Opposite in vitro and in vivo regulation of hepatic apolipoprotein A-I gene expression by retinoic acid. Absence of effects on apolipoprotein A-II gene expression.

Berthou, Laurence; Staels, Bart; Saldicco, I; Berthelot, Karine; Casey, James W.; Fruchart, Jean‐Charles; Denèfle, Patrice; Branellec, Didier

doi:10.1161/01.atv.14.10.1657

Cited by 26 publications

(12 citation statements)

References 52 publications

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“…By contrast, a significant decrease in serum HDL-cholesterol was observed after 1 month of treatment. This finding is consistent with a previous study reporting down-regulation of the expression of apolipoprotein A-I mRNA in rat hepatocytes, a major component of HDL-cholesterol, by alltrans retinoids (15). Both the increase in insulin levels and the decrease in HDL-cholesterol were transient, suggesting that in the long term other metabolic regulatory pathways may override the subtle alterations in glucose and lipid metabolism induced by retinoids.…”

Section: Discussionsupporting

confidence: 92%

Effects of retinoid therapy on insulin sensitivity, lipid profile and circulating adipocytokines

et al. 2006

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Objective: In vitro and in vivo models indicate that all-trans retinoic acids influence glucose and lipid metabolism. We aimed to evaluate the effects of chronic treatment with acitretin, an all-trans retinoic acid, on glucose metabolism, lipid profile and adiponectin and resistin levels. Design: Ten normoglycemic, normolipemic patients affected with psoriasis vulgaris were studied before and after 1 and 3 months of oral treatment with 35 mg of acitretin. Methods: Glucose metabolism, lipid profile, and adiponectin and resistin levels were evaluated in basal conditions and after acitretin treatment. Ten healthy subjects matched for age, body mass index (BMI) and insulin sensitivity were studied as controls. Results: One-month acitretin treatment reduced psoriasis activity, insulin sensitivity, evaluated as QUICKI values (0.364^0.034 versus 0.329^0.051; P , 0.05) and HOMA-IR index (1.53^0.73 versus 2.59^1.41; P , 0.05), and high-density lipoprotein (HDL)-cholesterol levels (45.2^11.7 versus 39.4^10.4 mg/dl; P ¼ 0.01). The impairment in glucose and lipid homeostasis was transient and not associated to BMI variations. Adiponectin levels did not change during the treatment, while resistin levels, which were higher in untreated patients than in controls (9.4^4.4 versus 6.2^2.1 ng/ml; P ¼ 0.05), fell within the normal range after 1 and 3 months of therapy. The normalization of resistin levels occurred without significant changes in circulating tumor necrosis factor a (TNFa) levels, which persisted elevated throughout the treatment. Conclusions: Treatment with a low dose of acitretin induced a mild, transient reduction of insulin sensitivity and HDL-cholesterol levels that was not related to modifications of adiponectin, resistin and TNFa levels. Although the role of resistin in humans remains elusive, the levels of this adipocytokine seem to be affected, at least in part, by retinoids. European Journal of Endocrinology 154 83-86

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Section: Discussionsupporting

confidence: 92%

Effects of retinoid therapy on insulin sensitivity, lipid profile and circulating adipocytokines

et al. 2006

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“…Positive RAR/RXR DR-2 and RXR/RXR DR-1 sites have been identified in the apo A-I promoter A footprint (43,44). Furthermore, retinoids increase apo A-I mRNA levels and secretion in human, monkey, and rat hepatocytes (45)(46)(47). Similarly, a RXRE has been localized in the apo A-II promoter J-site, which mediates the induction of apo A-II expression in human hepatocytes (31).…”

Section: Discussionmentioning

confidence: 99%

“…Similarly, a RXRE has been localized in the apo A-II promoter J-site, which mediates the induction of apo A-II expression in human hepatocytes (31). However, the physiological consequence of the effects of retinoids on the expression of these HDL apolipoproteins is unclear, since retinoid administration may decrease plasma HDL (5), without changing plasma apo A-I (48, 49) and apo A-II (50) concentrations in humans, whereas liver apo A-I gene expression decreases in rats in vivo (45,51). By contrast, both in humans and rats, retinoids induce a hypertriglyceridemia (5,52,53) with a mixed lipemia lipoprotein profile, such as in diabetes and familial combined hyperlipidemia (5,35), diseases in which apo C-III is an important factor (54,55).…”

Section: Discussionmentioning

confidence: 99%

Retinoids increase human apo C-III expression at the transcriptional level via the retinoid X receptor. Contribution to the hypertriglyceridemic action of retinoids.

Vu‐Dac¹,

Gervois²,

Pineda-Torra³

et al. 1998

J. Clin. Invest.

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125

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“…These observations indicate that RA suppressed the expression of apo A-I in rats. In contrast, a stimulatory effect on apo A-I synthesis was noted in hepatoma cell lines (6) and in primary cultures from cynomolgus monkey (30). The reason for the discrepancy among studies is not fully clear.…”

mentioning

confidence: 91%

Effect of retinoic acid on cell proliferation and differentiation as well as on lipid synthesis, lipoprotein secretion, and apolipoprotein biogenesis

Grenier

Maupas²,

Beaulieu³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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Dietary vitamin A and its active metabolites are essential nutrients for many functions as well as potent regulators of gene transcription and growth. Although the epithelium of the small intestine is characterized by rapid and constant renewal and enterocytes play a central role in the absorption and metabolism of alimentary retinol, very little is known about the function of retinoids in the human gastrointestinal epithelium and mechanisms by which programs engage the cell cycle are poorly understood. We have assessed the effects of 10 μM 9- and 13- cis-retinoic acid (RA) on proliferation and differentiation processes, lipid esterification, apolipoprotein (apo) biogenesis and lipoprotein secretion along with nuclear factor gene transcription. Treatment of Caco-2 cells with RA at different concentrations and incubation periods revealed the reduction of thymidine incorporation in 60% preconfluent or 100% confluent cells. Concomitantly, RA 1) modulated D-type cyclins by reducing the mitogen-sensitive cyclin D1 and upregulating cyclin D3 expressions and 2) caused a trend of increase in p38 MAPK, which triggers CDX2, a central protein in cell differentiation. RA remained without effect on lipoprotein output and apo synthesis, even for apo A-I that possesses RARE in its promoter. RA, in combination with 22-hydroxycholesterol, could induce apo A-I gene expression without any impact on apo A-I mass. Only the gene expression of peroxisome proliferator-activated receptor (PPAR)β, retinoic receptor (RAR)β, and RARγ was augmented and no alteration was noted in PPARα, PPARγ, liver X receptor (LXR)α, LXRβ, and retinoid X receptors. Taken together, these data highlight RA-induced cell differentiation via specific signaling without a significant impact on apo A-I synthesis.

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Opposite in vitro and in vivo regulation of hepatic apolipoprotein A-I gene expression by retinoic acid. Absence of effects on apolipoprotein A-II gene expression.

Abstract: We studied the pharmacological potential of retinoids to modulate apolipoprotein (apo) A-I and apoA

Cited by 26 publications

References 52 publications

Effects of retinoid therapy on insulin sensitivity, lipid profile and circulating adipocytokines

Effects of retinoid therapy on insulin sensitivity, lipid profile and circulating adipocytokines

Retinoids increase human apo C-III expression at the transcriptional level via the retinoid X receptor. Contribution to the hypertriglyceridemic action of retinoids.

Effect of retinoic acid on cell proliferation and differentiation as well as on lipid synthesis, lipoprotein secretion, and apolipoprotein biogenesis

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