scholarly journals Insulin, not C-peptide (proinsulin), is present in crinophagic bodies of the pancreatic B-cell.

1984 ◽  
Vol 98 (1) ◽  
pp. 222-228 ◽  
Author(s):  
L Orci ◽  
M Ravazzola ◽  
M Amherdt ◽  
C Yanaihara ◽  
N Yanaihara ◽  
...  
Keyword(s):  
B Cell ◽  
Secretory Granule ◽  
Secretory Granules ◽  
Core Material ◽  
Insulin Degradation ◽  
C Peptide ◽  
Lysosomal Compartment ◽  
Pancreatic B Cell ◽  
Ready Access ◽  
Gain Access

We have obtained evidence by autoradiography and immunocytochemistry that mature secretory granules of the pancreatic B-cell gain access to a lysosomal compartment (multigranular or crinophagic bodies) where the secretory granule content is degraded. Whereas the mature secretory granule content shows both insulin and C-peptide (proinsulin) immunoreactivities, in crinophagic bodies only insulin, but not C-peptide, immunoreactivity was detectable. The absence of C-peptide (proinsulin) immunoreactivity in multigranular bodies, i.e., in early morphological stages of lysosomal digestion, was compatible with the ready access and breakdown of C-peptide and/or proinsulin by lysosomal degrading enzymes, while the insulin crystallized in secretory granule cores remained relatively protected. However, in the final stage of lysosomal digestion, i.e., in residual bodies where the secretory granule core material is no longer present, insulin immunoreactivity became undetectable. Lysosomal digestion thus appears to be a normal pathway for insulin degradation in the pancreatic B-cell.

Glucose intolerance in thyrotoxicosis roles of insulin, glucagon and somatostatin

1987 ◽  
Vol 114 (2) ◽  
pp. 228-234 ◽  
Author(s):  
Karen S. L. Lam ◽  
Rose T. T. Yeung ◽  
Patricia W. M. Ho ◽  
S. K. Lam
Keyword(s):  
B Cell ◽  
Glucose Intolerance ◽  
Plasma Glucose ◽  
Insulin Response ◽  
Oral Glucose ◽  
Insulinogenic Index ◽  
C Peptide ◽  
Pancreatic B Cell ◽  
Significant Difference ◽  
Glucose Ingestion

Abstract. The responses in plasma glucose, insulin, C-peptide, glucagon and somatostatin to an oral glucose load were studied in 10 thyrotoxic patients and 10 matched euthyroid controls. The thyrotoxic patients had higher mean fasting plasma glucose (P < 0.05) and responded to oral glucose with an earlier peak at 30 min which was higher than the corresponding glucose level in the controls (P < 0.05). Impaired glucose tolerance was found in 3 patients. Fasting insulin and C-peptide levels were normal in the thyrotoxic patients when corrected for the higher glucose levels. Following glucose ingestion, there was no significant difference between the areas under the insulin or C-peptide curves in patients and controls, but Seltzer's insulinogenic index was reduced in the patients (P < 0.01) suggesting an impaired pancreatic B-cell response to oral glucose. Mean basal glucagon was normal in the thyrotoxic patients. However, while in the controls plasma glucagon became suppressed following glucose ingestion (P < 0.0001), no significant suppression was found in the patients. In the thyrotoxic patients, mean basal somatostatin was normal, but the area under the somatostatin curve following glucose ingestion was significantly increased (P < 0.02). Our findings suggest that décreased glucagon suppression and impaired insulin response after glucose ingestion are involved in glucose intolerance in thyrotoxicosis. Enhanced somatostatin responses to oral glucose in thyrotoxicosis may have contributed to the observed impairment in pancreatic B-cell responsiveness.

scholarly journals SNAP-25 is expressed in islets of Langerhans and is involved in insulin release.

1995 ◽  
Vol 128 (6) ◽  
pp. 1019-1028 ◽  
Author(s):  
K Sadoul ◽  
J Lang ◽  
C Montecucco ◽  
U Weller ◽  
R Regazzi ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Insulin Secretion ◽  
B Cell ◽  
Insulin Release ◽  
Islet Cells ◽  
Secretory Granules ◽  
Cell Types ◽  
Pancreatic B Cell ◽  
Pancreatic Endocrine Cells ◽  
Presynaptic Plasma Membrane

SNAP-25 is known as a neuron specific molecule involved in the fusion of small synaptic vesicles with the presynaptic plasma membrane. By immunolocalization and Western blot analysis, it is now shown that SNAP-25 is also expressed in pancreatic endocrine cells. Botulinum neurotoxins (BoNT) A and E were used to study the role of SNAP-25 in insulin secretion. These neurotoxins inhibit transmitter release by cleaving SNAP-25 in neurons. Cells from a pancreatic B cell line (HIT) and primary rat islet cells were permeabilized with streptolysin-O to allow toxin entry. SNAP-25 was cleaved by BoNT/A and BoNT/E, resulting in a molecular mass shift of approximately 1 and 3 kD, respectively. Cleavage was accompanied by an inhibition of Ca(++)-stimulated insulin release in both cell types. In HIT cells, a concentration of 30-40 nM BoNT/E gave maximal inhibition of stimulated insulin secretion of approximately 60%, coinciding with essentially complete cleavage of SNAP-25. Half maximal effects in terms of cleavage and inhibition of insulin release were obtained at a concentration of 5-10 nM. The A type toxin showed maximal and half-maximal effects at concentrations of 4 and 2 nM, respectively. In conclusion, the results suggest a role for SNAP-25 in fusion of dense core secretory granules with the plasma membrane in an endocrine cell type- the pancreatic B cell.

Priming of insulin granules for exocytosis by granular Cl− uptake and acidification

2001 ◽  
Vol 114 (11) ◽  
pp. 2145-2154
Author(s):  
Sebastian Barg ◽  
Ping Huang ◽  
Lena Eliasson ◽  
Deborah J. Nelson ◽  
Stefanie Obermüller ◽  
...  
Keyword(s):  
B Cell ◽  
Metabolic Regulation ◽  
Secretory Cell ◽  
Secretory Granules ◽  
Cell Types ◽  
Disulfonic Acid ◽  
Exact Nature ◽  
Pancreatic B Cell ◽  
Insulin Granules ◽  
Cl Channels

ATP-dependent priming of the secretory granules precedes Ca2+-regulated neuroendocrine secretion, but the exact nature of this reaction is not fully established in all secretory cell types. We have further investigated this reaction in the insulin-secreting pancreatic B-cell and demonstrate that granular acidification driven by a V-type H+-ATPase in the granular membrane is a decisive step in priming. This requires simultaneous Cl− uptake through granular ClC-3 Cl− channels. Accordingly, granule acidification and priming are inhibited by agents that prevent transgranular Cl− fluxes, such as 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (DIDS) and an antibody against the ClC-3 channels, but accelerated by increases in the intracellular ATP:ADP ratio or addition of hypoglycemic sulfonylureas. We suggest that this might represent an important mechanism for metabolic regulation of Ca2+-dependent exocytosis that is also likely to be operational in other secretory cell types.

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.

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