Effects of Carbohydrase-inhibiting Polyphenols on Glycaemic Response in Vivo

The world health organisation has reported that over 220 million people suffer from diabetes worldwide and that by the year 2030, this number will be doubled. The WHO also reports that in 2004, about 3.4 million people died from high blood sugar (WHO fact sheet number 312, January 2011). About 90% of all diabetes cases is due to type II diabetes. Type 2 diabetes is largely due to overweight and lack of physical activity characterised by high glucose levels (hyperglycaemia).

In the human diet, the source of blood glucose are carbohydrates. Dietary carbohydrate is important to maintain glycaemic homeostasis and provides the most of the energy in the diets of most people. The control of blood glucose is a hormonal process and it is very important to human physiology. Hormonal processes involve the release of insulin from the β- cells of the pancreatic cells which stimulates the uptake of glucose after a meal, to other tissues either for utilisation (glycolysis) or to be stored in the liver as glycogen (glycogenesis). When blood glucose falls below normal, glucagon is secreted from the pancreatic α-cells and it promotes liver glucose production by inducing the generation of glucose from non carbohydrate substrates such as amino and fatty acids (gluconeogenesis) and the generation of glucose from glycogen (glycogenolysis). In addition to insulin and glucagon, there are gut hormones which also play a role in controlling plasma glucose concentrations in the body. The two important peptide hormones are called Glucagon like peptides-1 (GLP-1) and Gastric Inhibitory Polypeptide (GIP). They are said to have incretin activity (promotion of glucose dependent insulin secretion). GIP is secreted from the upper small intestines by the K cells and its primary function is to stimulate glucose-dependent insulin secretion by acting on pancreatic islets. It also stimulates glucagon and it is said to respond to the presence of nutrients (Seino et al., 2010). GLP-1 is secreted from the lower intestine and colon by the L cells following exposure to ingested nutrients. It also stimulates insulin secretion and biosynthesis but inhibits glucagon. GLP-1 is said to have other health and disease related functions (Marathe et al., 2013).

When the glucose homeostasis hormonal control fails, it entails high blood glucose levels (postprandial hyperglycaemia) which can lead to metabolic syndrome which includes obesity, impaired glucose tolerance (IGT), hypertension and dyslipidemia. Disturbance of glucose homeostasis can also lead to other symptoms such as inflammation and oxidative stress at the whole body level as well as disturbances of the functionality in several organs as well as diabetes (Hanhineva et al). Therefore, as much as carbohydrates are required in the human body as a major source of energy, too much in the diet can have adverse health effects especially the one with high glycaemic effect.

The proposed mechanism adapted from (Aston, 2006) of how carbohydrates may affect human health is that when there is a continual presence of high glycaemic index foods in the diet, this gives rise to postprandial glucose rise as well as high insulin demand to act on the high blood glucose levels in the blood. This is by the action of the hormones GIP and GLP-1 which stimulates insulin release when they sense the presence of nutrients. Postprandial glucose rise and high insulin demand may lead to insulin resistance which is the major component of metabolic syndrome. High insulin demand may also lead to β-cell failure which may also result in hyperglycaemia which is also a cause of insulin resistance. Insulin resitance and hyperglycaemia are risk factors for metabolic syndrome and diabetes type 2.

Scientific evidence suggest that postprandial hyperglycaemia in humans has a major role to play in health priorities like type 2 diabetes and blood glucose control. It has been reported that about 90% of all diabetes cases consist of type 2 diabetes. Apart from type I and type 2 diabetes, there are other related conditions which include pre-diabetes (impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) as well as metabolic syndrome (obesity, hypertension and insulin resistance). It has been reported that pre-diabetes and metabolic syndrome increases the risk of developing cardiovascular disease and diabetes mellitus (Coutinho et al., 1999). The glycaemic index was originally proposed with the aim of managing diabetes. However, recent studies have shown that the GI has potential in the prevention of type 2 diabetes as well as in the treatment of metabolic syndrome. Research has shown that high GI diets are associated with increased risk of developing type 2 diabetes (Hodge et al., 2004) and (Steven et al., 2002). More research by (Mckeown et al., 2004) and (Scaglioni et al., 2004) have shown that high GI diet is associated with a number of abnormalities like increased metabolic syndrome and insulin resistance. In the same way, a low GI diet is said to improve insulin sensitivity but more research is needed to support this. A few studies like that of (Frost et al., 1996) have shown this to be the case. However it was observed that it was difficult to know whether this was as a result of improved insulin sensitivity, or improved insulin secretion or due to reduced rate of glucose absorption.