ABSTRACT
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.
Subject(s)
Adiponectin/metabolism , Aldehyde Dehydrogenase/metabolism , Diet, High-Fat/adverse effects , Gene Expression Regulation/physiology , Receptors, Retinoic Acid/metabolism , 3T3-L1 Cells , Adipocytes/physiology , Adiponectin/genetics , Adipose Tissue/physiology , Aldehyde Dehydrogenase/genetics , Aldehyde Dehydrogenase 1 Family , Alkaloids , Animal Feed/analysis , Animals , Dietary Supplements , Down-Regulation/physiology , Male , Mice , Mice, Knockout , Obesity , Oxindoles , Receptors, Retinoic Acid/genetics , Retinal Dehydrogenase , Signal Transduction/physiology , Tretinoin/metabolism , Up-Regulation , Vitamin A/administration & dosageABSTRACT
BACKGROUND: Brucellosis can involve almost any organ system and may present with a broad spectrum of clinical presentations. In this study, we present a case of deep vein thrombosis due to human brucellosis. CASE PRESENTATION: A 15- year old boy presented with acute pain and swelling in his left thigh in June 2011, when he complained of fever, chills and lower extremity pain in which he could barely walk. In family history, his older brother had brucellosis 3 weeks ago and appropriate medication was given. The tubal standard agglutination test (wright test) and 2ME test were positive (in a titer of 1/1280 and 1/640, respectively). Peripheral venous doppler ultrasound of left lower extremity showed that common iliac, femoral, external iliac, superficial and deep femoral vein and popliteal vein were enlarged and contained with echogenous clot. He was treated with rifampicin 600 mg once a day, doxycycline 100 mg twice a day (both for three months) and amikacin 500 mg twice a day (for 2 weeks) accompanied with anti-coagulant. Ten days after the onset of this treatment, thrombophlebitis was cured. The follow up of the patient showed no abnormality after approximately one year later. CONCLUSION: In brucellosis endemic areas, the clinicians who encounter patients with deep vein thrombosis and current history of a febrile illness, should consider the likelihood of brucellosis.