In a physiological context, fasting may refer to:
- The metabolic status of a person who has not eaten overnight.
- The metabolic state achieved after complete digestion and absorption of a meal.
Several metabolic adjustments occur during fasting, and some diagnostic tests are used to determine a fasting state. For example, a person is assumed to be fasting after 8–12 hours. Metabolic changes toward the fasting state begin after absorption of a meal (typically three to five hours after a meal); "post-absorptive state" is synonymous with this usage, in contrast to the "post-prandial" state of ongoing digestion. A diagnostic fast refers to prolonged fasting (from 8–72 hours depending on age) conducted under observation for investigation of a problem, usually hypoglycemia. Finally, extended fasting has been recommended as therapy for various conditions by health professionals of most cultures, throughout history, from ancient to modern.
During fasting, post-absorptive state, fatty acid oxidation contributes proportionately more to energy expenditure than does carbohydrate oxidation. This phenomenon is due largely to greater lipid and lower carbohydrate availability, as plasma non-esterified fatty acid (NEFA) concentrations rise in response to lower insulin and higher counter-regulatory hormone concentrations.
Post-absorptive plasma glucose concentration has been discovered to be physiologically maintained within the range of 70 mg/dl [3.9 mmol/l] to 110 mg/dl [6.1 mmol/l] in humans . This is accomplished via increased glucose levels from glucagon and decreased glucose levels from insulin. However, there has not yet been any convincing evidence of the involvement of glucagon in post-absorptive plasma glucose concentration maintenance.
Combined deficiency of insulin and glucagon results in an initial drop in plasma glucose levels, but is followed by an increase in plasma glucose levels. This indicates that there is support of post-absorptive plasma glucose concentrations from glucagon, when in concert with insulin. Changes in plasma glucose concentrations also result from changes in glucose production, but not from glucose utilization. Furthermore, during insulin and partial glucagon deficiency, and the exclusive partial deficiency of glucagon, the rate of glucose appearance increases to a point greater than the rate of glucose disappearance. This rate increase seems to be even larger than during insulin and glucagon deficiency, as well as when glucagon is made exclusively deficient. Both scenarios result in much higher plasma glucose concentrations.
Increases in plasma glucose levels are ultimately followed by plateaus. These plateaus occur within a postabsorptive physiological range, and after octreotide-induced suppression of insulin and glucagon secretion. It has been determined that hormones and additional factors are involved in postabsorptive glucose level maintenance, after short periods of time. However, chronic insulin and glucagon deficiencies still remain victims of diabetes. Therefore, insulin has been proven to contribute to the maintenance of postabsorptive plasma glucose concentrations, while high levels of glucagon are not required to onset diabetes.
These findings do not distinguish the individual roles of insulin and of glucagon. However, chronic insulin and glucagon deficiencies have been proven to cause hyperglycemia and, therefore, strongly suggest that insulin is the predominant factor of postabsorptive glucose levels.