Glucose-induced oscillations of cytoplasmic Ca2+ in the pancreatic β-cell

Grapengiesser, Eva; Gylfe, Erik; Hellman, Bo

doi:10.1016/s0006-291x(88)80503-5

Cited by 152 publications

(81 citation statements)

References 19 publications

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“…Intracellular calcium concentration is a key regulator of insulin vesicle secretion (17,43), and in previous publications, oscillations in intracellular calcium concentration have been recorded in both intact islets (44) and in single pancreatic ␤-cells (45). In isolated ␤-cells from mice, three classes of intracellular calcium oscillation have been described, with periods ranging from tens of seconds to a few minutes (46).…”

Section: Discussionmentioning

confidence: 96%

Human Insulin Vesicle Dynamics During Pulsatile Secretion

Michael

Xiong²,

Geng³

et al. 2007

Diabetes

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In healthy individuals, plasma insulin levels oscillate in both fasting and fed states. Numerous studies of isolated pancreata and pancreatic islets support the hypothesis that insulin oscillations arise because the underlying rate of insulin secretion also oscillates; yet, insulin secretion has never been observed to oscillate in individual pancreatic ␤-cells. Using expressed fluorescent vesicle cargo proteins and total internal reflection fluorescence (TIRF) microscopy, we demonstrate that glucose stimulates human pancreatic ␤-cells to secrete insulin vesicles in short, coordinated bursts of ϳ70 vesicles each. Randomization tests and spectral analysis confirmed that the temporal patterns of secretion were not random, instead exhibiting alternating periods of secretion and rest, recurring with statistically significant periods of 15-45 s. Although fluorescent vesicles arrived at the plasma membrane before, during, and after stimulation, their rate of arrival was significantly slower than their rate of secretion, so that their density near the plasma membrane dropped significantly during the cell's response. To study in greater detail the vesicle dynamics during cyclical bursts of secretion, we applied trains of depolarizations once a minute and performed simultaneous membrane capacitance measurements and TIRF imaging. Surprisingly, young fluorescent insulin vesicles contributed at least half of the vesicles secreted in response to a first train, even though young vesicles were vastly outnumbered by older, nonfluorescent vesicles. For subsequent trains, young insulin vesicles contributed progressively less to total secretion, whereas capacitance measurements revealed that total stimulated secretion did not decrease. These results suggest that in human pancreatic ␤-cells, young vesicles are secreted first, and only then are older vesicles recruited for secretion.

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Section: Discussionmentioning

confidence: 96%

Human Insulin Vesicle Dynamics During Pulsatile Secretion

Michael

Xiong²,

Geng³

et al. 2007

Diabetes

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“…'],-oscillations in single B-cells and small B-cell aggregates from mouse [2] are prevented by activation of PKC. Repolarization is an inlikely explanation to the termination of these oscillations, since PKCactivation has been shown to have no effect on average membrane potential in cell suspensions of gIucase stimu!atcd B=ce!…”

Section: Discussionmentioning

confidence: 99%

“…Slow oscillations in [Ca2.c]ir with a period of l-3 min, have previously been demonstrated in single mouse B-cells [2] and in single rat B-cells, purified by autofluorescence-activated cell-sorting [3]. Single mouse B-cells, stimulated with S-10 mM glucose, exhibit bursts of action potentials separated by repolarized intervals with durations ranging between 1 and 4 min [4].…”

Section: Introductionmentioning

confidence: 99%

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

et al. 1992

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“…In 1988 it was discovered that glucose-stimulated individual β-cells show pronounced [Ca 2+ ] i oscillations with a periodicity of 2-6 min (Grapengiesser et al, 1988b). These slow [Ca 2+ ] i oscillations are classical membrane oscillations that depend on the presence of extracellular Ca 2+ and are inhibited by blockers of voltage-dependent Ca 2+ channels ((Grapengiesser et al, 1989a); Table 1).…”

Section: The Cytoplasmic Ca 2+ Concentrationmentioning

confidence: 99%

Oscillatory control of insulin secretion

Tengholm

Gylfe

2009

Molecular and Cellular Endocrinology

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163

169

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Pulsatile insulin secretionSince insulin is the only blood glucose-lowering hormone, its secretion is essential for glucose homeostasis, and disturbances are associated with glucose intolerance and diabetes.Glucose is the major stimulus for insulin release but secretion is enhanced also by other nutrients and is under stimulatory and inhibitory control by hormones and neurotransmitters.Although the external factors are essential determinants of insulin secretion, there are also input-independent variations in hormone release. Regular oscillations of the circulating insulin concentrations in normal subjects consequently occur without accompanying changes

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Glucose-induced oscillations of cytoplasmic Ca2+ in the pancreatic β-cell

Cited by 152 publications

References 19 publications

Human Insulin Vesicle Dynamics During Pulsatile Secretion

Human Insulin Vesicle Dynamics During Pulsatile Secretion

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

Oscillatory control of insulin secretion

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Glucose-induced oscillations of cytoplasmic Ca2+ in the pancreatic β-cell

Cited by 152 publications

References 19 publications

Human Insulin Vesicle Dynamics During Pulsatile Secretion

Human Insulin Vesicle Dynamics During Pulsatile Secretion

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

Oscillatory control of insulin secretion

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Product

Resources

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