Abstract
Vitamin A deficiency is a public health problem in most developing countries, especially in children and pregnant women. It is thus a priority in health policy to improve preformed vitamin A and/or provitamin A carotenoid status in these individuals. A more accurate understanding of the molecular mechanisms of intestinal vitamin A absorption is a key step in this direction. It was long thought that β-carotene (the main provitamin A carotenoid in human diet), and thus all carotenoids, were absorbed by a passive diffusion process, and that preformed vitamin A (retinol) absorption occurred via an unidentified energy-dependent transporter. The discovery of proteins able to facilitate carotenoid uptake and secretion by the enterocyte during the past decade has challenged established assumptions, and the elucidation of the mechanisms of retinol intestinal absorption is in progress. After an overview of vitamin A and carotenoid fate during gastro-duodenal digestion, our focus will be directed to the putative or identified proteins participating in the intestinal membrane and cellular transport of vitamin A and carotenoids across the enterocyte (i.e., Scavenger Receptors or Cellular Retinol Binding Proteins, among others). Further progress in the identification of the proteins involved in intestinal transport of vitamin A and carotenoids across the enterocyte is of major importance for optimizing their bioavailability.
Highlights
Vitamin A is essential for normal cell growth, cell differentiation, immunological functions and vision [1]
It occurs as provitamin A carotenoids, which can be cleaved and metabolized into retinol after absorption by the intestinal cells (Table 1)
Micellar retinol absorption efficiency was around 30% in 1 h, but less than 5% for micellar provitamin A carotenoids [46]. This may be explained by the presence of an efficient specific transporter for retinol, whereas provitamin A carotenoids are absorbed via non-specific transporters
Summary
Vitamin A is essential for normal cell growth, cell differentiation, immunological functions and vision [1]. Vitamin A deficiency is still a public health problem in more than half of all countries, especially in Africa and South-East Asia where meat intake is low, and in young children and pregnant women. It is a priority in health policy to improve preformed vitamin. It occurs as provitamin A carotenoids (mainly β-carotene, α-carotene and β-cryptoxanthin), which can be cleaved and metabolized into retinol after absorption by the intestinal cells (Table 1). Recent studies completed over the past ten years have once again addressed these hypotheses, and have shown that the mechanisms of retinol and carotenoid absorption are more complex than previously thought. After an overview of the fate of retinol and carotenoid in the human upper gastrointestinal lumen, we will focus on the putative or identified proteins participating in the intestinal membrane and cellular transport of vitamin A and carotenoids across the enterocyte identified until 2013
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