Succinate to boost mitochondrial function?


I've been trying to boost mitochondrial function and scavenge glutamate with high doses of oxaloacetate...but it's expensive and I'm not actually sure it's doing anything.

I saw this diagram...and it got me wondering about succinate instead.

Screenshot 2016-09-05 16.55.27.png

If I'm theoretically not making *enough* GABA due to GAD antibodies, maybe this is a way to bypass that system?

Strangely enough, succinate is also used for menopausal symptoms. I can't quite make that connection yet myself. But the most popular product, Amberen, also contains MSG and that seems counterproductive when there are products available without it.

J Pharmacol Exp Ther. 2008 Mar;324(3):1155-62. Epub 2007 Nov 30.
Succinate ameliorates energy deficits and prevents dysfunction of complex I in injured renal proximal tubular cells.

Nowak G1, Clifton GL, Bakajsova D.


We previously reported that mitochondrial function, intracellular ATP levels, and complex I activity are decreased in renal proximal tubular cells (RPTC) after oxidant (tert-butyl hydroperoxide; TBHP)-induced injury.

This study examined the hypothesis that succinate supplementation decreases mitochondrial dysfunction, ameliorates energy deficits, and increases viability in TBHP-injured RPTC.

Basal and uncoupled respirations in injured RPTC decreased 33 and 35%, respectively, but remained unchanged in injured RPTC supplemented with 10 mM succinate (electron donor to respiratory complex II). State 3 respiration supported by electron donors to complex I decreased 40% in injured RPTC but improved significantly by succinate supplements. The activity of mitochondrial complex I in TBHP-injured RPTC decreased 48%, whereas complex II activity remained unchanged. Succinate supplementation prevented decreases in complex I activity. ATP levels decreased 43% in injured RPTC but were maintained in injured cells supplemented with succinate. Lipid peroxidation increased 19-fold in injured RPTC but only 9-fold in injured cells supplemented with succinate. Exposure of primary cultures of RPTC to TBHP produced 24% cell injury and lysis but no apoptosis. In contrast, no cell lysis was found in RPTC supplemented with succinate.

We conclude that mitochondrial dysfunction and energy deficits in oxidant-injured RPTC are ameliorated by succinate, and we propose that succinate supplementation may prove therapeutically valuable.

Succinate 1) uses an alternate pathway of mitochondrial energy metabolism, 2) improves activity of complex I and oxidation of substrates through complex I, and 3) decreases oxidative stress and cell lysis in oxidant-injured RPTC.


From the supplement info:

Succinic acid or amber acid is a dicarboxylic acid and is an essential component of the Krebs or citric acid cycle, a key metabolic pathway regulating respiratory chain in mitochondria.

Succinic acid expresses various biologic activities: 1) it serves as a natural antibiotic due to its modest acidic or caustic nature; 2) it reduces fatigue and improves brain performance; 3) it decreases gastric secretion relaxes gastric/duodenal smooth muscles; 4) it eases perimenopausal hot flashes; 5) it reduces the effects of hangovers by activating the degradation of acetaldehyde - a toxic byproduct of alcohol metabolism - into CO2 and H2O through aerobic metabolism; 6) it reduces hyperactivation of immune system associated with acute and chronic infectious processes; 7) it reduces joint pain; 8) it accelerates iron absorption; 9) it normalizes adrenal function; 10) it improves glucose control and protects liver function.

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