The explanation for T2D from the PDF paper from your own link explicitly singles out carbs and explains why they are critical to causing the disease process you describe.

> During any one period of time, if more calories are ingested than metabolized then any fat excess is stored either subcutaneously, viscerally or in the liver. But any excess carbohydrate cannot be stored once the glycogen depots are full. If more glucose is ingested than can be oxidized for energy or stored as glycogen, it has to be turned into fat by the process of de novo lipogenesis. This process only happens in the liver in humans, and triglyceride synthesized in situ is particularly likely to be stored in hepatocytes rather than exported for safe storage in subcutaneous adipose tissue.

> The newly synthesized fat has three possible fates: it can be oxidized for energy; exported as VLDL in the plasma to be delivered to other tissues or it can be stored in a rather full liver. As de novo lipogenesis is stimulated by insulin, those people who are relatively insulin resistant in muscle—and who therefore have a raised plasma insulin level—are especially likely to accumulate fat in the liver. This could explain the reason why muscle insulin resistance is the first detectable signal of risk for Type 2 diabetes.

https://www.ncl.ac.uk/media/wwwnclacuk/newcastlemagneticreso...