QUOTE from Dr Fung (emphasis mine):
“INSULIN IS NORMALLY released when we eat. It directs some of the incoming glucose to be used as energy and some to be stored for later use. In the short term, glucose is stored as glycogen in the liver, but the liver’s storage space for glycogen is limited. Once it’s full, excess glucose is stored as fat: that is, the liver begins manufacturing fat from glucose through de novo lipogenesis. After the meal, as insulin levels fall, this process reverses. With no food energy coming in, stored food energy must be retrieved. Glycogen and fat stores in the liver are turned back into glucose and distributed to the rest of the body for energy.
The liver acts like a balloon. As energy comes in, it fills up. As energy is needed, it deflates. Balancing feeding and fasting periods over a day ensures that no net fat is gained or lost.
But what happens if the liver is already crammed full of fat? Insulin then tries to force more fat and sugar into the liver, even though it’s already full of fat and sugar. Just as it is more difficult to inflate a fully inflated balloon, insulin has more difficulty trying to shove more fat into a fatty liver. It takes higher and higher levels of insulin to move the same amount of food energy into a fatty liver. The body is now resistant to the efforts of insulin, since normal levels will not be enough to push sugar into the liver. Voilà—insulin resistance in the liver.
The liver, like an overinflated balloon, will try to expel the sugar back into circulation, so continuously high insulin levels are also required to keep it bottled up in the liver. If insulin levels start to drop, the stored fat and sugar comes whooshing out. To compensate, the body keeps raising its insulin levels. Thus, insulin resistance leads to higher insulin levels. High insulin levels encourage more storage of sugar and fat in the liver, which causes even more over-cramming of fat in the already fatty liver, causing more insulin resistance—a classic vicious cycle.” 
NOTE (my commentary)
Fatty liver is already a major concern for insulin resistance, but it’s also a disease in its own right. Dr Fung mentions the reality that the pancreas also becomes clogged with fat, like a fatty liver, and that this is a major problem with insulin production. It’s not that the insulin-producing cells become tired and exhausted, it’s that they are unable to function because the pancreas is clogged with fat particles just like the liver.
Insulin then tries to force more fat and sugar into the liver, even though it’s already full of fat and sugar.
These fat particles are fuel for consumption, and when the body burns fat for fuel they will be consumed by preference. Studies related to people with bariatric surgery indicate that it is the loss of this organ fat which leads directly to the reversal of insulin resistance in type 2 diabetes. Bariatric patients recover from diabetes before they have lost a great deal of weight. Therefore it is the fat in the liver and pancreas which is a significant cause of both insulin resistance and type 2 diabetes.
If insulin levels start to drop, the stored fat and sugar comes whooshing out.
This “whooshing out” explains the Dawn Phenomenon. But it’s positive – sugar comes out from where it was hidden in the liver and now is visible in the blood. When it is gone, fat burning will begin.
STRATEGY: Do not be perturbed by unexpected increases in blood sugar while fasting. If you are not eating, and increase, by definition, comes from sugar in hiding. It, too, must be consumed.
What gets my attention?
Do I understand the need or problem?
Do I understand the potential solution?
Do I understand how to apply that strategy?
What questions do I have for the experts? What might be the answers?
Who needs to hear this?
What do I do next?
SOURCE – Footnotes:
 “The Obesity Code: Unlocking the Secrets of Weight Loss” by Dr. Jason Fung, Timothy Noakes, page 165.
Image: On-Off Switch.jpg From Wikimedia Commons
Please review the page How and Why We Use Quotes.
Key: Fung01-16.69 Last Revision: 01/13/2022.