Insulin release: biochemical and biophysical aspects.
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Biophysical Phenomena↗
Biomedical subjects
I Valverde
Publications and source records attributed to I Valverde.
In vivo stimulation of insulin release by succinic acid methyl esters.
Both the monomethyl and dimethyl esters of succinic acid, administered intravenously to fasted and anesthetized rats, caused a rapid increase in plasma insulin. A positive insulin secretory response to succinic acid monomethyl ester was also observed after intraperitoneal injection to fed and conscious rats. On a molar basis, stimulation of the insulin release, evoked by succinic acid esters, represented about twice that caused by D-glucose. It is speculated that succinic acid esters may be efficient insulin secretagogues even in those models of noninsulin-dependent diabetes characterized by a site-specific defect in the transport of D-glucose or in the early steps of its catabolism in the pancreatic B-cell.
Anesthesia↗
D-glucose metabolism in tumoral pancreatic islet cells with rapid or decreased mitotic activity.
The metabolism of D-glucose was investigated in tumoral islet cells of the RINm5F line with either unaltered or decreased mitotic activity, resulting from the incorporation of D, L-alpha-difluoromethylornithine (DFMO) in the culture medium. In DFMO-treated cells, the oxidation of D-[3,4-14C]glucose was less severely affected than the utilization of D-[5-3H] glucose, at least at hexose concentrations in the 1.0 to 16.7 mM range. This coincided with restoration of the process of glucose-induced stimulation of 3HOH generation from [2-3H]glycerol. Pretreatment with DFMO also resulted in a decreased circulation in the pentose phosphate pathway and the restoration of a preferential stimulation of D-[2-14C]glucose or D-[6-14C]glucose oxidation relative to D-[5-3H]glucose utilization when raising the hexose concentration from 0.2 to 1.0 mM. It is proposed that the interference of cell growth with the metabolic and functional responses of RINm5F cells to D-glucose is relevant to the difference between such responses otherwise found when comparing the behaviour of foetal or neonatal to adult normal islets.
Animals↗
Stimulation of insulin release caused by intraduodenal administration of succinic acid methyl esters.
The methyl esters of succinic and glutamic acid are currently under investigation as possible tools for stimulation of insulin biosynthesis and release in non-insulin-dependent diabetes mellitus. The present study deals with the secretory response of the pancreatic B-cell to these esters after intraduodenal administration to anaesthetized rats. The dimethyl ester of succinic acid and, to a lesser extent, its monomethyl ester both increased the plasma insulin concentration, whilst the dimethyl ester of glutamic acid virtuality failed to do so. The stimulation of insulin release, caused by the dimethyl ester of succinic acid, was faster and more pronounced than that evoked by an equimolar amount of glucose. The present study thus reveals that the latter ester, when administered via the gastrointestinal tract, evokes a more brisk and more ample secretory response of the pancreatic B-cell than that evoked by glucose.
Animals↗