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[Correction by succinic acid of behavioral and physiological parameters of neurosis-like condition in white rats].

The neurosis-like state of white rats is accompanied by development of cerebral hypoxia. Negative symptoms of the neurosis-like state (behavioral, anatomic and energy) were decreased by per os administration of succinate (30 mg/kg) during the second half of the neurotization process. Succinate provided chiefly the delayed action on the system arterial tension, on the succinate dehydrogenase and NADH dehydrogenase activity. The effects depended on the propensity of a rat to the catatonic "freezing". The "freezing" was detected by a specific breathing pattern: a short inhale and a long pause. In "freezing" rats succinate corrected the system tension to a greater extent, while in "non-freezing" animals it corrected to a greater extent the succinate and NADH dehydrogenase activities. The positive effect of succinate administration is probably associated with its antihypoxic properties.

Animals↗
PubMed1988

Glyceraldehyde phosphate and methyl esters of succinic acid. Two "new" potent insulin secretagogues.

We discovered that two physiologically occurring metabolic intermediates, glyceraldehyde phosphate and succinate, are potent insulin secretagogues. No other glycolytic intermediate besides glyceraldehyde phosphate was insulinotropic. Succinate, when added to islets as either its monomethyl or dimethyl ester to increase its cellular permeability, was also insulinotropic. In islets, as in other cell types, these esters are apparently hydrolyzed intracellularly to succinate. Unesterified succinate and other unesterified citric acid-cycle intermediates did not stimulate insulin release. Initiation of insulin release by esters of succinate suggests that mitochondrial metabolism alone is sufficient to initiate and support insulin release. However, this is specific for succinate in that esters of fumarate, pyruvate, and citrate were not insulinotropic.

Animals↗