I understand that insulin resistance occurs when one surpasses their personal fat threshold, insulin sensitivity in adipocytes and muscle becomes resistant to energy and energy begins to be deposited around and in the liver and pancreas.
But what about cases of Ketogenic diet?
As far as I know the energy is transported into the cell independent of insulin via acylation stimulating protein and hormone sensitive lipase (open to being wrong). If that was the case then technically insulin receptor sensitivity wouldn’t be an issue? Unless these other mechanisms are also affected?
Trying to be logical about it, I am guessing fat goes to the liver, converted to glucose then released back into the blood stream, causing high blood sugar, even in the presence of low dietary carbohydrate.
It also brings up the question of really overweight individuals, 500lbs+ surely they would have long surpassed their personal fat threshold, yet they still build up significant subcutaneous fat all over the body and not just centrally.
I’m not sure what you’re asking exactly, as low carbohydrate diets- even ketogenic ones- don’t “cause” insulin resistance unless they lead to an energy surplus. Yes, people will still store fat in an energy surplus even if they already have excess adiposity.
I do not think the mechanisms presented here are useful for dietary management, as they are part of much more complex systems.
Apologies, the situation was assumed caloric surplus. What I meant was, given insulin resistance is characterised in part by adipocytes and muscle cells not being able uptake energy due to their reduced sensitivity to insulin… in the low carb/ketogenic diet where insulin levels are low fat is stored via other mechanistic pathways (as opposed to insulin)…
Are these pathways all affected when someone becomes insulin resistant?
I wasn’t trying to use it to infer nutritional changes, but just understand the pathophysiology of insulin resistance onset.
Insulin levels are not low during Calorie surplus with a ketogenic or lower carbohydrate diet. In some studies, they are not lower than what is seen in an individual eating a similar energy level, but with higher carbohydrates. Insulin resistance pathophysiology is very complicated and beyond the scope of what I can answer in a forum reply at this point.
I have seen some overfeeding studies where compared to PUFAs Saturated fat increased hepatic fat significantly more, would this be upstream of insulin resistance onset?