When our bodies are deprived of normal amounts of food they consume their own fat reserves, with the fat inside organs used up first. The idea of Taylor's diet is to use up the fat that is clogging up the pancreas and preventing it from creating insulin, until normal glucose levels return. With my GP's blessing and a home glucose-testing kit, I began my experiment.
Eight categories of diabetes medicine are available in pill form: metformin (a biguanide), sulfonylureas, thiazolidinediones, meglitinides, alpha-glucosidase inhibitors, sodium-glucose transporter 2 (SGLT2), dipeptidyl peptidase-4 (DPP-4) inhibitors, and bile acid sequestrants. Each medicine has good points and bad points. Your doctor will decide which medicine is right for you.
Chronic exposure of β-cells to triacylglycerol or fatty acids either in vitro or in vivo decreases β-cell capacity to respond to an acute increase in glucose levels (57,58). This concept is far from new (59,60), but the observations of what happens during reversal of diabetes provide a new perspective. β-Cells avidly import fatty acids through the CD36 transporter (24,61) and respond to increased fatty acid supply by storing the excess as triacylglycerol (62). The cellular process of insulin secretion in response to an increase in glucose supply depends on ATP generation by glucose oxidation. However, in the context of an oversupply of fatty acids, such chronic nutrient surfeit prevents further increases in ATP production. Increased fatty acid availability inhibits both pyruvate cycling, which is normally increased during an acute increase in glucose availability, and pyruvate dehydrogenase activity, the major rate-limiting enzyme of glucose oxidation (63). Fatty acids have been shown to inhibit β-cell proliferation in vitro by induction of the cell cycle inhibitors p16 and p18, and this effect is magnified by increased glucose concentration (64). This antiproliferative effect is specifically prevented by small interfering RNA knockdown of the inhibitors. In the Zucker diabetic fatty rat, a genetic model of spontaneous type 2 diabetes, the onset of hyperglycemia is preceded by a rapid increase in pancreatic fat (58). It is particularly noteworthy that the onset of diabetes in this genetic model is completely preventable by restriction of food intake (65), illustrating the interaction between genetic susceptibility and environmental factors.