The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
we know the people with pre-diabetic physiology or diabetic physiology have higher levels of free fatty acids in the blood those are also called non-esterified fatty acids and those fatty acids in the blood signal to the muscles and signal to the liver to become insulin resistant
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the earliest changes you basically see is that they already have elevated levels of free fatty acid circulating so already you can see that in these populations whether the South Asians or Hispanics their visceral fat is already out putting a little bit of extra free fatty acid and we know that free fatty acid is a chemical signal for interrupting insulin resistance sort of signaling so at that point I'm thinking that yes it probably is a capacity issue but I think that early signal is limiting the ability of the muscle to really store that glycogen because it's already inhibiting glycogen synthesis basically at that level already