From that linked study:
>>...These drugs therefore do not restore the defective incretin effect in patients. By contrast, some bariatric surgical procedures enhance GLP-1 responses and also restore the incretin effect in obese individuals with type 2 diabetes. ...

So even bariatric surgery enhances GLP-1 response, *not* GIP response. I had *no* idea - but a minor bit of digging brought up a bit of research proposing that this is an effect of 'persistent hyperglycemia' (high glucose) blocking glucose from entering a number of cells, including alpha cells. https://www.diabetesresearchclinicalpractice.com/article/S0168-8227(24)00815-5/fulltext
The issue seems to be with one of the kinases so in principle similar to insulin resistance in myocytes (skeletal muscle).
Articles like this one that reveal a rabbit hole to dive into are why I subscribe to and read Medium. Thanks for this one!
Also, I'd thought that alpha (and beta) cells had GLUT2 gluclose receptors like those in hepatic (liver) cells, so no insulin required to allow glucose to move across the cell wall. Did I get that wrong?