A study in human colon cells describes a diet-responsive regulatory network that controls vitamin A production from beta-carotene and intestinal lipid absorption.
Based on the findings (1), the researchers predict that there would be significant differences in beta-carotene utilization in populations with a high versus a low vitamin A status: In vitamin A deficiency, enhanced expression of specific genes in the small intestine ensures that even small amounts of dietary beta-carotene can be efficiently absorbed and used for vitamin A production. When sufficient dietary vitamin A is available, absorption of beta-carotene is blocked preventing excess production of toxic amounts of vitamin A (retinoic acid) making beta-carotene a safe source of vitamin A.
Additionally, the findings imply that dietary vitamin A impacts lipid absorption more generally. A certain vitamin A (retinoic acid)-dependent protein facilitates the intestinal absorption not only of beta-carotene, but also of fatty acids, cholesterol, vitamin E, and other carotenoids.
Vitamin A insufficiency not only is a problem in developing countries but also is widespread in Western society. Approximately 15% of individuals aged 19–24 years in the UK have a total vitamin A intake below the lower recommended intake level (2) and almost half of American postmenopausal women may experience frank or marginal vitamin A deficiency (3).
There is considerable genetic variability in beta-carotene utilization in the general population. Many people have a reduced ability to convert beta-carotene to vitamin A (4). Inadequate supply of dietary vitamin A and/or genetic variability may constitute risk factors for human lipid disorders (dyslipidemia). The role of dietary vitamin A in preventing dyslipidemia associated disorders, such as cardiovascular and neurodegenerative diseases, needs further research and is of unquestionable relevance for human health.