Well, this is largely rooted in speculation, but for curiosity's sake - stay with me.
The theory is based on mitochondrial efficiency, or how well the electron transport chain can create and maintain a H+ concentration gradient across the inner mitochondrial membrane. This concentration gradient is used to drive ATPsynthase to generate ATP. If you had a leaky membrane and you were losing hydrogen ions, you'd be losing that gradient you worked so hard to create. Like trying to fill a bucket with a hole in the bottom, you'd have to turn up the water (substrate) to get it to fill up.
Uncoupling proteins essentially act as holes in the mitochondrial membrane, allowing protons to pass through them without harnessing their potential energy and this makes the electron transport chain less efficient - requiring more substrate to create "X" amount of ATP.
|Depiction of an uncoupling protein releasing H+ from intermembrane space|
Could uncoupling proteins be the culprit? How does training effect mitochondrial efficiency? Could obese people just be really efficient at making ATP? Does it matter?