Most of the carbohydrates in your diet are starches. Starches are long chains of glucose that are found in grains, potatoes and various foods. But not all of the starch you eat gets digested. Sometimes a small part of it passes through your digestive tract unchanged. In other words, it is resistant to digestion.

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Resum: The main objective of the present thesis was to evaluate the principal digestive and metabolic consequences of the resistant starch consumption using the pig as a model. To reach this objective 3 experiments were designed. Two of them to study the digestive adaptations and lipogenic responses during the medium- and long-term, and the third one to study the postprandial metabolism. In all the experiments, pigs were feed with 2 diets containing 2 different starches: corn starch CS and raw potato starch RPS as examples of digestible and resistant starch type II.

Colonic starch fermentation resulted in an increase on microbial activity reflected as a higher concentrations of purine bases PB and volatile fatty acids VFA on colonic digesta. As a result of the increased butyrate production in the large bowel digesta of the RPS fed pigs a reduction on the number of apoptosis per crypt of the colonic mucosa 0. Metabolic responses At the end of the experiments, pigs were euthanized and samples of muscular tissues and fat depots were collected in order to study the effect of resistant starch on the activity of lipogenic enzymes ACX, ME, G6PDH and on the intramuscular fat content.

No differences between diets were observed on the intramuscular fat content after a period of adaptation of 38 days. In contrast, resistant starch consumption during a period of 97 days, reduced the intramuscular fat content To explain the differences observed on lipogenic enzyme activities, an additional trial was performed.

In this trial, pigs were fitted with catheters and infused with 6,6-D2 glucose and C acetate in order to study variations between treatments on the glucose and acetate rates of appearance in the systemic pool, and on the plasmatic concentrations of glucose and insulin.

Both glucose and insulin plasmatic concentrations, and the glucose rate of appearance were reduced as a result of RPS consumption. However no differences were observed on the acetate rate of appearance.

This results suggested that the mechanism by which resistant starch consumption decreased lipogenic enzyme activities was through a reduction on the postprandial glycaemia and insulinaemia. The overall results demonstrate that resistant starch consumption promotes adaptations of the gastrointestinal tract in response of the chronic load of substrate to the large bowel.

In addition resistant starch consumption affects the general metabolism, reducing the glucose and insulin postprandial concentrations and as a consequence decreasing lipogenesis.


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