n elevated glycaemic response to food is increasingly being seen as a causative factor in the aetiology of the metabolic syndrome. This is problematic because the metabolic syndrome is associated with an increased risk of obesity, cardiovascular disease and type 2 diabetes. The health benefits of fibre are thought to stem in part from its ability to decrease the absorption rates of glucose and thus lower the glycaemic effect of carbohydrates. Legumes are particularly beneficial at reducing glycaemia because they contain high concentrations of soluble fibre that can provide a physical barrier to glucose absorption in the small intestine. However other factors may explain the benefits of legumes including the presence of enzyme inhibitors that block carbohydrate digestion. Legumes are also good sources of protein, and protein is increasingly being found to inhibit gastric emptying and thus delay glucose absorption and improve glycaemic response.
The mechanism by which protein can cause delays to gastric emptying has been extensively researched in the nutritional literature. The general effect is likely one of a physical barrier, because the presence of undigested protein in the stomach results in the release of hormones that inhibit the opening of the pyloric sphincter and thus inhibit passage of food from the non-absorptive surface of the stomach to the absorptive surface of the small intestine. This glycaemic lowering effect for protein has been demonstrated in a number of studies. For example, in one study published in the American Journal of Clinical Nutiriton1 researchers compared the glycaemic effects of a 300 ml drink containing 50 grams glucose with a 300 mL drink containing 50 grams glucose and 30 grams of gelatine. The results showed that the presence of protein in the form of gelatine decreased the glycaemic effects of the glucose when compared to the glucose alone.
In the study, protein also decreased the gastric emptying rate when compared to glucose alone, suggesting that the pyloric sphincter had been inhibited and that the protein caused a containment of the glucose in the stomach. The process by which this occurs is likely a hormonal feedback system involving cholecystokinin (CCK). The presence of undigested protein in the small intestine stimulates I cells in the mucosa of the duodenum, and this causes the release of cholecystokinin into plasma. The cholecystokinin subsequently acts on receptors in the stomach, causing a decrease in motility by inhibition of gastric wall smooth muscle, and limits further food intake by decreasing gastric emptying. Protein also results in a reduction in circulating ghrelin levels when compared to carbohydrate, which is likely the mechanisms by which protein increases satiety and reduces food intake. The evidence that shows high protein intakes are associated with weight loss, supports an appetite regulatory role for protein.
In addition, protein is known to stimulate the release of insulin, with whey protein being particularly insulinogenic. This mechanisms may also explain the lower blood glucose levels seen after carbohydrate consumption with protein, compared to protein alone. The insulinogenic effects of whey protein may relate to the ability of digested and partially digested (hydrolysed) protein (amino acids and peptides) to cause a greater release of glucose-dependent insulinotrophic peptide (GIP) and glucagon-like peptide 1 (GLP-1). These compounds, knows as incretins, are responsible for the release of insulin following an oral glucose load, and explain why insulin release is lower following intravenous glucose, because intravenous glucose does not stimulate incretin release. Both GLP-1 and GIP act on β-cells of the pancreas and have glucose lowering effects, and this explains some of the glycaemic effects of protein.
RdB
