Abstract
Dietary intake and tissue levels of carotenoids have been associated with a reduced risk of several chronic diseases, including cardiovascular diseases, type 2 diabetes, obesity, brain-related diseases and some types of cancer. However, intervention trials with isolated carotenoid supplements have mostly failed to confirm the postulated health benefits. It has thereby been speculated that dosing, matrix and synergistic effects, as well as underlying health and the individual nutritional status plus genetic background do play a role. It appears that our knowledge on carotenoid-mediated health benefits may still be incomplete, as the underlying mechanisms of action are poorly understood in relation to human relevance. Antioxidant mechanisms - direct or via transcription factors such as NRF2 and NF-κB - and activation of nuclear hormone receptor pathways such as of RAR, RXR or also PPARs, via carotenoid metabolites, are the basic principles which we try to connect with carotenoid-transmitted health benefits as exemplified with described common diseases including obesity/diabetes and cancer. Depending on the targeted diseases, single or multiple mechanisms of actions may play a role. In this review and position paper, we try to highlight our present knowledge on carotenoid metabolism and mechanisms translatable into health benefits related to several chronic diseases.
Highlights
Carotenoids are typically C-40 based tetraterpenoid secondary plant compounds, more recently, C-30(1) and C-50(2) based carotenoids in bacteria have been described, resulting in over 1100 known carotenoids[3]
It is highly likely that the adverse effects of β-carotene that were observed in about 1 % of the subjects who were enrolled in the ATBC and Carotene and Retinol Efficacy (CARET) studies were due to peculiar genotypes in the genes involved in either the bioavailability and the metabolism of β-carotene and/or in lung cancer related genes that are targets for β-carotene metabolites
Carotenoids may act in humans as antioxidants and photoprotective compounds, while likely a larger activity range is mediated via the transcription factors NF-κB and NRF2 as well as the nuclear hormone receptors retinoic acid receptors (RARs) and retinoid X receptors (RXRs)
Summary
Carotenoids are typically C-40 based tetraterpenoid secondary plant compounds, more recently, C-30(1) and C-50(2) based carotenoids in bacteria have been described, resulting in over 1100 known carotenoids[3]. Typically ranging around 10 to over 100 μM in in vitro experiments, as well as high nutritional dosages in human in vivo intervention trials (approximately 5–120 mg/d) have shown potential antioxidant activities, as shown by decreased markers of oxidative stress in mid-to-long-term human studies[33,151], proposing protective effects of carotenoids on e.g. cellular membranes and lipoprotein particles. Whether these effects are based primarily on direct antioxidant effects or are transmitted via interactions with transcription factors such as NRF2 and NF-κB is rather unclear. Smokers and asbestos-exposed subjects have an increased lung cancer
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