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Biologically Occurring Ketone Bodies.

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Tutorial Series On Lipids

Tutorials and lectures on lipids Index Set of Powerpoint files covering Lipid Chemistry and Lipid Metabolomics Lipids defined Lipid Definition Categories of lipids Fatty Acyls [FA] Glycerolipids [GL] Glycerophospholipids [GP] Sphingolipids [SP] Sterol lipids [ST] Prenol lipids [PR] Saccharolipids [SL] Polyketides [PK] Biological functions References References and resources See Also Author Recommendations and tools Tutorial Series on Lipid Chemistry and Lipid Metabolomics Presented as a set of Powerpoint files A: Lipid Chemistry Lipid chemistry and classification B: Lipid Metabolomics Lipid Definition A lipid is generally considered to be any molecule that is insoluble in water and soluble in organic solvents. Biological lipids usually refer to a broad grouping of naturally occurring molecules which includes fatty acids, waxes, eicosanoids, monoglycerides, diglycerides, triglycerides, phospholipids, sphingolipids, sterols, terpenes, prenols, fat-soluble vitamins (such as vitamins A, D, E and K) and others [1,2,3], in contrast to the other major groupings of biological molecules, namely the nucleic acids, amino acids, and carbohydrates (sugars). The main biological functions of lipi Continue reading >>

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Popular Questions

  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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