Context #1. The easiest way to explain gluconeogenesis (GNG) is how it relates to starvation. If you’re not eating food, your brain still needs a steady supply of fuel. Mostly glucose at first (ketones come later), but since you’re not eating anything, glucose comes from hepatic GNG (huge potential supply*) or glycogenolysis (limited supply). *One of the precursors for GNG, glycerol, comes from stored fat (which you’ll die of something else before you run out of stored fat bc GNG).
In this case, it is mostly true that GNG is demand-driven.
If you’re interested in this, more HERE.
Context #2. Protein (which also contains GNG precursors) doesn’t acutely increase glucose. But you might think protein does convert to glucose via GNG but protein also induces a splash of insulin which is why blood glucose doesn’t rise. Read this blog post at least up to the awesome Fromentin study: “8% of the blood glucose produced under optimal gluconeogenic conditions came from dietary protein.” But also check out the Conn & Newburgh studies. And Gannon.
This is usually the reason recreational keto dieters say they can be high protein, which either ends up looking like PSMF or it’s probably not very ketogenic (which doesn’t really matter in this #context; protein is restricted in therapeutic ketogenic diets).
#BenignDietaryKetosis #BDK
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Context #3. the mouse doctor is in 🙂
Context #3b. Chronic high protein.
Context #4. Random thoughts on animal foods.
measure urinary acetoacetate (AcAc) and reflect the degree of ketosis in the blood probably about 2-4 hours ago. 
measure beta-hydroxybutyrate (bHB) right now. bHB fluctuates to a greater degree, eg, it plummets after a meal whereas AcAc takes longer to decline. AcAc/bHB is usually around 1, but increases after a meal (