When fat cells become hypertrophic, they release inflammatory mediators and experience macrophage infiltration, which is associated with insulin resistance and vascular endothelial dysfunction.

“They release all sorts of inflammatory mediators, and they have macrophage infiltration, inflammation in the adipocyte depots. Adipose macrophage infiltration is associated with insulin resistance and vascular endothelial dysfunction in obese subjects.”

“There's very good evidence that in individuals who are insulin resistant, fat cells are broken. I'll talk about why later in this podcast, but fat cells are broken, and they cannot divide. They cannot do hyperplasia, they can only hypertrophy. So, the fat cells get bigger and bigger and bigger, and they balloon, and they get inflamed, and there's infiltration of macrophages and other immune cells. They release lipokines, they release inflammatory mediators, they release non-esterified fatty acids, and all of human physiology goes into the toilet because you become insulin resistant when your fat cells can't divide.”

“as these fat cells expand they become distended they release inflammatory mediators they release lipokines they become resistant to the signals of insulin and they start releasing free fatty acids all of the time”

“insulin resistance is is dysfunction of the adipose tissue dysfunction of the fatty the fat tissue in the human body where the fat tissue becomes sort of like hypertrophic instead of hyperplastic so the fat cells can't divide anymore they just get really really big and they leak out inflammatory mediators lipokines and then they actually leak out non-sterified fatty acids signaling to the periphery to become insulin resistant inappropriately”