Some Questions ...
1. It is known that the adult human brain consumes roughly 23% of total daily caloric expenditure for the "average person". Glucose utilization by the brain has been determined to be at least 100 g/day, the most common figure I've seen is 125-130 g/day, and I've seen up to 150 g/day. In light of this (and absent rare brain GLUT transporter deficiency disease), wouldn't EVERY human have a "carbohydrate tolerance" of at least 100 g/day?
2. Low carb advocates like to focus on the fact that there are approximately 1 to 2 teaspoons or somewhere between 4 to 10 grams of sugar (glucose) dissolved in circulation at any given time. However normal individuals "clear" several times that amount in fairly short order (an OGTT runs 50 to 100 grams of glucose). The "insulin resistance" paradigm implicates a backlog of glucose in the blood stream due to cells with filled up glycogen stores. This sounds like common sense. Why, then, does someone who has restricted carbohydrate for even a day not perform better on an OGTT?
3. If high blood sugars impact ketogenesis, why then do untreated Type 1's go into ketoacidosis along with raging hyperglycemia?
Go ... :-)
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The pivotal role of pyruvate dehydrogenase kinases in metabolic flexibility
http://www.nutritionandmetabolism.com/content/11/1/10
From this perspective, you "should" be able to eat, say, a cup of cooked oatmeal or 3/4 cup of rice or a couple slices of bread with each meal, 3 meals per day, and still be on a "low carb" diet, or at least a "moderate carb" diet.
2) This argument never made sense to me, either. Your car's fuel line probably only contains a few tablespoons of gasoline at a time, but you wouldn't fill up your gas tank with a teaspoon.
2. Physiological IR, due to elevated serum FFA's/NEFA's.
3. They don't. High blood insulin inhibits hepatic ketogenesis. Untreated Type 1's don't have any/enough insulin.
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