These articles [Aiello et al., 1983: (http://jds.fass.org/cgi/reprint/67/8/1707.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/6480960); Henning and Hird, 1972: (http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1174516&blobtype=pdf)(http://www.ncbi.nlm.nih.gov/pubmed/4664932)] show that butyrate, such as from the highly-soluble sodium butyrate, is an effective ketogenic substrate in hepatocytes (in the livers of cows) (Aiello et al., 1983) or in the epithelial cells of parts of the GI tract in rabbits (Henning and Hird, 1972). There's nothing that's really magical about a ketogenic compound, and even glucose is obviously an indirect, ketogenic substrate. But the issues of interest are the efficiencies with which different compounds can be converted into ketones and the extents to which increases in the availabilities of different compounds can increase ketone formation or oxidation, etc. Increasing glucose in one's diet is unlikely to increase ketone formation very efficiently, past a certain point, for example.
I should mention that the accumulation of short-chain or branched-chain or long-chain or any other types of acyl-CoA thioesters can potentially contribute to fatty liver disease in the long term or under other circumstances, in different individuals. That's my opinion, and acyl-CoAs just inhibit all sorts of different mitochondrial enzymes and inhibit ATP production, etc., and are thought to contribute to the development of fatty liver disease (http://scholar.google.com/scholar?num=100&hl=en&lr=&q=acyl-CoA+%22fatty+liver%22+mitochondrial). I've discussed this in past postings. Although there is research showing that high-fat diets can sometimes actually be beneficial to fatty liver disease, to the extent that high-protein, low-carbohydrate diets can reduce insulin levels, I find it hard to believe that most people would be able to sustain very high-fat, "ketogenic" diets. Increasing one's fat intake is not necessarily going to cause fatty liver disease, but the point is that cells in the liver and other parts of the bodies of adult humans (such as in astrocytes, in the brain) do not have as much of a capacity to oxidize fatty acids as the cells of children and adolescents do. Most of the research, in my opinion, shows that high fat diets, in combination with the carbohydrates that most people eat and that are almost impossible not to eat, do increase a person's risk of developing fatty liver disease. It's just something to be aware of, given that ketogenic substrates, such as HMB and butyrate, can cause the accumulation of acyl-CoAs that can become toxic, in my opinion.
I think there can be a tendency for people to think that they have to either commit to a full-blown, restrictive, "ketogenic diet" or to do nothing, but those are not the only approaches. I understand that carbohydrate ingestion tends to suppress ketone formation, but this is only true to a certain point, in my view. It's not an all-or-nothing phenomenon. Eating carbohydrates doesn't shut down ketone formation completely, and one doesn't, in my opinion, need to eat 100 grams a day of liquid fats to slightly increase ketone formation by astrocytes or by the liver or intestinal epithelial cells. One approach would be to, of course, talk to one's doctor before taking anything and to discuss the possibility of taking small doses of some of these ketogenic substrates. Researchers are discussing the potential usefulness of an increase in ketone availability in many different conditions, including Alzheimer's disease and psychiatric conditions, etc. But combining small doses of some of these ketogenic compounds with something like resistance exercise, which tends to increase ketone formation and utilization in a more subtle and physiologically-sustainable way, seems, in my opinion, to be a more rational approach than does the use of one of these drastic, high-dose-or-nothing, dietary interventions.
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