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Filter by:Human beings are 'omnivores' meaning that all principal components of food (i.e. the macronutrients: carbohydrates, fat, proteins) can be assimilated by the gastrointestinal tract. When the gut mucosa is exposed to dietary changes it adjusts its functional behaviour. For example, a fatty diet demands certain digestive mechanisms, whereas others are needed to take care of a carbohydrate rich diet. Such dietary induced changes in appearance and functionality of the small intestinal mucosa have been described in animals but only little is known about it in man. The present project aims at elucidating in man if a 2 weeks diet dominated by either fat or carbohydrates, but with similar energy content, is associated with changes in the small intestinal mucosal appearance and metabolic signalling capacity.
Endothelial dysfunction of conduit arteries contributes to the increased morbidity and cardiovascular mortality in patients with essential hypertension and appears increasingly as an independent therapeutic target. We have shown previously that besides a decrease in the availability of NO and other endothelium-derived vasodilators factors, the epoxyeicosatrienoic acids, an increase in the vasoconstrictor endothelin-1 (ET-1) may play a role in the pathophysiology of this endothelial dysfunction. Indeed, the local concentrations of endothelin-1 during the endothelium-dependent dilation of the radial artery in response to a sustained increase in blood flow decreased significantly in healthy volunteers controls but not in hypertensive patients. This lack of adaptation of the endothelinergic system could be due to a decreased clearance of endothelin-1 by endothelial ETB receptors, potentiating the vasoconstrictor action of endothelin-1 mediated by ETA receptor activation at the muscular level. However, to validate this hypothesis , it is needed to demonstrate the physiological role of ETA receptor and ETB in sustained flow-mediated dilatation of conduit arteries.