Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pone.0015414
Title: Neuronal calcium sensor synaptotagmin-9 is not involved in the regulation of glucose homeostasis or insulin secretion
Authors: Gustavsson N.
Wang X.
Wang Y.
Seah T.
Xu J.
Radda G.K.
Südhof T.C.
Han W. 
Keywords: calcium ion
glucose
insulin
synaptotagmin
synaptotagmin 9
unclassified drug
calcium
glucose
insulin
synaptotagmin
animal tissue
article
body weight
calcium signaling
controlled study
exocytosis
gene deletion
glucose blood level
glucose homeostasis
glucose tolerance
in vivo study
insulin blood level
insulin release
isolated pancreas islet
mouse
nonhuman
animal
cell membrane
cell membrane potential
drug effect
electric capacitance
electron microscopy
female
genetics
glucose tolerance test
homeostasis
male
metabolism
mouse mutant
nerve cell
pancreas islet
pancreas islet beta cell
patch clamp
physiology
secretion
ultrastructure
Mus
Animals
Body Weight
Calcium
Cell Membrane
Electric Capacitance
Exocytosis
Female
Glucose
Glucose Tolerance Test
Homeostasis
Insulin
Insulin-Secreting Cells
Islets of Langerhans
Male
Membrane Potentials
Mice
Mice, Knockout
Microscopy, Electron
Neurons
Patch-Clamp Techniques
Synaptotagmins
Issue Date: 2010
Citation: Gustavsson N., Wang X., Wang Y., Seah T., Xu J., Radda G.K., Südhof T.C., Han W. (2010). Neuronal calcium sensor synaptotagmin-9 is not involved in the regulation of glucose homeostasis or insulin secretion. PLoS ONE 5 (11) : e15414. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0015414
Rights: Attribution 4.0 International
Abstract: Background:Insulin secretion is a complex and highly regulated process. It is well established that cytoplasmic calcium is a key regulator of insulin secretion, but how elevated intracellular calcium triggers insulin granule exocytosis remains unclear, and we have only begun to define the identities of proteins that are responsible for sensing calcium changes and for transmitting the calcium signal to release machineries. Synaptotagmins are primarily expressed in brain and endocrine cells and exhibit diverse calcium binding properties. Synaptotagmin-1, -2 and -9 are calcium sensors for fast neurotransmitter release in respective brain regions, while synaptotagmin-7 is a positive regulator of calcium-dependent insulin release. Unlike the three neuronal calcium sensors, whose deletion abolished fast neurotransmitter release, synaptotagmin-7 deletion resulted in only partial loss of calcium-dependent insulin secretion, thus suggesting that other calcium-sensors must participate in the regulation of insulin secretion. Of the other synaptotagmin isoforms that are present in pancreatic islets, the neuronal calcium sensor synaptotagmin-9 is expressed at the highest level after synaptotagmin-7. Methodology/Principal Findings: In this study we tested whether synaptotagmin-9 participates in the regulation of glucose-stimulated insulin release by using pancreas-specific synaptotagmin-9 knockout (p-S9X) mice. Deletion of synaptotagmin-9 in the pancreas resulted in no changes in glucose homeostasis or body weight. Glucose tolerance, and insulin secretion in vivo and from isolated islets were not affected in the p-S9X mice. Single-cell capacitance measurements showed no difference in insulin granule exocytosis between p-S9X and control mice. Conclusions:Thus, synaptotagmin-9, although a major calcium sensor in the brain, is not involved in the regulation of glucose-stimulated insulin release from pancreatic b-cells. © 2010 Gustavsson et al.
Source Title: PLoS ONE
URI: https://scholarbank.nus.edu.sg/handle/10635/161797
ISSN: 19326203
DOI: 10.1371/journal.pone.0015414
Rights: Attribution 4.0 International
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