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"Insulin is a natural protein that regulates energy consumption and blood sugar levels in the body. "While not exactly untrue, what it leaves out is so huge that it is wrong. While insulin has an effect on BG levels; the relative sensitivity to insulin is just as an important part of the control loop.
Insulin also has MANY other effects::
What is most important to realize is that insulin-sensitivity is
just as important for glucose regulation as insulin. And it
is also important to realize there is not one insulin-sensitivity
- muscles, liver, and adipose tissue react differently.
And you HAVE to be a bit insulin resistant to lose weight.
So how to get insulin resistance in adipose tissue with-out having high BG? low-carb diet - and avoiding PUFA’s
I was asked: "If you eat low carb you become insulin resistant?"
Yes! - hopefully. Any diet that works - has to create insulin resistance. Insulin resistance is what lets fat leave adipose tissue(fat cells). ( You can also get into ketosis by any calorie restriction - normal people are in ketosis when they wake up - and this state includes some insulin resistance.)
If you are insulin sensitive and/or have a high insulin level - fat accumulates in adipose tissue. Only when you are insulin resistant and have lower insulin can fat leave these cells.
From wikipedia: There is a constant flux of FFA (Free Fatty Acids) entering and leaving adipose tissue. The net direction of this flux is controlled by insulin and leptin—if insulin is elevated, then there is a net inward flux of FFA, and only when insulin is low can FFA leave adipose tissue. Insulin secretion is stimulated by high blood sugar, which results from consuming carbohydrates.
The adipose insulin sensitivity is controlled by the F:N ratio that Petro talks about:
LPL move fat in to fat cells. HSL moves fat out of fat cells.
insulin is known to activate LPL in adipocytes
HSL is inhibited by insulin.
So here is the take home - there is nothing wrong with being insulin resistant - IF BG and thus insulin is low. Two ways to get there - starvation diet or low-carb.
This is a simplification - other bits are involved - leptin, ASP
are also involved and there are effects of the autonomic nervous
system as well. Remember that man does not know his biology
completely - so likely there are bits we are missing.Also insulin
apparently has the opposite effect on muscle tissue - as it should
see Effects of
insulin and exercise on muscle lipoprotein lipase activity in
man and its relation to insulin action.
"LPL isozymes are regulated differently depending on the tissue. For example, insulin is known to
activate LPL in adipocytes and its placement in the capillary endothelium. By contrast, insulin has
been shown to decrease expression of muscle LPL. Muscle and myocardial LPL is instead activated
by glucagon and adrenaline. This helps to explain why during fasting, LPL activity increases in
muscle tissue and decreases in adipose tissue, whereas after a meal, the opposite occurs."
So apparently the type of LPL is different depending on the tissue? Opposite for adipose tissue?
This little detail had bothered me for a while.. sort of a lose-end to tie up.. Can't get at all the
references - but I think this is correct.
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