Could you elaborate on the differences? The stim use is more of an acute-IR effect? Of course that would probably still be a bad thing to someone "pre-disposed" to developing T2DM (perhaps an endomorph?), no?
My T2DM references were used as an example of population that is insulin-resistant. Doesn't insulin-resistance and leptin-resistance tend to go hand-in-hand, along with some of the other issues you named, regardless of the development of full-blown T2DM? Doesn't IR lead to LR by the liver overloading the blood with free fatty acids converted from the excess sugar? Therefor, wouldn't increasing insulin sensitivity (such as the metformin study) also increase leptin senitivity and help correct/stabilize many of the issues associated with T2DM & metabolic syndrome?
I think of it as comparing apples to oranges, and the apples have worms in them.
T2DM patients are predisposed to insulin resistance. They can watch what they eat, exercise regularly and still develop some level of IR regardless. I have a family member that falls into this category...she eats very well, exercises every day, maintains a very healthy BMI for her height, and still pulls ~100-105 on a fasting glucose. They have a genetic predisposition because their body handles nutrients differently than those without said predisposition.
It becomes hard to compare a transient IR d/t stimulant use in a normal individual to long-term IR d/t genetic factors in a T2DM individual.
It becomes impossible to compare the exact mechanisms, especially with a disease such as T2DM, because of the multigenic inheritance pattern. There are many genes that can contribute to T2DM, each effecting a different pathway and each having various levels of response to environmental stimuli (overeating, lack of exercise, sedentary lifestyle, etc). One person with T2DM might be very well controlled with metformin for the remainder of their life, while another might require escalating dosages and eventual progression to an oral hypoglycemic with insulin. In these people, not only do they have IR but also an inadequate production of insulin.
Regardless, I think the point of this thread is moot. IR from stimulant use (with concomitant increase in cortisol levels) is transient at best and probably isn't relevant when talking about a cutting cycle...the increase in BMR and liberation of FFAs is a greater reward than the risk of transient IR. Of course, this is all with a GOOD diet. IR in a caloric surplus isn't a good thing, because your body will be aiming to store calories and finds itself having trouble.
Now, someone who abuses caffeine regularly for years and years, sits at work for 10 hours everyday, consumes an excess of (dirty) calories, and hasn't walked more than 15 feet from the couch to the kitchen since they were a teen...well, thats a different story.
mfg: