abdominal subcutaneous blood flow increased by 50% in the presence of unchanged glycerol concentrations, indicating stimulated abdominal lipolysis.
It looks like fasting promoted fat burn off the belly rather than elsewhere? This might be useful background with respect to an IF regime. I do not know of an IF advocate that says you should go for 72 hours between feeds, but these mechanisms are good to know about.
I am not sure what to make of the insulin resistance issue (in his Ultimate Diet 2.0 Lyle McDonald says "Now, insulin is a storage hormone, affecting nutrient storage in tissues such as liver, muscle and fat cells. In that same ideal world, we'd have high insulin sensitivity in skeletal muscle (as this would tend to drive more calories into muscle) and poor insulin sensitivity in fat cells (making it harder to store calories there). This is especially true when you're trying to gain muscle.
When you diet, it's actually better to be insulin resistant (note that two of the most effective diet drugs, GH and clenbuterol/ephedrine cause insulin resistance). By limiting the muscle's use of glucose for fuel, insulin resistance not only spares glucose for use by the brain, but also increases the muscles use of fatty acids for fuel." ) UD2.0 is a fantastic book by the way, a real good introduction to nutrition and biochemistry)
Anyway, I hope to get hold of the full article and that is always more helpful than the abstract. The abstract is below:
Effects of a 3-day fast on regional lipid and glucose metabolism in human skeletal muscle and adipose tissue.
Aim: Fasting is characterized by increased whole body lipolysis and lipid oxidation, decreased glucose oxidation and insulin resistance. To identify the regional sources and underlying mechanisms, we studied 10 healthy male volunteers post-absorptively and after 72 h of fasting.
Methods: Each study comprised a 3-h basal period and a 3-h hyperinsulinaemic euglycaemic clamp and we used a combination of leg and forearm arteriovenous techniques, upper and lower body microdialysis and glucose and palmitate tracers.
Results: In the basal state, plasma levels, fluxes and oxidation rates of free fatty acids all roughly doubled after fasting. Palmitate fluxes across the forearm and leg also increased by two to threefold and interstitial leg muscle glycerol concentrations doubled. Subcutaneous femoral glycerol concentrations and blood flows were unaltered, but abdominal subcutaneous blood flow increased by 50% in the presence of unchanged glycerol concentrations, indicating stimulated abdominal lipolysis. During the clamp, we observed whole body insulin resistance and glucose uptake across the leg and forearm decreased by 60%.
Conclusion: Our data show that fasting induces insulin resistance in upper and lower body muscles and suggest that increased lipolysis, is primarily due to the activation of lipolysis in muscle-associated fat (in the leg) and in upper body subcutaneous fat, whereas peripheral subcutaneous fat is spared.