Too bad the study he used is behind a paywall. One thing Dr. Fung writes about glucagon being found to not contribute to the effectiveness of the interventions, and there was little difference between the interventions for this. Interesting though, since one of the interventions had them eating lots of carbs, yet their glucagon is described as being insignificantly different from when they ate zero carb or fasted--this in itself is an elevated glucagon in the carb-fed period, since dietary carbohydrate should have driven glucagon down.
Something I also find interesting is how the insulin acts in the second graph. It looks like the total area for insulin is roughly half what it is for the carb-free diet when fasting, and the carb free insulin is roughly half what it is for the standard carby diet. This sort of implies a reserve of insulin secretion capacity in the low carb group. Which is interesting in light of this;
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The overnight fasting glucose concentration decreased from 196 (standard diet) to 160 (carbohydrate-free diet) to 127 mg/dl (fasting)
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Or as Dr. Fung puts it;
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Even then, the carb-free diet does remarkably well – giving you 71% of the benefits of the fasting, without actual fasting.
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Which sort of begs the question--why don't the beta cells secrete the bit of extra insulin needed to bring the blood glucose down in the low carb period, as low as it went in the fasting period? Insufficient
potential insulin secretion doesn't seem to be the problem...
One thing I think could be a factor--that glucagon that didn't decrease, it's possible that the effect of glucagon on the liver's blood glucose production is partly driven by the liver's capacity to produce glucose. In a prolonged fast, the rate of gluconeogenesis is substrate-driven, as protein and carbohydrate metabolism decrease through the fast in favour of fat, availability of amino acids for glucose production decreases.
None of this says that glucagon isn't a good target for intervention, if you could find a way to do it, it would bring down glucose, that would bring down insulin.
Also, none of my babbling really detracts from Dr. Fung's statement that it's the insulin, stupid--because failure of glucagon to decrease with the carbohydrate feeding is likely due to insulin resistance by some cell or other--either the cells that themselves produce glucagon, or the cells that produce other hormones etc. that drive glucagon release.