PMC:7573190 / 20307-21419 JSONTXT

{"project":"MyTest","denotations":[{"id":"33088259-1683279-29829811","span":{"begin":147,"end":149},"obj":"1683279"},{"id":"33088259-1683279-29829812","span":{"begin":364,"end":366},"obj":"1683279"},{"id":"33088259-9892224-29829813","span":{"begin":552,"end":554},"obj":"9892224"},{"id":"33088259-1371193-29829814","span":{"begin":644,"end":647},"obj":"1371193"},{"id":"33088259-1371193-29829815","span":{"begin":1106,"end":1109},"obj":"1371193"}],"namespaces":[{"prefix":"_base","uri":"https://www.uniprot.org/uniprot/testbase"},{"prefix":"UniProtKB","uri":"https://www.uniprot.org/uniprot/"},{"prefix":"uniprot","uri":"https://www.uniprot.org/uniprotkb/"}],"text":"The initial evidence that NO played a role in the regulation of insulin secretion came from Laychock and colleagues in 1991 (Laychock et al., 1991[70]). They found that sodium nitroprusside by increasing the cGMP level in rat islets, stimulated insulin secretion, while inhibition of NOS decreased glucose- and arginine-induced cGMP release (Laychock et al., 1991[70]). This was further supported by the finding that L-arginine-derived NO increases basal and GSIS in isolated mouse islets (Henningsson and Lundquist, 1998[51]; Henningsson et al., 1999[48]) and the glucose-responsive clonal pancreatic β-cell line HIT-T15 (Schmidt et al., 1992[110]). A concomitant release of insulin and NO is induced by L-arginine in the presence of D-glucose, with the median effective arginine concentrations (EC50) for insulin and NO release equal to 150 µM and 50 µM, respectively, both of which are within the physiological range of circulating L-arginine levels. Interestingly, L-arginine also decreases the EC50 for D-glucose's stimulation of both NO and insulin release (from 15 mM to 5 mM) (Schmidt et al., 1992[110])."}

{"project":"2_test","denotations":[{"id":"33088259-1683279-29829811","span":{"begin":147,"end":149},"obj":"1683279"},{"id":"33088259-1683279-29829812","span":{"begin":364,"end":366},"obj":"1683279"},{"id":"33088259-9892224-29829813","span":{"begin":552,"end":554},"obj":"9892224"},{"id":"33088259-1371193-29829814","span":{"begin":644,"end":647},"obj":"1371193"},{"id":"33088259-1371193-29829815","span":{"begin":1106,"end":1109},"obj":"1371193"}],"text":"The initial evidence that NO played a role in the regulation of insulin secretion came from Laychock and colleagues in 1991 (Laychock et al., 1991[70]). They found that sodium nitroprusside by increasing the cGMP level in rat islets, stimulated insulin secretion, while inhibition of NOS decreased glucose- and arginine-induced cGMP release (Laychock et al., 1991[70]). This was further supported by the finding that L-arginine-derived NO increases basal and GSIS in isolated mouse islets (Henningsson and Lundquist, 1998[51]; Henningsson et al., 1999[48]) and the glucose-responsive clonal pancreatic β-cell line HIT-T15 (Schmidt et al., 1992[110]). A concomitant release of insulin and NO is induced by L-arginine in the presence of D-glucose, with the median effective arginine concentrations (EC50) for insulin and NO release equal to 150 µM and 50 µM, respectively, both of which are within the physiological range of circulating L-arginine levels. Interestingly, L-arginine also decreases the EC50 for D-glucose's stimulation of both NO and insulin release (from 15 mM to 5 mM) (Schmidt et al., 1992[110])."}