Sucrose is a disaccharide composed of a fructose and glucose moiety linked through a glucosidic bond. When ingested sucrose is hydrolysed by the sucrase enzyme to form fructose and glucose within the small intestine. The glucose and fructose are then both absorbed, but have quite different fates. The glucose enters the blood and contributes to the rise in blood glucose levels seen postprandially. This glucose can be passed into tissues to provide energy, with the skeletal muscles and brain making up a large proportion of the recipient tissue. Alternatively the glucose can pass into the liver to undergo a number of fates including the synthesis into glycogen or fatty acids depending on the metabolic needs of the individual. However, the fructose that is absorbed from the gut can only be processed in the liver. The fate of fructose is therefore to be converted to glucose and subsequently stored as glycogen, to be converted to fatty acids, or to be used as a source of energy by the liver cells.
Because fructose is processed by the liver no insulin is released when it enters the blood. In contrast glucose stimulates the release of insulin from the beta cells of the pancreas. The insulin release by glucose is stimulated by gut hormones called incretins in the entero-insulin axis. Two incretins that have been identified as playing a pivotal role in this process are gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP 1). Both of these incretins also decrease glucagon release, which makes sense as glucagon is the antagonistic hormone to insulin and is primarily tasked with raising levels of blood sugar. Evidence suggests that consumption of high intakes of sucrose causes the development of insulin resistance in mammals including humans in just a few short weeks. The exact reason for this is not fully understood, but it is evident that it is the fructose moiety that is responsible for this because fructose alone has a similar effect. Part of the effect of the sucrose might be an inhibitory effect of incretin release.
For example, the response of 19 healthy men and women aged 35 to 55 years to diets containing either starch or sucrose was investigated1. The subjects consumed a normal mixed diet comprised of 43 % carbohydrate, 42 % protein and 15 % fat for 6 weeks, with 30 % of the calories coming from either starch or sucrose. Each diet was followed for 6 weeks, before subjects switched to the alternative diet. The results showed that the GIP response to a sucrose load of 2 grams per kg body weight was significantly greater following consumption of the sucrose diet in comparison to the starch diet. The largest increase in GIP was seen 0.5 hours and 1 hours postprandially when increases of 30 % and 16.3 % were detected. Therefore there is an increase in insulin response in response to sucrose feeding for 6 weeks. The increase in the GIP seen following the sucrose diet may relate to the development of insulin resistance in the peripheral tissues, something that is countered through an increase in the release of insulin.
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