Quote:
Originally posted by Natrushka
Gluconeogenesis takes place under the influence of glucagon, not insulin. If you have extra glucagon floating around in your system, insulin cannot be present in large quantities (and vice versa). So, if insulin is not present, how can this knock you out of ketosis?
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OK, I seem to have answered my own question again
I am
quoting here , from a biochemist who answered my question elsewhere. His answer is taken from
Koolman and Röhm, 1994
Gluconeogenesis, or the
de novo synthesis of glucose, occurs predominantly in the liver. The kidneys also have high gluconeogenetic activity. However, because of the much smaller mass of these cells, the contribution of the kidneys to the synthesis of glucose is only about 10% of the total. The main precursors of gluconeogenesis are
amino acids derived from the muscles. Prolonged fasting, therefore, results in a massive degradation of muscle protein. A further important precursor is lactate, which is formed in red blood cells and in muscles when oxygen is in short supply. Glycerol produced from the degradation of fats can also sustain gluconeogenesis. In contrast, the conversion of fatty acids to glucose is not possible in animal metabolism. Humans can synthesize several hundred grams of glucose per day by gluconeogenesis.
Cortisol,
glucagon, and
epinephrine promote gluconeogenesis, whereas
insulin inhibits it.
When the body senses a drop in the blood glucose level, the liver relies on glycogen (or muscle starch) degradation to supply glucose. Even though the muscles have glycogen, they can’t degrade it so the glucose molecules are sent into the blood stream so other tissues can use them. Moreover, the amount of liver glycogen is very limited, so it can rely on its degradation to supply blood glucose for only a limited period of time. Glycogen reserves are already depleted after a day of fasting, and the blood glucose level begins to fall. Not much later, however, it regains its original value, and the glycogen reserves of the liver also begin to recover. Both effects are due to the onset of gluconeogenesis.
So, it is possible to make glucose out of proteins, in fact we do that all the time. Whenever the blood glucose level drops, signals are sent to put the gluconeogenetic machinery to work. However, this process is under the control of glucagon, cortisol or epinephrine, the three of them acting under different circumstances. Glucagon and insulin don’t work both at the same time “
on”. That is, if glucagon is “
on” and controlling gluconeogenesis, insulin is “
off”, and vice versa. Following this reasoning, if insulin is off (actually that means not present in excess), fat storage is also controlled, and fat release from the fat cells is favored (another process influenced by glucagon).
The process of gaining weight by storing fat into the fat cells needs fat, on one side, and insulin on the other side to activate the process. The process of gaining weight by making fat requires excess carbohydrates on one side and insulin on the other side to activate fat synthesis. With glucagon being released instead, a signal of low carbohydrate, these processes are inhibited. Thus, the mere conversion of amino acids into glucose by gluconeogenesis should not be misunderstood as a mechanism through which fat can be synthesized or deposited into the fat cells. The glucose produced by gluconeogenesis has a “
tag” on it, if you will, and it will serve to supply for blood glucose when the levels fall.
Ketones are produced from fatty acids. Other triggering situations that increase the production of ketone bodies are starvation (true starvation), prolonged severe exercise and uncontrolled diabetes. Suppose that your muscles are well adjusted now to use fatty acids very efficiently for the production of respiratory energy. Saying that the muscles are well adjusted to the utilization of fatty acids for production of energy is not the same as saying that the muscles utilize ketone bodies all the time. They are different things, and even though ketosis may be detected at any given time, it doesn't mean that all the energy is being produced from their metabolism. If muscles are well adapted for fatty acid utilization, the amount available for ketosis is limited and ketones may not increase at any given time.
It is important to note that the utilization of fatty acids seems to be regulated at four different levels. First, the rate of lipolysis itself from triglycerides (to form free fatty acids). Second, the mobilization of fatty acids from the adipose tissue. Third, their transport into the mitochondrion, and finally the availability of important co-enzymes inside the mitochondria for beta oxidation of fatty acids, and the presence of a key enzyme as well.
When the muscle is adapted to fatty acid utilization for respiratory energy, those factors play in such way that the source for ketones may be restricted. That could explain why ketosis may not be always detected, not really because they are completely utilized (which can also occur), but because they are not being made so they can accumulate in the first place.
Nat
L-Gltamine and ketosis
Testing for ketosis, however, can be tricky. What you eat, how much water you drink, and how much exercise you do, all greatly effect your readings- or lack there of.
They are tempermental devices, at the best of times.
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