Ketoacidosis Causes

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Diabetes With Ketone Bodies In Dogs

Studies show that female dogs (particularly non-spayed) are more prone to DKA, as are older canines. Diabetic ketoacidosis is best classified through the presence of ketones that exist in the liver, which are directly correlated to the lack of insulin being produced in the body. This is a very serious complication, requiring immediate veterinary intervention. Although a number of dogs can be affected mildly, the majority are very ill. Some dogs will not recover despite treatment, and concurrent disease has been documented in 70% of canines diagnosed with DKA. Diabetes with ketone bodies is also described in veterinary terms as diabetic ketoacidosis or DKA. It is a severe complication of diabetes mellitus. Excess ketone bodies result in acidosis and electrolyte abnormalities, which can lead to a crisis situation for your dog. If left in an untreated state, this condition can and will be fatal. Some dogs who are suffering from diabetic ketoacidosis may present as systemically well. Others will show severe illness. Symptoms may be seen as listed below: Change in appetite (either increase or decrease) Increased thirst Frequent urination Vomiting Abdominal pain Mental dullness Coughing Continue reading >>

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Popular Questions

  1. Christian

    I read conflicting views about whether or not the human body can create glucose out of fat. Can it?

  2. David

    Only about 5–6% of triglyceride (fat) can be converted to glucose in humans.
    This is because triglyceride is made up of one 3-carbon glycerol molecule and three 16- or 18-carbon fatty acids. The glycerol (3/51-to-57 = 5.2–5.9%) can be converted to glucose in the liver by gluconeogenesis (after conversion to dihydroxyacetone phosphate).
    The fatty acid chains, however, are oxidized to acetyl-CoA, which cannot be converted to glucose in humans. Acetyl-CoA is a source of ATP when oxidized in the tricarboxylic acid cycle, but the carbon goes to carbon dioxide. (The molecule of oxaloacetate produced in the cycle only balances the one acetyl-CoA condenses with to enter the cycle, and so cannot be tapped off to gluconeogenesis.)
    So triglyceride is a poor source of glucose in starvation, and that is not its primary function. Some Acetyl-CoA is converted to ketone bodies (acetoacetate and β-hydroxybutyrate) in starvation, which can replace part — but not all — of the brain’s requirement for glucose.
    Plants and some bacteria can convert fatty acids to glucose because they possess the glyoxylate shunt enzymes that allow two molecules of Acetyl-CoA to be converted into malate and then oxaloacetate. This is generally lacking in mammals, although it has been reported in hibernating animals (thanks to @Roland for the last piece of info).

  3. blu potatos

    To be more detailed it is the irreversibly of the reaction carried by Pyruvate dehydrogenase that makes the conversion of the fatty acid chains to glucose impossible. The fatty acids chains are converted to acetyl-CoA.
    Acetyl-CoA to be converted into pyruvate need an enzyme that can do the Pyruvate Dehydrogenase's inverse reaction (in humans there is no such enzyme). Than the pyruvete inside the mitochondria is converted into glucose(gluconeogenesis).

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