Proposed Physiological Mechanisms

Elegant homeostatic regulatory mechanisms exert tight control over blood glucose concentrations during the postprandial period to ensure a smooth transition from the fed to the postabsorptive state. In the normal fed state, nutrients stimulate release of incretins, including glucagon-like peptide-1 (GLP1) and glucose-dependent insulinotropic polypeptide (GIP), into the circulation from endocrine cells located in the gut. The incretins augment the effects of rising blood glucose in stimulating insulin release from the P-cells. Insulin promotes an anabolic response characterized by glucose uptake in liver and muscle, and fat uptake in adipose tissue. In the postabsorptive state, counter-regulatory hormones (i.e., glucagon, epinephrine, cortisol, growth hormone) antagonize insulin action, stimulating release of stored metabolic fuels to maintain euglycemia. Metabolic fuels are directed away from storage via increased hepatic glycogenolysis, lipolysis, and gluconeogenesis.

Meals that are high in GI challenge these regulatory mechanisms, as presented in Fig. 1. To illustrate the dynamic changes that occur following a meal, the postprandial period can be divided into early, middle, and late phases (60). During the early phase (0-2 h after a meal), hyperglycemia can be more than twofold greater following consumption of a high-GI food (e.g., potatoes) compared with a macronutrient-controlled portion of a low-GI food (e.g., legumes) (24,61). Exaggerated hyperglycemia accentuates release of gut hormones and promotes primary hyperinsulinemia, along with hypoglucagonemia. This hormonal milieu enhances the normal anabolic response to feeding described above. The middle postprandial phase (2-4 h after a meal) is marked by a decline in nutrient absorption from the gastrointestinal tract. However, persistent elevation of circulating insulin relative to glucagon stimulates continued glucose uptake by insulin-sensitive tissues, often causing a rapid drop in blood glucose to concentrations below premeal levels. Suppressed circulating free fatty acid concentrations also indicate continued partitioning of nutrients toward storage and away from oxidation. As the body attempts to restore homeostasis, hunger increases due to limited availability of metabolic fuels. During the late postprandial phase (4-6 h after a meal), an exaggerated counterregulatory response elicits increased glycogenolysis, gluconeogenesis, and hepatic glucose output to restore euglycemia. In addition, there is an increase in lipolysis and elevated circulating free fatty acid concentrations. This metabolic state typically would be expected only after fasting for several hours beyond the postprandial period (62).

The adverse effects of a high-GI meal or snack seem to persist beyond the postprandial period, thereby compromising glucose uptake following a subsequent meal. This phenomenon is known as the "second-meal effect" (63). The underlying mechanism likely involves decreased insulin sensitivity with increased concentrations of circulating free fatty acids during the late postprandial phase (64). The second-meal effect has been observed during the postprandial period following breakfast in response to a high-GI dinner or evening snack on the previous day (63,65,66). Likewise, the GI of breakfast can affect glucose disposal at lunch on the same day (67-70).

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