Retinoids and retinoid-metabolic gene expression in mouse adipose tissues

2011 ◽  
Vol 89 (6) ◽  
pp. 578-584 ◽  
Author(s):  
Aurelia Sima ◽  
Daniel-Constantin Manolescu ◽  
Pangala Bhat
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Adipocyte Differentiation ◽  
Binding Protein ◽  
Retinol Binding Protein ◽  
Retinol Dehydrogenase ◽  
Adipose Tissues ◽  
Fat Depots ◽  
Retinoid Metabolism ◽  
Metabolic Gene Expression

Vitamin A and its analogs (retinoids) regulate adipocyte differentiation. Recent investigations have demonstrated a relationship among retinoids, retinoid-binding-protein 4 (RBP4) synthesized in adipose tissues, and insulin-resistance status. In this study, we measured retinoid levels and analyzed the expression of retinoid homeostatic genes associated with retinol uptake, esterification, oxidation, and catabolism in subcutaneous (Sc) and visceral (Vis) mouse fat tissues. Both Sc and Vis depots were found to contain similar levels of all-trans retinol. A metabolite of retinol with characteristic ultraviolet absorption maxima for 9-cis retinol was observed in these 2 adipose depots, and its level was 2-fold higher in Sc than in Vis tissues. Vis adipose tissue expressed significantly higher levels of RBP4, CRBP1 (intracellular retinol-binding protein 1), RDH10 (retinol dehydrogenase), as well as CYP26A1 and B1 (retinoic acid (RA) hydroxylases). No differences in STRA6 (RBP4 receptor), LRAT (retinol esterification), CRABP1 and 2 (intracellular RA-binding proteins), and RALDH1 (retinal dehydrogenase) mRNA expressions were discerned in both fat depots. RALDH1 was identified as the only RALDH expressed in both Sc and Vis adipose tissues. These results indicate that Vis is more actively involved in retinoid metabolism than Sc adipose tissue.

Identification of genes expressed differentially in subcutaneous and visceral fat of cattle, pig, and mouse

2005 ◽  
Vol 21 (3) ◽  
pp. 343-350 ◽  
Author(s):  
Daisuke Hishikawa ◽  
Yeon-Hee Hong ◽  
Sang-gun Roh ◽  
Hisae Miyahara ◽  
Yukihiko Nishimura ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
Animal Species ◽  
Fat Deposition ◽  
High Fat ◽  
Adipose Tissues ◽  
Fat Accumulation ◽  
Fat Depots ◽  
Visceral Adipose

The factors that control fat deposition in adipose tissues are poorly understood. It is known that visceral adipose tissues display a range of biochemical properties that distinguish them from adipose tissues of subcutaneous origin. However, we have little information on gene expression, either in relation to fat deposition or on interspecies variation in fat deposition. The first step in this study was to identify genes expressed in fat depot of cattle using the differential display RT-PCR method. Among the transcripts identified as having differential expression in the two adipose tissues were cell division cycle 42 homolog (CDC42), prefoldin-5, decorin, phosphate carrier, 12S ribosomal RNA gene, and kelch repeat and BTB domain containing 2 (Kbtbd2). In subsequent experiments, we determined the expression levels of these latter genes in the pig and in mice fed either a control or high-fat diet to compare the regulation of fat accumulation in other animal species. The levels of CDC42 and decorin mRNA were found to be higher in visceral adipose tissue than in subcutaneous adipose tissue in cattle, pig, and mice. However, the other genes studied did not show consistent expression patterns between the two tissues in cattle, pigs, and mice. Interestingly, all genes were upregulated in subcutaneous and/or visceral adipose tissues of mice fed the high-fat diet compared with the control diet. The data presented here extend our understanding of gene expression in fat depots and provide further proof that the mechanisms of fat accumulation differ significantly between animal species.

scholarly journals Gene expression of PPARγ and PGC-1α in human omental and subcutaneous adipose tissues is related to insulin resistance markers and mediates beneficial effects of physical training

2010 ◽  
Vol 162 (3) ◽  
pp. 515-523 ◽  
Author(s):  
Karen Ruschke ◽  
Lauren Fishbein ◽  
Arne Dietrich ◽  
Nora Klöting ◽  
Anke Tönjes ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Cardiovascular Risk ◽  
Mrna Expression ◽  
Physical Training ◽  
Adipose Tissues ◽  
Beneficial Effects ◽  
Fat Depots

ObjectiveObesity and type 2 diabetes (T2D) are reaching epidemic proportions in Western societies, and they contribute to substantial morbidity and mortality. The peroxisome proliferator-activated receptor γ (PPARγ) and PPARγ coactivator-1α (PGC-1α) system plays an important role in the regulation of efficient energy utilization and oxidative phosphorylation, both of which are decreased in obesity and insulin resistance.Design and methodsWe measured the metabolic parameters and the expression of PPARγ and PGC-1α mRNA using quantitative real-time PCR in omental and subcutaneous (SC) adipose tissues in an observational study of 153 individuals as well as in SC fat and skeletal muscle in an interventional study of 60 subjects (20 each with normal glucose tolerance, impaired glucose tolerance, and T2D) before and after intensive physical training for 4 weeks.ResultsPPARγ and PGC-1α mRNA expression in both fat depots as well as in skeletal muscle is associated with markers of insulin resistance and cardiovascular risk. PGC-1α mRNA expression is significantly higher in SC fat than in omental fat, whereas PPARγ mRNA expression is not significantly different between these fat depots. Skeletal muscle and SC fat PPARγ and PGC-1α mRNA expression increased significantly in response to physical training.ConclusionsGene expression of PPARγ and PGC-1α in human adipose tissue is related to markers of insulin resistance and cardiovascular risk. Increased muscle and adipose tissue PPARγ and PGC-1α expression in response to physical training may mediate the beneficial effects of exercise on insulin sensitivity.

233-LB: Spinal Cord Injury Inhibited-FGF21 Signaling Is Associated with Dysregulation of Metabolic Gene Expression in Mouse Liver and Adipose Tissue

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 233-LB
Author(s):  
XIN-HUA LIU ◽  
LAUREN HARLOW ◽  
ZACHARY GRAHAM ◽  
JOSHUA F. YARROW ◽  
KENNETH CUSI ◽  
...  
Keyword(s):  
Gene Expression ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Adipose Tissue ◽  
Mouse Liver ◽  
Metabolic Gene ◽  
Metabolic Gene Expression ◽  
Cord Injury

scholarly journals A direct role for C/EBP and the AP-I-binding site in gene expression linked to adipocyte differentiation.

1989 ◽  
Vol 9 (12) ◽  
pp. 5331-5339 ◽  
Author(s):  
R Herrera ◽  
H S Ro ◽  
G S Robinson ◽  
K G Xanthopoulos ◽  
B M Spiegelman
Keyword(s):  
Gene Expression ◽  
Transcriptional Activation ◽  
Adipocyte Differentiation ◽  
Binding Protein ◽  
Point Mutations ◽  
Chloramphenicol Acetyltransferase ◽  
Lipid Binding ◽  
Direct Role ◽  
New Genes ◽  
Chloramphenicol Acetyltransferase Gene

Adipocyte differentiation is accompanied by the transcriptional activation of many new genes, including the gene encoding adipocyte P2 (aP2), an intracellular lipid-binding protein. Using specific deletions and point mutations, we have shown that at least two distinct sequence elements in the aP2 promoter contribute to the expression of the chloramphenicol acetyltransferase gene in chimeric constructions transfected into adipose cells. An AP-I site at -120, shown earlier to bind Jun- and Fos-like proteins, serves as a positive regulator of chloramphenicol acetyltransferase gene expression in adipocytes but is specifically silenced by adjacent upstream sequences in preadipocytes. Sequences upstream of the AP-I site at -140 (termed AE-1) can function as an enhancer in both cell types when linked to a viral promoter but can stimulate expression only in fat cells in the intact aP2 promoter. The AE-1 sequence binds an adipocyte protein identical or very closely related to an enhancer-binding protein (C/EBP) that has been previously implicated in the regulation of several liver-specific genes. A functional role for C/EBP in the regulation of the aP2 gene is indicated by the facts that C/EBP mRNA is induced during adipocyte differentiation and the aP2 promoter is transactivated by cotransfection of a C/EBP expression vector into preadipose cells. These results indicate that sequences that bind C/EBP and the Fos-Jun complex play major roles in the expression of the aP2 gene during adipocyte differentiation and demonstrate that C/EBP can directly regulate cellular gene expression.

scholarly journals Cellular retinol-binding protein type III is a PPARγ target gene and plays a role in lipid metabolism

2008 ◽  
Vol 295 (6) ◽  
pp. E1358-E1368 ◽  
Author(s):  
Cynthia F. Zizola ◽  
Gary J. Schwartz ◽  
Silke Vogel
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Free Fatty Acid ◽  
Target Gene ◽  
Binding Protein ◽  
Retinol Binding Protein ◽  
Wild Type ◽  
Type Iii ◽  
Cellular Retinol Binding Protein

Cellular retinol-binding protein (CRBP) type III (CRBP-III) belongs to the family of intracellular lipid-binding proteins, which includes the adipocyte-binding protein aP2. In the cytosol, CRBP-III binds retinol, the precursor of retinyl ester and the active metabolite retinoic acid. The goal of the present work is to understand the regulation of CRBP-III expression and its role in lipid metabolism. Using EMSAs, luciferase reporter assays, and chromatin immunoprecipitation assays, we found that CRBP-III is a direct target of peroxisome proliferator-activated receptor-γ (PPARγ). Moreover, CRBP-III expression was induced in adipose tissue of mice after treatment with the PPARγ agonist rosiglitazone. To examine a potential role of CRBP-III in regulating lipid metabolism in vivo, CRBP-III-deficient (C-III-KO) mice were maintained on a high-fat diet (HFD). Hepatic steatosis was decreased in HFD-fed C-III-KO compared with HFD-fed wild-type mice. These differences were partly explained by decreased serum free fatty acid levels and decreased free fatty acid efflux from adipose tissue of C-III-KO mice. In addition, the lack of CRBP-III was associated with reduced food intake, increased respiratory energy ratio, and altered body composition, with decreased adiposity and increased lean body mass. Furthermore, expression of genes involved in mitochondrial fatty acid oxidation in brown adipose tissue was increased in C-III-KO mice, and C-III-KO mice were more cold tolerant than wild-type mice fed an HFD. In summary, we demonstrate that CRBP-III is a PPARγ target gene and plays a role in lipid and whole body energy metabolism.

scholarly journals Expression of adipocytokine genes and their content in various adipose tissue sites in patients with heart diseases

2020 ◽  
Author(s):  
Olga Gruzdeva ◽  
Yulia Dyleva ◽  
Ekaterina Belik ◽  
Daria Borodkina ◽  
Maxim Sinitsky ◽  
...  
Keyword(s):  
Gene Expression ◽  
Coronary Artery Disease ◽  
Adipose Tissue ◽  
Coronary Artery ◽  
Mitral Valve ◽  
Valve Replacement ◽  
Mitral Valve Replacement ◽  
Biologically Active ◽  
Fat Depots ◽  
Artery Disease

Abstract Background Adipose tissue (AT) is an endocrine and paracrine organ that synthesizes biologically active adipocytokines, which affect inflammation, fibrosis, and atherogenesis. Epicardial and perivascular fat depots are of great interest owing to potential effects on the myocardium and blood vessels. Objective To assess expression and secretion of adipocytokine genes in adipose tissue in patients coronary artery disease (CAD) and patients with aortic or mitral valve replacement. Methods The study included 84 patients with CAD and 50 patients with aortic or mitral valve replacement. Adipocytes were isolated from subcutaneous (SAT), epicardial (EAT), and perivascular AT (PVAT) samples. Isolated adipocytes were cultured for 24 h after which, gene expression and secretion levels of selected adipokines and cytokines in the culture medium were determined. Results The study parameters differed depending on the adipose tissue location. EAT adipocytes in CAD patients were characterized by a pronounced imbalance in the adipokine system. EAT had the lowest adiponectin gene expression and secretion, regardless of nosology and high expression levels of the leptin gene, its receptor, and interleukin-6 (IL-6) were detected. High leptin and IL-6 levels resulted in increased pro-inflammatory activity, as observed in both EAT and PVAT adipocytes, especially in individuals with coronary artery disease. Conclusion The "protective" potential of adipose tissue depends on its location.

scholarly journals Diet-related variation in cellular retinol-binding protein type II gene expression in rat jejunum

2005 ◽  
Vol 94 (6) ◽  
pp. 890-895 ◽  
Author(s):  
Kazuhito Suruga ◽  
Masaaki Kitagawa ◽  
Hiromitsu Yasutake ◽  
Sachiko Takase ◽  
Toshinao Goda
Keyword(s):  
Gene Expression ◽  
Fatty Acid ◽  
Binding Protein ◽  
Dietary Fatty Acids ◽  
Retinol Binding Protein ◽  
Rat Jejunum ◽  
Type Ii ◽  
Feeding Period ◽  
Related Variation ◽  
Cellular Retinol Binding Protein

Cellular retinol-binding protein type II (CRBPII) is involved in the transport of vitamin A and its metabolism in the small intestine. In the present study, we demonstrated diet-related variations in CRBPII expression in rat jejunum. The CRBPII protein and mRNA levels increased in parallel after the start of feeding period regardless of whether the feeding period was restricted to the hours of darkness or of light. In addition, this variation was observed in the rats fed high-fat diet or low-fat diets, but not in those fed a fat-free diet or in fasted rats. A similar diet-induced variation was seen in the mRNA of liver-type fatty acid-binding protein in rat jejunum. In the transient transfection experiment, unsaturated fatty acid increased rat CRBPII gene promoter activity via the PPARα/retinoid X receptor-α heterodimer. Taken together, these results suggest that the diet-related variation in CRBPII expression in rat jejunum may be brought about by the transcriptional induction of CRBPII gene expression mainly triggered by dietary fatty acids.

Sign in / Sign up

Export Citation Format

Share Document