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In-vitro expansion of functional beta cells from the limited number of donated adult human pancreata is an attractive approach for generating an abundant source of cells for beta-cell replacement therapy of diabetes.
The constitutive deleter mice induce deletion in nearly all beta cells from the immediate postnatal period to adulthood and they display normal control of body weight and glycaemia.
Although the beta cells from the cryopreserved islets tended to show a larger Ca2+ entry in response to depolarisation, this was not statistically significant.
Bitransgenic offspring of a cross between both lines then enabled the collection of purified populations of alpha and beta cells from the same islets.
Of the 2,485 beta cells from the three transplant cases that were analysed by confocal microscopy (Fig. 5), the frequency of opposite-sex insulin-expressing cells was 1.5%.
We show that Ins1Cre mice induce efficient and selective recombination of floxed genes in beta cells from the time of birth, with no recombination in the central nervous system.
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Interestingly, PLA2G6 has been reported to protect beta cells from apoptosis via the generation of arachidonic acid and prostaglandin E2 [ 47] and the repair of mitochondrial membrane peroxidation [ 48] as well as modulating oscillations and transients of [Ca+2]i in response to ATP in these cells [ 49].
Cultured beta cells from d20 secreted the same amount of insulin in 15.6 mM than in 5.6 mM glucose (basal conditions), and were characterized by a high basal insulin secretion.
For type 2 diabetes, it would be of considerable interest to study beta cells from subjects with the genetic associations found in GWAS [ 37].
Proinsulin, insulin, and C peptide are stored in granules in the beta cells, from which they are released into the capillaries of the islets in response to appropriate stimuli.
An alternative strategy is to replenish beta cells from stem cells, if the stem cells have the capacity to differentiate into functional beta cells.
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