Fasting is the simplest and fastest method to force your body to burn sugar for energy. Glucose in the blood is the most easily accessible source of energy for the body. Fasting is merely the flip side of eating – if you are not eating you are fasting. When you eat, your body stores food energy. When you fast, your body burns food energy. If you simply lengthen out your periods of fasting, you can burn off the stored sugar.
To make matters worse for the inactive, carb addict, when the body senses glucose in the bloodstream, the pancreas releases a hormone called insulin (perhaps you’ve heard of it?) to signal the body to store the glucose as glycogen. If the glycogen receptors are full and it can’t do this, the body thinks that the cells didn’t get the message and releases even more insulin.
A: Fasting plasma glucose and weight change 2 years after randomization either to gastric banding or to intensive medical therapy for weight loss and glucose control. Data plotted with permission from Dixon et al. (13). B: Early changes in fasting plasma glucose level following pancreatoduodenal bypass surgery. A decrease into the normal range was seen within 7 days. Reproduced with permission from Taylor (98).

Some medical professionals use an Oral Glucose Tolerance Test (OGTT) to test for diabetes. If you’ve ever been pregnant and had to drink the sickeningly sweet sugar cocktail and then have blood drawn, you are familiar with this one. Basically, a patient is given 50-75 grams of glucose in concentrated solution and his blood sugar response is measured. I’m not a fan of this test because no one should be ingesting that much concentrated glucose, and the test is not a completely accurate measure. (Just a side note: if you are a drinker of the “Big Gulp” drinks or large amounts of soda, you are putting your body through a similar test each day! Eventually, your body will respond, probably with something like “Fine, you want diabetes, I’ll show you diabetes!)
Storage of liver fat can only occur when daily calorie intake exceeds expenditure. Sucrose overfeeding for 3 weeks has been shown to cause a 30% increase in liver fat content (37). The associated metabolic stress on hepatocytes was reflected by a simultaneous 30% rise in serum alanine aminotransferase (ALT) levels, and both liver fat and serum ALT returned to normal levels during a subsequent hypocaloric diet. Superimposed upon a positive calorie balance, the extent of portal vein hyperinsulinemia determines how rapidly conversion of excess sugars to fatty acid occurs in the liver. In groups of both obese and nonobese subjects, it was found that those with higher plasma insulin levels have markedly increased rates of hepatic de novo lipogenesis (2,38,39). Conversely, in type 1 diabetes the relatively low insulin concentration in the portal vein (as a consequence of insulin injection into subcutaneous tissue) is associated with subnormal liver fat content (40). Initiation of subcutaneous insulin therapy in type 2 diabetes brings about a decrease in portal insulin delivery by suppression of pancreatic insulin secretion and, hence, a decrease in liver fat (41). Hypocaloric diet (42), physical activity (43), or thiazolidinedione use (23,44) each reduces insulin secretion and decreases liver fat content. Newly synthesized triacylglycerol in the liver will be either oxidized, exported, or stored as hepatic triacylglycerol. Because transport of fatty acid into mitochondria for oxidation is inhibited by the malonyl-CoA produced during de novo lipogenesis, newly synthesized triacylglycerol is preferentially directed toward storage or export. Hence, hepatic fat content and plasma VLDL triacylglycerol levels are increased.
During this 8-week study, β-cell function was tested by a gold standard method that used a stepped glucose infusion with subsequent arginine bolus (21). In type 2 diabetes, the glucose-induced initial rapid peak of insulin secretion (the first phase insulin response) typically is absent. This was confirmed at baseline in the study, but the first phase response increased gradually over 8 weeks of a very-low-calorie diet to become indistinguishable from that of age- and weight-matched nondiabetic control subjects. The maximum insulin response, as elicited by arginine bolus during hyperglycemia, also normalized. Pancreas fat content decreased gradually during the study period to become the same as that in the control group, a time course matching that of the increase in both first phase and total insulin secretion (Fig. 3). Fat content in the islets was not directly measured, although it is known that islets take up fat avidly (24) and that islet fat content closely reflects total pancreatic fat content in animal models (25). Although a cause-and-effect relationship between raised intraorgan fat levels and metabolic effect has not yet been proven, the time course data following the dietary intervention study are highly suggestive of a causal link (21).

Like the sulfonylureas, meglitinides is a class of drugs that work by promoting insulin secretion from the pancreas. Unlike the sulfonylureas, which last longer in the body, repaglinide (Prandin) and nateglinide (Starlix) are very short acting, with peak effects within one hour. For this reason, they are given up to three times a day just before meals.