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Mechanism of Action of Vitamin A
Published in Ayse Serap Karadag, Berna Aksoy, Lawrence Charles Parish, Retinoids in Dermatology, 2019
Retinoids may be acquired as retinyl esters (from animals) or β-carotene (from plants) and are absorbed in the small intestine, where they are carried to the liver by chylomicrons as retinyl-esters. In the liver, retinyl esters may be stored or are hydrolyzed to produce retinol that circulates bound to retinol-binding protein 4 (RBP4). It may enter the target cell using the stimulated by retinoic acid gene 6 (STRA6) homologs transporter or may cross the cell membrane by passive diffusion.
Effects of aerobic exercise and a high-carbohydrate diet on RBP4 expression in rat skeletal muscle
Published in Robert Hofstra, Noriyuki Koibuchi, Suthat Fucharoen, Advances in Biomolecular Medicine, 2017
Nuroh Najmi, Yunia Sribudiani, Bethy S. Hernowo, Hanna Goenawan Setiawan, Vita M. Tarawan, Ronny Lesmana
The main carbohydrate source in the Indonesian diet is rice. High carbohydrate intake can increase the risk factor of diabetes mellitus. Increased blood glucose can induce insulin release from pancreatic β-cells. Insulin mediates glucose uptake in peripheral tissues such as muscle, adipose tissue, and kidneys (Ma et al. 2016). The increasing glucose concentration can induce glycogen storage in the liver and muscle. High carbohydrate consumption for a long period increases the risk factor of insulin resistance (Alapatt et al. 2013). Retinol-Binding Protein 4 (RBP4) is a vitamin A transport protein, which is also one of the potential indicators of insulin resistance (Kotnik et al. 2011). RBP4 is a adipocytokine that is secreted mainly from the liver and adipose tissue. Some studies have revealed that serum RBP4 levels correlated with the metabolic syndrome. Therefore, RBP4 levels could be used to detect insulin resistance.
Lymphocyte trafficking from inductive sites to effector sites
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Valerie Verhasselt, William Agace, Oliver Pabst, Andrew Stagg
The specific capacity of small intestine-derived DC to induce CCR9 and α4β7 integrin on T lymphocytes appears to result from their enhanced ability to metabolize vitamin A. Vitamin A is a dietary vitamin that is taken up in the small intestine and transported to the liver, where it is stored as retinyl esters. Retinol is released into the circulation, primarily from the liver, in association with retinol-binding protein 4 and is taken up by tissue cells, where it is further metabolized. The major active metabolite of vitamin A is retinoic acid (RA). RA is generated by the consecutive oxidation of retinol to retinal and from retinal to RA. The oxidation of retinol to retinal is catalyzed by a family of alcohol dehydrogenases, which seem to be ubiquitously expressed in a wide range of tissues, and the oxidation of retinal to RA is catalyzed through an irreversible reaction by a family of retinal dehydrogenases, which seem to have more tissue- and cell-restricted expression patterns. Once generated, RA can be used by the cell generating it or released into the local environment to regulate the function of neighboring cells. RA signaling is mediated through retinoic acid receptor (RAR)–retinoid X receptor (RXR) heterodimers that function as ligand-induced transcription factors bound to DNA target sequences. The addition of low (subnanomolar) concentrations of RA to stimulated T lymphocytes in vitro is sufficient to induce expression of the gut-homing receptors CCR9 and α4β7 integrin on responding T cells; more importantly, the ability of intestinal DCs to induce gut-homing receptors on responding T cells is blocked by the addition of antagonists of retinoic acid receptors. In this regard, small intestinal-derived migratory DCs express higher levels of key enzymes involved in vitamin A metabolism and have been shown to induce enhanced RA signaling in responding T cells (Figure 16.7). Numerous additional cells in the intestinal mucosa, including epithelial cells of the intestinal wall and stromal cells in the mesenteric lymph nodes, also have the capacity to metabolize vitamin A and probably contribute to generating an RA-rich environment at these sites that helps drive the selective generation of gut-homing T cells in the mesenteric lymph node in vivo. The ability of RA to induce gut-homing receptors is also not restricted to T cells, because RA also induces the expression of gut-homing receptors on B cells. As one might expect from these findings, mice whose vitamin A stores have been depleted by being kept on a diet deficient in vitamin A for a long period have markedly reduced numbers of T cells and B cells in the intestinal mucosa. These findings probably explain some of the beneficial effects of dietary supplementation with vitamin A in reducing childhood mortality from persistent diarrhea induced by infectious disease in developing countries.
A novel homozygous c.67C>T variant in retinol binding protein 4 (RBP4) associated with retinitis pigmentosa and childhood acne vulgaris
Published in Ophthalmic Genetics, 2020
J. Cehajic-Kapetanovic, K. M. Jasani, M. Shanks, P. Clouston, R. E. MacLaren
Informed consent for DNA blood sampling was subsequently taken from the patient. Molecular analysis using the 111-gene panel associated with retinitis pigmentosa and retinitis pigmentosa like phenotype was undertaken using the HaloPlex Target Enrichment system (Agilent Technologies, California, USA). An abnormal homozygous signal at the RBP4 c.67 oligonucleotide position was detected, with a C > T change, that is predicted to lead to a stop codon (p.Arg23*) causing a premature termination of translation. This variant had not previously been described in the literature, and in view of a single nucleotide change, the pathogenicity remained uncertain. However, given the potential systemic manifestations of retinol deficiency, we specifically questioned the patient, who admitted to having severe acne as a child (Figure 3), making the diagnosis of RBP4-related retinal degeneration much more plausible. In addition, the affected brother also had a history of severe acne vulgaris whereas the unaffected brother did not, confirming that mutations in RBP4 segregated with the acne vulgaris phenotype in this family. The genetic testing of the affected brother confirmed the presence of the same homozygous variant c.67 C > T. Although the unaffected brother was not available for genetic testing, the family history is clear that he did not have the severe acne vulgaris phenotype of the affected probands.
Association between plasma retinol binding protein 4 levels and severe preeclampsia
Published in Journal of Obstetrics and Gynaecology, 2018
Yanping Zhang, Tao Wang, Shunping Gui, Xijing Liu, Li Dai, Bin Zhou, Rong Zhou, Yunhui Gong
Retinol binding protein 4 (RBP4) is a recently-added member of the adipokines family (Yang et al. 2005). A previous study has revealed that systolic and diastolic blood pressure were higher in the RBP4 – over expressing mice, and lower in the RBP4 – knockout mice, compared with BP in the wild-type mice (Kraus et al. 2015), which suggested that RBP4 could engage in the regulation of blood pressure. Large epidemiologic studies have also demonstrated that elevated circulating RBP4 levels are a biomarker for insulin resistance (Sun et al. 2013). The definite function of RBP4 in insulin resistance is hypothesised to be implicated in PE. Moreover, alternation in circulating concentrations of RBP4 could affect physiologic metabolic adaptations during normal pregnancy, and kinds of pregnancy complications, including PE (Mazakitovi et al. 2007, 2009).
Association of vitamin A and its organic compounds with stroke – a systematic review and meta-analysis
Published in Nutritional Neuroscience, 2023
Sajjad Farashi, Siamak Shahidi, Abdolrahman Sarihi, Mohammad Zarei
In Zhu et al. [45] the association of the level of Retinol-Binding Protein 4 (RBP4), and the outcomes of stroke was evaluated. RBP4 is a carrier of vitamin A and a potential biomarker for stroke diagnosis [47]. This study showed significantly higher RBP4 values in poor outcome stroke patients. This result was in accordance with [48] and contradicted with [49]. In another study conducted by LIombart et al. [47], the difference between ischemic stroke and intracerebral hemorrhagic stroke patients in point of RBP4 plasma level was evaluated. The results showed that RBP4 was a capable biomarker for separating ischemic and hemorrhagic types of stroke (p < 0.05).