PMID- 19212007
OWN - NLM
STAT- MEDLINE
DCOM- 20090408
LR  - 20220310
IS  - 1899-1505 (Electronic)
IS  - 0867-5910 (Linking)
VI  - 59
IP  - 4
DP  - 2008 Dec
TI  - Short term 13-cis-retinoic acid treatment at therapeutic doses elevates 
      expression of leptin, GLUT4, PPARgamma and aP2 in rat adipose tissue.
PG  - 731-43
AB  - Temporary defects in the plasma lipid and glucose homeostasis are frequent 
      complication accompanying chronic treatment with 13-cis-retinoic acid (13cRA). 
      White adipose tissue acts as an endocrine organ producing a variety of hormones 
      (adipocytokines) including leptin, adiponectin, tumor-necrosis factor alpha 
      (TNFalpha) and angiotensin II (Ang II), which influence lipid metabolism, 
      systemic insulin sensitivity and inflammation. To study the effect of a 
      short-term 13cRA administration on metabolism of epididymal fat tissue, we 
      treated Wistar rats with five identical therapeutic doses of 13cRA (0.8 mg/kg 
      b.w.) by gavage during a period of 10 days. Expression of adiponectin, leptin, 
      TNFalpha and selected proteins such as adipocyte fatty acid binding protein 
      (aP2), insulin-dependent glucose transporter GLUT4, peroxisome 
      proliferator-activated receptor gamma (PPARgamma) and retinoid X receptors (RXRs) 
      was investigated using RT-PCR. Short-term treatment with therapeutic doses of 
      13cRA caused significant increase of the aP2, PPARgamma and moderately RXRalpha 
      gene expression. Similarly, the relative amount of mRNA for leptin and GLUT4 was 
      increased, while the TNFa transcript was decreased after treatment with 13cRA. 
      The gene expression and plasma concentration of adiponectin were without any 
      significant changes. Since local adipose renin-angiotensin system (RAS) has been 
      presumed to be involved in the regulation of fat tissue metabolism, we also 
      investigated the gene expression of RAS components in epididymal fat depot. Our 
      data has shown that 13cRA elevated Ang II receptor type 1 (AT(1) receptor)--at 
      both, mRNA and protein level. Thus, our results demonstrate that short-term 13cRA 
      treatment is inducing alterations in fat tissue metabolism in relation to 
      stimulated adipogenesis.
FAU - Krskova-Tybitanclova, K
AU  - Krskova-Tybitanclova K
AD  - Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, 
      Slovakia.
FAU - Macejova, D
AU  - Macejova D
FAU - Brtko, J
AU  - Brtko J
FAU - Baculikova, M
AU  - Baculikova M
FAU - Krizanova, O
AU  - Krizanova O
FAU - Zorad, S
AU  - Zorad S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Poland
TA  - J Physiol Pharmacol
JT  - Journal of physiology and pharmacology : an official journal of the Polish 
      Physiological Society
JID - 9114501
RN  - 0 (Dermatologic Agents)
RN  - 0 (Fatty Acid-Binding Proteins)
RN  - 0 (Glucose Transporter Type 4)
RN  - 0 (Leptin)
RN  - 0 (PPAR gamma)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptor, Angiotensin, Type 1)
RN  - 0 (Retinoid X Receptors)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EH28UP18IF (Isotretinoin)
SB  - IM
MH  - Adipose Tissue, White/drug effects/metabolism
MH  - Animals
MH  - Dermatologic Agents/*toxicity
MH  - Fatty Acid-Binding Proteins/drug effects/genetics
MH  - Gene Expression Regulation/*drug effects
MH  - Glucose Transporter Type 4/drug effects/genetics
MH  - Isotretinoin/*toxicity
MH  - Leptin/genetics/metabolism
MH  - Male
MH  - PPAR gamma/deficiency/drug effects/genetics
MH  - RNA, Messenger/drug effects/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Receptor, Angiotensin, Type 1/drug effects/genetics
MH  - Retinoid X Receptors/drug effects/genetics
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Tumor Necrosis Factor-alpha/drug effects/genetics
EDAT- 2009/02/13 09:00
MHDA- 2009/04/09 09:00
CRDT- 2009/02/13 09:00
PHST- 2008/04/02 00:00 [received]
PHST- 2008/11/06 00:00 [accepted]
PHST- 2009/02/13 09:00 [entrez]
PHST- 2009/02/13 09:00 [pubmed]
PHST- 2009/04/09 09:00 [medline]
PST - ppublish
SO  - J Physiol Pharmacol. 2008 Dec;59(4):731-43.