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Tissue-engineered skin is a significant advance in the field of wound healing. It has mainly been developed because of limitations associated with the use of autografts and allografts where the donor site suffers from pain, infection, and scarring. Recently, tissue-engineered skin replacements have been finding widespread application, especially in the case of burns, where the major limiting factor is the availability of autologous skin. The development of a bioartificial skin facilitates the treatment of patients with deep burns and various skin-related disorders. The present review gives a comprehensive overview of the developments and future prospects of scaffolds as skin substitutes for tissue repair and regeneration.

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The portal appearance of enteral alpha-ketoglutarate (AKG) and the effect of enteral or parenteral AKG on portal net appearance of glucose, short-chain fatty acids, alanine, aspartate, glutamate, glutamine, proline and insulin were investigated in three growing pigs. During the experimental samplings the pigs were fed hourly with a standard feed mix with 5% glucose (control), 5% AKG (enteral) or no feed additive but continuously infused with AKG into the mesenteric vein in an amount equivalent to 5% of feed intake (parenteral). The arterial plasma concentration of AKG increased (p < 0.05) following both enteral (from 16+/-2 to 22+/-3 micromol/l) and parenteral (from 16+/-2 to 425+/-27 micromol/l) administration of AKG. With the enteral treatment 4+/-1% of the AKG could be accounted for in the portal vein, however, with the parenteral treatment 86+/-5% could be accounted for in the portal vein. The arterial plasma concentration of proline increased (p < 0.05) with the enteral treatment (365 +/- 3 to 443 +/- 39 micromol/l), but was not affected by the parenteral treatment (p > 0.10). The plasma concentration glutamine decreased (p < 0.05) with the parenteral treatment only. The portal net appearance of proline showed a numerical increase with the enteral treatment but no other affects on arterial concentrations or portal net appearance were found. A small accompanying study showed that only small amounts of enteral AKG was present in the small intestine. It was therefore concluded that enteral AKG has a low availability to peripheral tissues either because it is absorbed and metabolized in the stomach and duodenum or because it is metabolized by microbes in the stomach. The study showed that AKG is metabolized differently following enteral and parenteral application in growing pigs.