I’ve been really trying to understand the mechanism of how T2D is caused by excessive fat gain.
I understand that the pancreas can no longer produce sufficient insulin to remove blood glucose, but what leads to this point? The obvious line of thought would be increased production of insulin due to excess carbohydrate intake.
However, what about a low-carb diet? Technically people can still excessive weight and get diabetes this way (without the choric rise in insulin).
Has it got something to do with hormone-sensitive lipase?
Or do pro-inflammatory cytokines from excess adiposity have an independent impact on pancreas function?
Brilliant thank you, I will take a listen
I have read this a couple times now over the last few months, it explains it very well. Once specific physiology question I have that is not answered (as it’s pretty nuanced) is on the conversion of glucose to triglycerides.
It was my understanding that glucose is preferentially stored as glycogen, and increased glucose consumption meant increased glucose oxidation, therefore to store subcutaneous fat, liver glycogen must be at capacity?
Would that be correct? Or can one store glycogen and glucose (via conversion to TAGs) happen at the same time?
I think in the article it’s just explained as excess energy is stored as fat.
I am assuming in insulin resistance scenarios, the storage mechanism is the same, but the fat is now within the liver or visceral.
Edit: From further research it appears to be converted to FFA in the liver then transported to adipocytes?