Rising sugar levels after skipping meal

Look up dawn phenomenon (or foot on floor phenomenon as it’s also sometimes called). Basically your liver gives everyone a shot of glucose to get up and going. In diabetics that normal event is sometimes messed up and keeps on giving! In some people it continues for hours and is only turned off earlier with a small amount of food (differing people find non carb or carbs better). Kind of like the liver thinks you’re starving and keeps on “helping”. Eating makes it realise you’re not and it behaves. If you do coffee with cream or bulletproof this might be enough, some use a little cheese, yoghurt etc or a single egg.

I was very much one of these that suffered a lot but am very slowly finding now 10mnths into low carb/keto and fairly frequent 16/8 fasting it’s getting a little better and doesn’t go as high or continue for as long without food.

The language in this is a bit baffling but I think it explains this phenomenon. If anyone can simplify what it says so the layman can understand it, go right ahead . "
Hormonal Regulation Of Hepatic Glucose Production In Health And Disease
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3131084/
"
HGP and diabetes
Unlike muscle and adipose insulin resistance, which antedate hyperglycemia by years and remain relatively stable throughout the course of the disease (Weyer et al., 1999), the rise of HGP occurs ‘late’ in the natural history of diabetes, but appears to worsen progressively, and to become refractory to treatment (Monnier et al., 2007). In type 2 diabetes, HGP is higher in the post-absorptive state, and fails to be properly suppressed by insulin, resulting primarily from excessive gluconeogenesis, rather than glycogenolysis (Rizza, 2010). As HGP is inversely correlated to insulin levels (Bogardus et al., 1984), its increase likely reflects as much the plight of the β-cell as it does a deterioration of hepatic insulin action.

Several factors contribute to elevated gluconeogenesis in diabetes: (i) increased supply of glucogenic precursors to the liver (glycerol, amino acids, free fatty acids); (ii) increased liver lipid content; (iii) cytokines and adipokines; (iv) altered glucagon-to-insulin ratios; (v) in rodents, vagal control originating in the hypothalamus; and (vi) decreased insulin receptor signaling in hepatocytes (Figure 1)."

Some other baffling terms: https://www.nextgurukul.in/nganswer...emical-Coordination-and-Integration/82999.htm

Sorry, that probably wan't helpful, was it? My head is hurting trying to make sense of it. People talk about a "liver dump" causing a rise in BG when you skip a meal or after waking and moving around, but it's a more complicated to understand exactly what is going on... Is it glucose stored in the liver only that can be "dumped"? Is it glucose that was made from carbohydrates only or from other sources, like protein and does it make any difference anyway? Is it due to insulin resistance not being able to deal with the glucose being "dumped" by the liver that causes BG levels in diabetics to be higher at these times? Or is there some other hormonal aspect at play that makes the liver dump more in diabetics than in non-diabetics? Also, if you a eat low or zero carb diet long enough, does your liver eventually run out of stored glucose and the BG fasting levels would eventually come down, or does it still go on making glucose from the protein you are eating and continue to "dump" it out at a higher level than your insulin production / insulin resistance cells can keep up with?