I read the Richard K. Bernstein paper which describes tight control of glucose using low doses of insulin and a low carb diet, and then I watched the Robert Unger lecture I linked to in the previous post, and saw a slide of blood glucose
I read the Richard K. Bernstein paper which describes tight control of glucose using low doses of insulin and a low carb diet, and then I watched the Robert Unger lecture I linked to in the previous post, and saw a slide of blood glucose levels in a mouse with no beta cells, given insulin normally (wide fluctuations ranging into hypo- and hyperglycaemia) or given insulin plus a glucagon antagonist.
Also compare the recent case study "Type 1 diabetes mellitus successfully managed with the paleolithic ketogenic diet" by Tóth and Clemens.
"He was put on insulin replacement therapy (38 IU of insulin) and standard conventional diabetes diet with six meals containing 240 grams carbohydrate daily. He followed this regime for 20 days. While on this regime his glucose levels fluctuated between 68–267 mg/dL.
Average blood glucose level while on the standard diabetes diet with insulin was 119 mg/dL while 85 mg/dL on the paleolithic-ketogenic diet without insulin. Fluctuations in glucose levels decreased
as indicated by a reduction of standard deviation values from 47 mg/dL on the standard diabetes diet to 9 mg/dL on the paleolithic-ketogenic diet. Average postprandial glucose elevation on the standard diabetes diet was 23 mg/dL while only 5.4 mg/dL on the paleolithic-ketogenic diet."
Again the question - why does LCHF (or fasting) act like the glucagon receptor antagonist? Why does feeding glucose worsen hyperglycaemia and ketoacidosis, and fat improve them, when fat, and protein, not glucose, are the gluconeogenic and ketogenic substrates?
Could it be that in diabetes - when there is no insulin present, or when the cells of the liver are highly insulin-resistant, or when subcutaneous insulin fails to give attain an adequate concentration in the portal vein feeding the liver - glucose itself in some way promotes gluconeogenesis and ketogenesis?
Consider first that in uncontrolled diabetes blood glucose is very high and becomes even higher after carbohydrate feeding. This is especially so in the portal vein feeding the liver. Hepatocytes without insulin are not resistant to glucose, especially at high concentrations. The Glut2 receptor is not wholly controlled by insulin, though the metabolism of glucose within the cell is.
Concentrations of glucose approaching 10 mM are pre-diabetic levels. Concentrations of glucose above 10 mM are analogous to a diabetic condition within the cell culture system. This is important because the same processes that can affect cells and molecules in 