If I am rich enough to have a down payment for a Bay Area house I’ll be tremendously in debt. But that wouldn’t put me in the same boat as someone with oodles of credit card debt.

I’m guessing in endurance athletes it’s there because it’s about to be used. In the obese it’s there because they’re running out of places to put fat.

Right - but even then, if a super fit endurance athlete stops exercising, they don't immediately become diabetic. The upstream cause (what biochemical stimulus is driving the fat deposition?) is probably where the key insight lies.

If I recall correctly there were some studies that actually showed endurance runners have higher type 2 diabetes risk. And the suspect cause was the diet, specifically the carb loading practice and the abuse of high sugar products during the activity. So the three categories may actually share the same baseline, insulin resistance. It was quite controversial when it emerged (see Tim Noakes story), not sure if it's more accepted these days.

This is very interesting to a diabetic like myself, who is slightly underweight.

I've even had some people tell me I can't be diabetic because I don't have much, if any, extra fat.

Well yeah. You’re measuring the output to a multi-variate function. There should be no expectation that this one output drives other occasionally correlated outputs to other functions.

Doesn’t diabetes mean that the cells has to extract more energy from those lipid droplets instead of from the glucose pathway impacted by the diabetes? Thus in the cases of 2 and 3 those droplets is an additional significant source of energy.

I also think that in the case of 1 the cells may be starving on glucose pathways (pre-diabetes), similar to 3 during the exercise and to 2 in regular situation, and that causes the over-eating while all that food doesn’t feed the cells because of the original issue and thus goes into fat for storage and into the lipid droplets way of feeding the cells to workaround the original glucose pathway issue.