florant ◽  
A. K. Lawrence ◽  
K. Williams ◽  
W. A. Bauman
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
B Cell ◽  
Cell Function ◽  
Peripheral Resistance ◽  
The Body ◽  
Pancreatic B Cell ◽  
Peripheral Insulin Resistance ◽  
Body Weights ◽  
System Input

Fasting plasma insulin (PI) and glucose (PG) concentrations were measured throughout the body weight cycle of marmots. Animals gained weight during summer, and in late fall body weight peaked, after which they ceased feeding. Each month euthermic animals were injected intra-arterially with either dextrose (500 mg/kg) or porcine insulin (0.1 U/kg), and blood samples were collected over the subsequent 2 h. During weight gain fasting PI concentration and pancreatic B-cell response to injected dextrose increased markedly. Maximal insulin release to a dextrose challenge was measured during peak body weight or when body weight initially began to decline. The PG concentration after exogenous insulin administration was slight (less than 10%) in the fall but increased approximately 25% in the spring after marmots lost weight. Basal PG levels were not significantly different throughout the year. Basal fasting PI concentrations were significantly higher during the fall (P less than 0.01). It is suggested that in the fall, when marmots are obese, hyperinsulinemia and peripheral insulin resistance appear. Furthermore, in two animals with an increase in body weight of approximately 30% or less over the summer, peripheral resistance was demonstrable, albeit not as marked as in animals that appropriately doubled their body weights when given food ad libitum. Thus we hypothesize that factors other than adiposity, i.e., food intake, central nervous system input to the pancreatic B-cell, and/or changes in B-cell sensitivity to PG, may contribute to the observed peripheral insulin resistance and may be involved in body weight regulation.

scholarly journals Evidence for two different types of P2 receptors stimulating insulin secretion from pancreatic B cell

1998 ◽  
Vol 125 (6) ◽  
pp. 1368-1374 ◽  
Author(s):  
P Petit ◽  
D Hillaire-Buys ◽  
M Manteghetti ◽  
S Debrus ◽  
J Chapal ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
B Cell ◽  
P2 Receptors ◽  
Pancreatic B Cell ◽  
Different Types

scholarly journals The life story of the pancreatic B cell

Diabetologia ◽  
1984 ◽  
Vol 26 (6) ◽  
Author(s):  
C. Hellerstr�m
Keyword(s):  
B Cell ◽  
Life Story ◽  
Pancreatic B Cell

scholarly journals Protein kinase C activity affects glucose-induced oscillations in cytoplasmic free Ca2+ in the pancreatic B-cell

FEBS Letters ◽  
1992 ◽  
Vol 303 (1) ◽  
pp. 85-90 ◽  
Author(s):  
Henrik Kindmark ◽  
Martin Köhler ◽  
Suad Efendić ◽  
Patrik Rorsman ◽  
Olof Larsson ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
B Cell ◽  
Pancreatic B Cell ◽  
Kinase C ◽  
Protein Kinase C Activity
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