Retinoids and retinoid-metabolic gene expression in mouse adipose tissues

Sima, Aurélia; Manolescu, Daniel-Constantin; Bhat, Pangala V.

doi:10.1139/o11-062

Cited by 20 publications

(16 citation statements)

References 37 publications

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“…The endogenous concentration of RA is tightly regulated during embryonic and postnatal development and is essential for the proper functionality of adult tissues and cells. Several recent reports have indicated potential roles of retinoids (RA, retinol, retinal, and other vitamin A derivatives) in adipose tissue (32–34). Although the liver is the primary storage site of retinoids, adipose tissue is the second largest site and actively mediates retinoid metabolism (35,36).…”

Section: Discussionmentioning

confidence: 99%

Retinoic Acid Mediates Visceral-Specific Adipogenic Defects of Human Adipose-Derived Stem Cells

et al. 2016

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Increased visceral fat, rather than subcutaneous fat, during the onset of obesity is associated with a higher risk of developing metabolic diseases. The inherent adipogenic properties of human adipose-derived stem cells (ASCs) from visceral depots are compromised compared with those of ASCs from subcutaneous depots, but little is known about the underlying mechanisms. Using ontological analysis of global gene expression studies, we demonstrate that many genes involved in retinoic acid (RA) synthesis or regulated by RA are differentially expressed in human tissues and ASCs from subcutaneous and visceral fat. The endogenous level of RA is higher in visceral ASCs; this is associated with upregulation of the RA synthesis gene through the visceral-specific developmental factor WT1. Excessive RA-mediated activity impedes the adipogenic capability of ASCs at early but not late stages of adipogenesis, which can be reversed by antagonism of RA receptors or knockdown of WT1. Our results reveal the developmental origin of adipocytic properties and the pathophysiological contributions of visceral fat depots.

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Section: Discussionmentioning

confidence: 99%

Retinoic Acid Mediates Visceral-Specific Adipogenic Defects of Human Adipose-Derived Stem Cells

et al. 2016

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“…With regard to ligands other than ATRA, it is still unknown which RAR- and/or RXR-activating ligands could be synthesized upon ALDH1A1 expression in WAT, and we could not conclusively suggest a possible structure using our current analytical expertise (26, 53). However, several known and unknown candidates, including 9- cis - and all- trans -13,14-dihydroretinoic acid, retinal, apo-lycopenoic acids, apo-13′-carotenone, apo-10′-carotenoic acid, and apo-14′-carotenoic acid (20, 26, 44, 47, 64–72), were recently identified and could constitute potential endogenous retinoids.…”

Section: Discussionmentioning

confidence: 99%

Reduced adiponectin expression after high‐fat diet is associated with selective up‐regulation of ALDH1A1 and further retinoic acid receptor signaling in adipose tissue

et al. 2016

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Adiponectin is an adipocyte-derived adipokine with potent antidiabetic, anti-inflammatory, and antiatherogenic activity. Long-term, high-fat diet results in gain of body weight, adiposity, further inflammatory-based cardiovascular diseases, and reduced adiponectin secretion. Vitamin A derivatives/retinoids are involved in several of these processes, which mainly take place in white adipose tissue (WAT). In this study, we examined adiponectin expression as a function of dietary high-fat and high–vitamin A conditions in mice. A decrease of adiponectin expression in addition to an up-regulation of aldehyde dehydrogenase A1 (ALDH1A1), retinoid signaling, and retinoic acid response element signaling was selectively observed in WAT of mice fed a normal–vitamin A, high-fat diet. Reduced adiponectin expression in WAT was also observed in mice fed a high–vitamin A diet. Adipocyte cell culture revealed that endogenous and synthetic retinoic acid receptor (RAR)α- and RARγ-selective agonists, as well as a synthetic retinoid X receptor agonist, efficiently reduced adiponectin expression, whereas ALDH1A1 expression only increased with RAR agonists. We conclude that reduced adiponectin expression under high-fat dietary conditions is dependent on 1) increased ALDH1A1 expression in adipocytes, which does not increase all-trans-retinoic acid levels; 2) further RAR ligand–induced, WAT-selective, increased retinoic acid response element–mediated signaling; and 3) RAR ligand–dependent reduction of adiponectin expression.—Landrier, J.-F., Kasiri, E., Karkeni, E., Mihály, J., Béke, G., Weiss, K., Lucas, R., Aydemir, G., Salles, J., Walrand, S., de Lera, A. R., Rühl, R. Reduced adiponectin expression after high-fat diet is associated with selective up-regulation of ALDH1A1 and further retinoic acid receptor signaling in adipose tissue.

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“…However, not all PIs have the same effect since they enter and accumulate differently in different tissues and have different intracellular localizations [21,25,26]. Moreover, as it was recently reported, adipose tissue influences tissue distribution of carotenoids [26] and certainly of RAs [24]. Heightened RAs concentrations in different tissues [21] enhance the expression of various P450 CYP enzymes such as CYP 26A1, CYP 26B1 and CYP 26C1, resulting in increased RAs catabolism [10,27].…”

Section: Discussionmentioning

confidence: 99%

Combination antiretroviral therapy and chronic HIV infection affect serum retinoid concentrations: longitudinal and cross-sectional assessments

et al. 2012

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BackgroundSeveral lines of evidence suggest that retinoids (retinol-ROL or vitamin A, and its active metabolites, retinoic acids-RAs) play important pathogenic roles in HIV infection and combination antiretroviral therapy (cART)-related events. We previously reported that antiretrovirals alter RAs synthesis in vitro. We hypothesised that in vivo serum retinoid concentrations are affected by both cART and HIV infection. This might explain several clinical and laboratory abnormalities reported in HIV-infected patients receiving cART.MethodsThe effects of optimal cART and chronic HIV on serum retinoids were firstly assessed longitudinally in 10 HIV-infected adults (group1 = G1): twice while on optimal cART (first, during long-term and second, during short term cART) and twice during 2 cART interruptions when HIV viral load (VL) was detectable. Retinoid concentrations during optimal long term cART in G1 were compared with cross-sectional results from 12 patients (G2) with suboptimal cART (detectable VL) and from 28 healthy adults (G3). Serum retinoids were measured by HPLC with ultraviolet detection. Retinoid concentrations were correlated with VL, CD4+ T- cell count and percentages, CD8+38+ fluorescence, triglycerides, cholesterol and C-peptide serum levels.ResultsDuring optimal cART, G1 participants had drastically reduced RAs (0.5 ± 0.3 μg/dL; P < 0.01) but the highest ROL (82 ± 3.0 μg/dL) concentrations. During cART interruptions in these patients, RAs slightly increased whereas ROL levels diminished significantly (P < 0.05). G3 had the highest RAs levels (7.2 ± 1.1 μg/dL) and serum ROL comparable to values in North Americans. Serum ROL was decreased in G2 (37.7 ± 3.2 μg/dL; P < 0.01). No correlations were noted between RA and ROL levels or between retinoid concentrations and CD4+ T- cell count, CD8+38+ fluorescence, VL. ROL correlated with triglycerides and cholesterol in G1 (rs = 0.8; P = 0.01).ConclusionsSerum RAs levels are significantly diminished by cART, whereas ROL concentrations significantly decreased during uncontrolled HIV infection but augmented with optimal cART. These alterations in retinoid concentrations may affect the expression of retinoid-responsive genes involved in metabolic, hormonal and immune processes and be responsible for some adverse events observed in HIV-infected persons treated with antiretrovirals. Further studies should assess concomitant serum and intracellular retinoid levels in different clinical situations in larger, homogenous populations.

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Retinoids and retinoid-metabolic gene expression in mouse adipose tissues

Cited by 20 publications

References 37 publications

Retinoic Acid Mediates Visceral-Specific Adipogenic Defects of Human Adipose-Derived Stem Cells

Retinoic Acid Mediates Visceral-Specific Adipogenic Defects of Human Adipose-Derived Stem Cells

Reduced adiponectin expression after high‐fat diet is associated with selective up‐regulation of ALDH1A1 and further retinoic acid receptor signaling in adipose tissue

Combination antiretroviral therapy and chronic HIV infection affect serum retinoid concentrations: longitudinal and cross-sectional assessments

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