The author of this article [Fernandez-Mejia, 2005: (http://www.ncbi.nlm.nih.gov/pubmed/15992683)] discusses the way high-dose biotin (3-15 mg/d) can reduce fasting blood sugar and triglyceride levels, in part by enhancing glucokinase expression by cells in the liver or other tissues. In my opinion, the use of "high-dose" biotin is more "legitimate" than the use of high-dose pantothenic acid, for example. It's not entirely clear to me that those are even "pharmacological" or supraphysiological dosages, because no one's really researched the physiological responses that occur with graded increases in dosages. The choices for RDAs are essentially arbitrary and have no real basis in physiological reality, in my opinion, but that doesn't mean that every "B-vitamin" or nutrient "should" be increased to some random dosage. The authors of all of the articles discuss the fact that biotin is essentially nontoxic, but there tends to be some built-in reluctance to use those types of higher dosages in research. The authors of some papers still refer to 600-microgram dosages of biotin as "high-dose biotin," etc. There are several studies using the 15 mg/d dosage to lower fasting glucose and triglyceride levels, and humans with biotin-responsive basal ganglia disease (which is a genetic disorder that's distinct from biotinidase deficiency) take either 50 or 100 mg/d of biotin. Large dosages of lipoic acid have been shown to deplete biotin, but I think it wouldn't work in reverse. I mean, I don't think 15 mg/d of biotin would deplete lipoic acid, because, under normal circumstances, there's no free lipoic acid, supposedly (lipoic acid is biosynthesized truly "in situ," with the octanoic acid already attached to the proteins that are lipoylated). That's my sense of it, in any case.
There are some interesting phenomena with biotin, whereby increasing the intake of biotin, in a human, tends to increase the expression of biotin-dependent enzymes. Histone proteins can also be biotinylated by biotinidase, and so biotinidase is not just a "biotin-recycling" enzyme. I think one of the articles on that is called something like, "Biotinidase: not just for recycling biotin." Histone biotinylation can regulate gene expression and could account for some of the effects at higher dosages.
The biotin-dependent enyzyme propionyl-CoA carboxylase is a couple of enzymatic steps away from methylmalonyl-CoA mutase (MMM) in the propionate oxidation pathway, and vitamin B12 supplementation can compensate for the effects of biotin deficiency [Baugh et al., 1968:(http://www.ajcn.org/cgi/reprint/21/2/173.pdf) (http://www.ncbi.nlm.nih.gov/pubmed/5642891)]. Both normal biotin status and normal vitamin B12 (methylcobalamin, etc.) status are required for something like propionyl-L-carnitine to be metabolized normally and to exert its effects. Propionyl-CoA (and related compounds) increases and causes toxic effects in both vitamin B12 and biotin deficiencies, for example. There's research showing that biotin depletion can cause fatty liver disease (mitochondrial injury), and that's what one would expect (there's a series of articles referring to "fatty liver and kidney" syndrome in broiler chickens or something, and one could find the rest of the articles from that starting point) [Whitehead et al., 1976: (http://www.ncbi.nlm.nih.gov/pubmed/1244838); Awrich et al., 1983: (http://www.ncbi.nlm.nih.gov/pubmed/6644449)]. I saw one article talking about a theoretical concern that biotin repletion, meaning the maintenance of normal biotin status, could increase acetyl-CoA carboxylase activity and cause excessive fatty acid synthesis in the liver. In my opinion, that concern is not in line with the research. Awrich et al. (1983) discussed the way that low propionyl-CoA carboxylase activity, such as would result from biotin deficiency, seems to be most strongly linked to the "fatty liver and kidney" syndrome in broiler chickens, and the authors discuss the ways in which that syndrome can mimic Reye's syndrome (which is mitochondrial damage, essentially an acute, very severe form of fatty liver and hyperammonemia that can be induced by viral illnesses in combination with inhibitors of the beta-oxidation of fatty acids) (http://hardcorephysiologyfun.blogspot.com/2009/01/reyes-syndrome-and-coenzyme.html). Even if biotin deficiency doesn't perfectly mimic the severity of Reye's syndrome, Awrich et al. (1983) implied that propionyl-CoA carboxylase may be more sensitive to changes in biotin status than the other biotin-dependent enzymes are. Additionally, acetyl-CoA carboxylase is a highly-regulated enzyme. That would mean that trying to "hide" from acetyl-CoA carboxylase activity would, in my opinion, probably not work, given that acetyl-CoA carboxylase activity would be expected, as implied by Awrich et al. (1983) to be sustained in a person with marginal biotin status. So I don't see how biotin restriction would be a reasonable strategy for inhibiting fatty acid synthesis (by supposedly decreasing acetyl-CoA carboxylase activity). That type of approach tends to not work too well. At least that's my sense of things, based on the literature. And, in people with fatty liver disease, low fat diets tend to be useful in the long term, but a short-term, drastic decrease in fat intake can acutely worsen the liver damage. Propionyl-CoA is really toxic, and so are the "intermediate" metabolites that tend to be associated with elevations in propionyl-CoA (propionate, malonate, methylmalonic acid, methylcitric acid, etc.). Propionyl-CoA can inhibit urea cycle enzymes and thereby produce hyperammonemia and can inhibit the glycine cleavage system, leading to hyperglycinemia, etc. Both hyperglycinemia and hyperammonemia, especially, generally produce neurotoxicity. There are so many toxic effects of methylmalonic acid and propionic acid derivatives that I couldn't begin to cite all of them.
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