Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
As we age, we are all (including me) worried about neurodegeneration.
Okay, I ran across this - 3 things can help prevent neurodegeneration:
Some of the events in the neurodegenerative cascade can be counteracted in animal models by manipulations that *stabilize neuronal calcium* homeostasis including
1.dietary energy restriction,
2.agonists of glucagon-like peptide 1 receptors and
3.drugs that *activate* mitochondrial potassium channels
Liraglutide and Byetta are ***analogs of a hormone called GLP-1,*** which stimulates insulin secretion and expands insulin-making beta cells in the pancreas.
Of course now (2018) there is: Dulaglutide (Trulicity), a once-weekly glucagon-like peptide-1 (GLP-1) receptor agonist, is now approved as an *adjunct to* diet and exercise in the treatment of type 2 diabetes in adults.
“Berberine induces GLP-1 secretion through activation of bitter taste receptor pathways. Because berberine was found to be a ligand of bitter taste receptor, the results of present study may provide an explanation for some bitter taste substance obtain hypoglycemic effect.”
Which may explain how Gluco-Reg works too (chromium + *BITTER melon,* etc.)
Berberine is one of the ingredients in a supplement called Brain Gain
Ahh…
Quinine is a bitter taste receptor agonist that has been studied its anti-pyretic, anti-malarial, anti-pain, and anti-inflammatory activity. Our data suggest that quinine stimulates the GLP-1 secretion through the bitter taste receptor-signaling pathway, and thus has the possibility of therapeutic agent of T2DM.
Did you all see the TV news re: a woman who stopped eating at 4pm (thus "fasting" longer every day = burn fats instead) lost something like 50 pounds? She ate normally up until 4pm.
So...eating fewer calories/fasting or using a Rx/supplement to lower blood glucose levels helps. Now for the "toughie" - #3
Mitochondria potassium channels:
It was recently reported that mitoKATP channel openers release Ca2+ from Ca2+-loaded mitochondria
I really do NOT want to encourage this (!!!), but I must be honest:
Opening of ATP-sensitive K+ (K(ATP)) channels by the uncoupler of oxidative phosphorylation, 2,4 dinitrophenol (DNP),
has been assumed to be secondary to metabolic inhibition and reduced intracellular ATP levels.
Herein, we present data which show that DNP (200 μM) *can induce opening of cardiac K(ATP) channels*, under whole-cell and inside-out conditions, despite millimolar concentrations of ATP (1-2.5 mM).
Proton-pumping NADH:ubiquinone oxidoreductase (respiratory complex I) is a large membrane protein complex of the inner mitochondrial membrane of most eukaryotes
Remember DNP appears to open the mitochondrial K-ATP channels -> which *inhibits* ROS production via the SAME complex (ubiquinone oxidoreductase) which is in OUR mitochondria AND in many bacteria.
What else can do the same i.e. inhibit ROS production by mitochondria complex 1?
They report that millimolar concentrations of
metformin
directly inhibit complex I activity in a non-competitive manner.
Like all meds AND/OR supplements, there can be dangers, problems, significant side effects for SOME persons (likely due to their underlying genetic handling of them).
The question is: do we want to restore the "health" of the infected cells' mitochondria = allowing the cells to properly finish their job OR do we want to destroy the infected cells and (hopefully) the pathogen is also destroyed at the same time?
SLOWLY destroying the infected cells is what the body IS doing via a route involving P13K -> apoptosis = IF cell death not being inhibited.
It looks like cells containing HIV, when destroyed, also destroys HIV:
HIV-1 infection extends the life span of macrophages by promoting the stress-induced activation of the PI3K/Akt cell survival pathway.
Importantly, various cancers also display the PI3K/Akt activation for long-term cell survival and outgrowth, and Akt inhibitors have been extensively searched as anti-cancer agents.
This led us to investigate whether Akt inhibitors could antagonize ***long-term survival*** and cytoprotective phenotype ***of HIV-1 infected macrophages.***
This study suggests that Akt inhibitors, such as ALP compounds, may serve as potential anti-HIV-1 agents specifically targeting long-living HIV-1 macrophages and microglia reservoirs.
It appears Bb and Cpn like to ultimately hang out in long living macrophages and even in HeLa (cancerous) cells.
Bottom line...there appears to be an intentional calcium overload in our mitochondria which disrupts the function of the mitochondria (our powerhouses)which might be our body's attempted alternative route to destroy the infected cell (ROS = DNA damage)- along with the pathogen which is parasitic (living off our nutrients).
I will try and find other alternatives that also impact ubiquinone oxidoreductase - complex I.
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