Postprandial glucose excursion is the precise, transient elevation in plasma glucose concentration that occurs following the ingestion and subsequent digestion of a carbohydrate-containing meal, reflecting the body’s acute metabolic load. This measurement is a critical physiological marker for assessing the efficiency of the body’s insulin-mediated glucose clearance and overall metabolic flexibility. An excessive or prolonged excursion indicates compromised insulin sensitivity or impaired pancreatic beta-cell function, serving as an early clinical indicator of developing metabolic dysregulation and chronic disease risk.
Origin
The term is derived from Latin: post (after), prandium (a meal), and excursion (a movement outward or deviation). The clinical significance of this measurement became central to endocrinology with the understanding of glucose homeostasis and the pathogenesis of Type 2 diabetes. It is a fundamental concept in assessing the acute stress placed upon the endocrine system by dietary intake.
Mechanism
The mechanism begins with the gastrointestinal absorption of glucose, leading to a rapid rise in blood sugar, which acts as the primary stimulus for the pancreatic beta-cells to secrete insulin. Insulin then binds to its peripheral receptors, primarily on muscle and adipose tissue, initiating the uptake and storage of glucose, thereby lowering the plasma concentration back to baseline. The magnitude and duration of the excursion are determined by the quantity and type of carbohydrate consumed, the functional capacity of the beta-cells, and the degree of peripheral tissue insulin sensitivity.
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