β-carotene in Obesity Research: Technical Considerations and Current Status of the Field

Abstract

Over the past decades, obesity has become a rising health problem as the accessibility to high calorie, low nutritional value food has increased. Research shows that some bioactive components in fruits and vegetables, such as carotenoids, could contribute to the prevention and treatment of obesity. Some of these carotenoids are responsible for vitamin A production, a hormone-like vitamin with pleiotropic effects in mammals. Among these effects, vitamin A is a potent regulator of adipose tissue development, and is therefore important for obesity. This review focuses on the role of the provitamin A carotenoid β-carotene in human health, emphasizing the mechanisms by which this compound and its derivatives regulate adipocyte biology. It also discusses the physiological relevance of carotenoid accumulation, the implication of the carotenoid-cleaving enzymes, and the technical difficulties and considerations researchers must take when working with these bioactive molecules. Thanks to the broad spectrum of functions carotenoids have in modern nutrition and health, it is necessary to understand their benefits regarding to metabolic diseases such as obesity in order to evaluate their applicability to the medical and pharmaceutical fields.

Keywords: Vitamin A; adipocyte; β-carotene oxygenase 1.

Figure 1

Schematic representation of carotenoid and vitamin A uptake and metabolism. Left: extracellular sources of provitamin A carotenoids (named carotenoids) and vitamin A and the relative concentration. * indicates that these sources can vary more than one order of magnitude depending on the fasting vs. fed conditions. Data show fasting values. Right: main proteins and conversion pathways involved in the uptake, cleavage/conversion and catabolism of carotenoids and vitamin A. For the purpose of this review, we only represented the proteins present in adipocytes and the hepatocytes in yellow and green, respectively. Dotted arrows are pathways not fully established. TTR, transthyretin; RBP4, retinol-binding protein 4; RBPR2, RBP4-receptor 2; STRA6, stimulated retinoic acid gene 6; NPC1L1, Niemann-Pick C1-Like 1; LDLr, Low-density lipoprotein receptor; SR-B1, scavenger receptor class B type 1; LPL, lipoprotein lipase; CD36, cluster of differentiation 36; REHs; Retinyl ester hydrolases; LRAT, lecithin:retinol acyl transferase, ARAT, acyl:retinol acyl transferase; ADHs, aldehyde hydrogenases; SDR, short-chain dehydrogenase/reductase; RALDH, retinaldehyde hydrogenases; 9-cisRA, 9-cis-retinoic acid; cis-DHRA, 9-cis-13,14-dihydroretinoic acid; CYP26s, cytochrome P450s; RARs, retinoic acid receptors; RXRs; retinoid X receptors; RAREs, retinoic acid-response element.

Figure 2

Purity and isomer variation between three commercial sources of β-carotene. HPLC chromatograms detected at 452 nm were obtained using YMC C30 column in three different commercially available β-carotene sources. The largest peak shows all-trans-β-carotene. Smaller peaks correspond to different carotenoid isomers (probably cis forms) in each commercial source. Arrows show the presence of two peaks only present in the orange chromatogram (probably β-carotene cis forms). AU, arbitrary units.