Great question.

I was researching similar myself. GLUT4 would, apparently be less active at the surface. GLUT4 status and ChREBP influence each other via a few feedback loops.

https://www.cell.com/cell-reports/pdf/S2211-1247(17)31411-0.pdf

https://www.nature.com/articles/nature10986/figures/2

Article Absence of Carbohydrate Response Element Binding Protein in ...

And I forgot to mention, some context: creating new fat cells is an adaptive response against insulin resistance. Overstuffed adipose cells cause inflammatory processes and lead to b-cell exhaustion and high insulin levels. (Check out attached file from Dr. Jason Feng). Europeans are more likely to be obese than other races, but when exposed to the same modern diet other races are more likely to become diabetic, without the obesity. This is because they are less capable of generating happy new tiny baby fat cells that can soak up glycerides and glucose without trouble -- if those are in excess, which is not ideal.

The above is part of the functional context within which the likes of ChREBP influence adiposite differentiation.

Thanks @Eric Klein, I've been reviewing lot's of diseases from their genetic basis, it's obvious that diabetes is polygenic (especially taking into account it's a multifactorial disease). Interesting, I haven't come across a study that reveled the creation of new fat cells and it's relationship within the European population in comparison to other races, but I definitely know it can be managed with manipulation of environmental factors (ex: diet, physical activity, etc.) Which alongside other biological factors, are superior in the prediction of diabetes as of now, since there are >70 genetic mutations associated with diabetes but aren't necessarily expressed in all diabetics cases.