Originally, this effect was attributed solely to prolonged glucose absorption. However, according to a newer study, the improvement is a result of the physiological properties of the carbohydrates that are typically found in LGI foods, not simply a diminished glucose response.1 Two major properties of carbohydrates affecting glucose tolerance after a second meal are presented below:
Prolonged Glucose Absorption:
A possible mode of action is that slower postprandial carbohydrate absorption minimizes postprandial glycemia, which, in turn, minimizes postprandial insulin levels. Reduced insulin levels should decrease the likelihood of glucose falling to below fasting levels and triggering the formation of ketone bodies and the release of nonesterified fatty acids (NEFAs). The net result is enhanced glucose uptake by peripheral tissues.
More recent data indicate that colonic fermentation, via short-chain fatty acids (SCFAs) can also play a major role in promoting the second-meal effect. Fermentable carbohydrates stimulate glucagon-like peptide-1 (GLP-1). Although a direct connection between colonic fermentation and carbohydrate metabolism has been established, 12 a detailed mechanism is not yet available. Likely, such a link is mediated through SCFAs that are produced as a result of colonic fermentation. A growing body of animal data indicates that SCFAs mediate GLP-1, an incretin hormone that is secreted by enteroendocrine L cells located in the distal small intestine and colon in response to food intake.13 According to Drucker et al,13 this hormone plays a key role in the regulation of carbohydrate metabolism in three ways: 1) It promotes increased beta-cell mass in the pancreas by stimulating beta-cell proliferation and by inhibiting apoptosis. 2) It helps to control glycemia by acting on glucose sensors, inhibiting gastric emptying, reducing food intake, and decreasing glucagon secretion. And, 3) it strongly stimulates insulin secretion in patients with type 2 diabetes.