T2DM is straightforward (ish). See:
Basically excess calories are stored as fatty acid in the liver. When it reaches a critical point, the fatty acids end up being stored elsewhere, including the pancreas. Liver storage creates problems with insulin sensitivity. Pancreatic storage creates problems with insulin production. Marked calorie loss = moblising from intra abdo organ stores = no more T2DM.
The liver usually prevents any postprandial peak in blood sugar, and when poisoned by excess fatty acid (how the body keeps stores of excess energy once glucose ok and liver glycogen stores replete, nothing to do with the form of energy it's taken in - fat, carbs, protein all stored in energy dense form) the glucose gets into the systemic circulation. Pancreas is prodded to make insulin and cannot adequately do so.
The genetics are probably a combination of appetite and where you store your fat (intra abdo/subcutaneous).
Since coming across this idea, it has massively simplified my understanding of T2DM and related areas. Patients' questions are easy to answer with this conceptual map.
DOI: family link to the work :-)