Thu, Jul-09-15, 13:18
|
 |
Senior Member
Posts: 15,075
|
|
Plan: mostly milkfat
Stats: 190/152.4/154
BF:
Progress: 104%
Location: Ontario
|
|
It's hard to do the low glucose without the high ketones. I guess that'd be called a coma.
There have been studies with exogenous ketones done by Dom D'Agostino's group.
Quote:
Ketone supplementation decreases tumor cell viability and prolongs survival of mice with metastatic cancer.
Poff AM1, Ari C, Arnold P, Seyfried TN, D'Agostino DP.
Author information
Abstract
Cancer cells express an abnormal metabolism characterized by increased glucose consumption owing to genetic mutations and mitochondrial dysfunction. Previous studies indicate that unlike healthy tissues, cancer cells are unable to effectively use ketone bodies for energy. Furthermore, ketones inhibit the proliferation and viability of cultured tumor cells. As the Warburg effect is especially prominent in metastatic cells, we hypothesized that dietary ketone supplementation would inhibit metastatic cancer progression in vivo. Proliferation and viability were measured in the highly metastatic VM-M3 cells cultured in the presence and absence of β-hydroxybutyrate (βHB). Adult male inbred VM mice were implanted subcutaneously with firefly luciferase-tagged syngeneic VM-M3 cells. Mice were fed a standard diet supplemented with either 1,3-butanediol (BD) or a ketone ester (KE), which are metabolized to the ketone bodies βHB and acetoacetate. Tumor growth was monitored by in vivo bioluminescent imaging. Survival time, tumor growth rate, blood glucose, blood βHB and body weight were measured throughout the survival study. Ketone supplementation decreased proliferation and viability of the VM-M3 cells grown in vitro, even in the presence of high glucose. Dietary ketone supplementation with BD and KE prolonged survival in VM-M3 mice with systemic metastatic cancer by 51 and 69%, respectively (p < 0.05). Ketone administration elicited anticancer effects in vitro and in vivo independent of glucose levels or calorie restriction. The use of supplemental ketone precursors as a cancer treatment should be further investigated in animal models to determine potential for future clinical use.
|
Something I've found interesting lately is how ketones participate in the Krebs cycle. There's an enzyme that converts succinyl-CoA to succinate. To convert acetoacetate back to acetyl-CoA for oxidation in the cycle, an alternate pathway is involved. This produces acetyl-Coa and succinate from the ketone and succinyl-CoA, bypassing that other enzyme. That makes it a possible work-around if mitochondrial respiration were compromised somewhere around that neighbourhood.
A lot of amino acids are synthesized from krebs cycle intermediates, with an added amine group, so you can see how subverting some portions of the krebs cycle could feed into cancer growth.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4235292/
edited to add link. |
Linear Mode
