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Insulin

False Narrative

"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.
But then...

Insulin also has MANY other effects::

Decreased autophagy - decreased level of degradation of damaged organelles. Postprandial levels inhibit autophagy completely.
controlling storage of fat - Decreased lipolysis
as a growth factor.
glycogen synthesis
Increased cellular potassium uptake
decreases production of glucose from noncarbohydrate substrates
Increased lipid synthesis
Increased production of trygly from fatty acids
decreased breakdown of proteins
forces cells to absorb circulating amino acids
forces arterial wall muscle to relax
Inhibits uric acid excretion
Increase in the secretion of hydrochloric acid in the stomach
Decreased renal sodium excretion
enhances learning and memory
increased fertility

( Apoptosis is a process of cell self-destruction, while autophagy is a process of cell self-eating

A couple of pedro's factoids

Liver becomes insulin resistant first, muscles second, adipocytes last.
Insulin levels in the obese remain about 10 times those of a normal person even under complete starvation.

Insulin vs Insulin-sensitivity( opposite of insulin resistance)

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:

Remember:
LPL moves 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.

From https://en.wikipedia.org/wiki/Lipoprotein_lipase#Regulation

<
"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.

Obesity is associated with macrophage accumulation in adipose tissue
https://en.wikipedia.org/wiki/Adipose_tissue_macrophages
(It seems that macrophages are involved in lipolysis regulation in some way )

Artificial Sugar

Insulin testing

Confounded by pro-insulin (has C-peptide attached) (pro insulin only 5% as active as insulin) - but chronically elevated insulin is always a problem (There is a test to see both insulin types).

ROS effects

Effects of Modestly High ROS

Insulin Signaling Pathways: Modestly elevated ROS can enhance insulin signaling pathways. ROS can activate kinases such as Akt and AMPK, which are critical for insulin action and glucose uptake.

    Cell Signaling:
        Stimulation: Modestly high ROS levels can act as signaling molecules, stimulating pathways that promote cell growth, proliferation, and differentiation.

    Mitochondrial Biogenesis:

    Increased Energy Production: Enhanced ROS levels can stimulate mitochondrial biogenesis through the activation of PGC-1α and AMPK, improving cellular energy metabolism and insulin sensitivity.

    Adaptive Stress Responses:
        Hormesis: Low levels of ROS can induce protective stress responses, enhancing the cell's ability to handle oxidative stress.

    Inflammation:
        Mild Activation: Modestly elevated ROS can activate inflammatory pathways, which, if not controlled, may lead to chronic inflammation.

Effects of Low ROS

    Reduced Cell Signaling:
        Diminished Response: Very low ROS levels can impair signaling pathways necessary for normal cell functions, potentially leading to reduced cell proliferation and survival.

    Lower Mitochondrial Biogenesis:

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