Today, there is a dramatic increase in the prevalence of metabolic disorders linked to the “insulin resistance syndrome”. In particular, obesity and maturity onset diabetes is being referred to as an epidemic, and from a public health perspective preventive actions are needed. One factor that could be exploited is a diet characterised by low GI foods. Such a diet has been implemented as one important tool in the prevention1,2 and treatment3,4 of diseases related to insulin resistance, and appears to ameliorate not only the insulin resistance per se, but also certain metabolic ramifications of a lowered insulin sensitivity.
There are several ways of altering the GI features of carbohydrate foods, either through the choice of raw material or food processing conditions. Of particular relevance is to exploit possibilities to optimise the GI of cereal products since a high GI characterizes most of the commonly produced bread and breakfast cereals5. Among the food factors that are known to lower the rate of glucose delivery to the blood from cereal products are the inclusion of coarse cereal grains and/or viscous cereal dietary fiber in bread and macromolecular interactions in pasta.8 In addition, certain organic acids have shown to lower postprandial blood glucose and insulin responses in healthy humans, when included in bread-based meals.9-11 In the case of bread added with the sodium salt of propionic acid, the reduced glycaemia observed in healthy humans was caused by a reduced gastric emptying rate.10,12 Also in a study with acetic acid, the improved glycaemia could be attributed to a decreased gastric emptying rate.
However, the lowering of glucose and insulin responses to bread with lactic acid could not be assigned to a reduced rate of gastric emptying, but instead to an obstruction of the amylolysis rate.12 Recent data have confirmed the hypothesis that the presence of lactic acid reduces the rate of starch digestion in bread. In addition, available data also suggest that the lactic acid needs to be present during baking of the bread, suggesting that this acid induce an enzyme barrier during heat-treatment of the starch substrate.
The nature of the enzyme barrier at the molecular level is not known. However, a higher level of gluten appears to promote a lowered rate of starch digestion in vitro, suggesting some interaction between starch and gluten in the presence of lactic acid. Until now the potential benefits of lactic acid has mainly been tested in vitro, and in acute11 or semi acute meal studies (“second-meal” studies) in healthy humans. In a previous study performed in obese Zucker (fa/fa) rats it was shown that orally supplied sodium salt of propionic acid lowered fasting plasma glucose, d excretion of glucose in urine and total liver cholesterol pools. Work by Tajiri et al, has shown that organic acids extracted from sediments of rice vinegar have the ability to reduce fasting blood glucose levels in diabetic mice and rats.
To evaluate the semi long-term metabolic impact of a diet containing lactic acid, we designed an intervention in rats. Obese and hyperinsulinaemic Zucker (fa/fa) rats were used because they are generally considered as a good model of human obesity, and related metabolic disturbances. The purpose was firstly, to evaluate potential effects of wheat bread containing lactic acid on glucose tolerance and blood lipids; and secondly to investigate if a wheat bread diet with added lactic acid differed regarding metabolic impact depending on whether or not lactic acid was added prior to, or after baking. Finally, since lactic acid is produced by certain Lactobacillus species, the possible impact of L plantarum 299v was investigated by adding this probiotic bacteria to a wheat bread diet; that is, in the absence of lactic acid. The level of lactic acid added before baking of the wheat bread, or added to the diet, was chosen to match a level that was previously reported to lower the rate of in vitro starch digestion.
