Fri, Jul-22-16, 05:21
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Senior Member
Posts: 15,075
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Plan: mostly milkfat
Stats: 190/152.4/154
BF:
Progress: 104%
Location: Ontario
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Quote:
Originally Posted by inflammabl
The increase in ketones after a meal of MCT might be indirect. That is the dietary fat goes into the energy pool.... reduces the bodies consumption of ketones... more AcAc and BHOB is converted into Acetone.... and acetone increases because it stops being metabolized when we eat more fat than our body is asking for.
So ketonix measures just one ketone, Acetone, a ketone that is not made directly from fat. Second ketones are a "difference" variable, that is a quantity that is the difference between two different processes, generation and consumption of ketones. So it's hard to say why, exactly, there are more or less.
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Interesting point... reminds me of this
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2671041/
Basically, looking at effects of MCT's vs hypoglycemia. They mention that MCT's can readily cross the blood brain barrier, so besides contributing to ketone production in the liver, they can get past that obstacle to fat oxidation as a direct energy source for the brain.
Quote:
Medium-chain triglycerides, a source of medium-chain fatty acids, have been widely used for nutritional support and in patients with malabsorption (10,25). Medium-chain fatty acids are rapidly absorbed and oxidized in the liver. This results in an excess of acetyl-CoA, and in turn the rapid production of ketones (10), an energy source for the brain (3,5,7). Furthermore, medium-chain fatty acids readily cross the BBB and are metabolized by the brain (13). Therefore, medium-chain fatty acids could directly and/or indirectly, via the generation of ketones, act to preserve brain function during hypoglycemia by provision of alternative fuels without raising blood glucose levels in patients with type 1 diabetes.
Medium-chain triglyceride ingestion raised plasma β-hydroxybutyrate and FFA levels during insulin-induced hypoglycemia, and thus both fuels might contribute to the observed effects on cognitive performance. The hippocampal slice data, however, suggest that the predominant impact of medium-chain fatty acids is mediated via the generation of ketones. β-Hydroxybutyrate supported synaptic transmission both at rest and during stimulus trains when glucose supply was deficient, whereas octanoate alone was ineffective. The failure to see an effect of octanoate in the hippocampal slice preparation reflects a time-dependent effect, and longer prior exposure to medium-chain fatty acids might have improved neuronal function. Alternatively, these findings may be explained by differences in brain metabolism of ketones and medium-chain fatty acids. Evidence suggests that octanoate is exclusively metabolized by astrocytes (13,26,27), whereas ketones are oxidized by both neurons and astrocytes (28,29). The finding that octanoate was able to improve the rate of recovery of synaptic function upon restoration of control glucose concentrations, but not the response to hypoglycemia itself, is consistent with the hypothesis that astrocytes may be critical for the restoration of synaptic function after a metabolic challenge such as hypoglycemia.
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