This is a fundamental pathophysiological fact of type 2 diabetes mellitus: sufficient residual insulin secretion suppresses lipolysis and hepatic ketogenesis, preventing diabetic ketoacidosis, which is why patients typically present with hyperosmolar hyperglycemic state instead.
The claim is a well-established physiological principle that does not require citation of specific retrieved literature to be verified, as it defines the classic distinction between type 1 and type 2 diabetes crises.