Biologically Occurring Ketone Bodies.

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Metabolic Intervention With Glp-1 Or Its Biologically Active Analogues To Improve The Function Of The Ischemic And Reperfused Brain

CROSS REFERENCE TO A RELATED APPLICATION This application is a continuation-in-part of provisional application No. 60/103,498 filed Oct. 8, 1998. FIELD OF THE INVENTION This invention relates to an/effective treatment to improve the function of the ischemic and reperfused brain. BACKGROUND OF THE INVENTION Strokes, or cerebrovascular accidents, are the result of an acute obstruction of cerebral blood flow to a region of the brain. There are approximately 500,000 cases each year in the United States, of which 30% are fatal, and hence stroke is the third leading cause of death in the United States. Approximately 80% of strokes are “ischemic” and result from an acute occlusion of a cerebral artery (usually a clot or thrombus), with resultant reduction in blood flow. The remainder are “hemorrhagic”, which are due to rupture of a cerebral artery with hemorrhage into brain tissue and consequent obstruction of blood flow due to local tissue compression, creating ischemia. Stroke commonly affects individuals older than 65 years, and the most powerful risk factor is hypertension. However, there are additional strong risk factors, of which the most important is diabetes mellitus, whi Continue reading >>

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  1. jayhiller21

    Anyone understand ketone bodies utilization?

    From what I can gather, ketone bodies are created during times of prolonged starvation, when OAA is diverted to gluconeogenesis. When OAA gets too low, the krebs cycle cannot continue so the accumulation of acetyl CoA is used to create ketone bodies. Here's what I don't get: Supposedly these ketone bodies are then transferred from the liver to the tissues, where it is turned back into acetyl co A to enter the krebs cycle.
    TLDR, I have one main question. 1) How is acetyl CoA that is made from ketone bodies able to enter the krebs cycle if there supposedly a lack of OAA (b/c of increased gluconeogenesis)?
    Is it that once the body resorts to forming ketone bodies, gluconeogenesis activity has declined, enabling krebs to continue?
    Clarification would be much appreciated!

  2. ryansmith1235515

    I think this answers your question... gluconeogensis occurs mainly in the LIVER. As a result it is true that there is less OAA in the liver now slowing down entry of acetyl coA (made from fatty acid oxidation) in the Krebs cycle. But, Ketone bodies can move in the bloodstream to other tissues where gluconeogensis is not occuring, therefore plenty of OAA to proceed through the Krebs Cycle.
    This is how the liver can use fats to make more energy by breaking down those fats and putting the byproducts (glycerol + fatty acid chains) into the metabolic cycles. I think you can view ketones as a vehicle in which the liver "shares" the breaking down of fats so all tissues in the body can use the energy.
    During long-term starvation, you're body is adapted to stop using as much gluconeogensis and increase ketogensis. The reason is gluconeogensis uses amino acids which requires the breakdown of proteins. You're body would rather breakdown fat than protein so it is advantageous to use fat as a fuel source rather than muscle.
    Let me know what you guys think about these explanations, I'm not 100% sure myself. Metabolism is such a tricky subject!

  3. jayhiller21

    This clears things up, thanks! Ketone bodies acting as an acetyl coa transporter are kind of analogous to how malate transports nadh into the mitochondria...

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