scholarly journals Evidence for a brown adipocyte specific enhancer in the first intron of the murine Ucp3 gene

2012 ◽  
Vol 1817 ◽  
pp. S41
Author(s):  
C. Hoffmann ◽  
T. Fromme ◽  
M. Klingenspor
Keyword(s):  
Brown Adipocyte ◽  
First Intron ◽  
Ucp3 Gene

scholarly journals PPARs in the Control of Uncoupling Proteins Gene Expression

PPAR Research ◽  
2007 ◽  
Vol 2007 ◽  
pp. 1-12 ◽  
Author(s):  
Francesc Villarroya ◽  
Roser Iglesias ◽  
Marta Giralt
Keyword(s):  
Gene Expression ◽  
Mitochondrial Membrane ◽  
Adipocyte Differentiation ◽  
Uncoupling Proteins ◽  
Membrane Transporters ◽  
Brown Adipocyte ◽  
Ucp3 Gene ◽  
Ucp2 Gene

Uncoupling proteins (UCPs) are mitochondrial membrane transporters involved in the control of energy conversion in mitochondria. Experimental and genetic evidence relate dysfunctions of UCPs with metabolic syndrome and obesity. The PPAR subtypes mediate to a large extent the transcriptional regulation of the UCP genes, with a distinct relevance depending on the UCP gene and the tissue in which it is expressed. UCP1 gene is under the dual control of PPARγand PPARαin relation to brown adipocyte differentiation and lipid oxidation, respectively. UCP3 gene is regulated by PPARαand PPARδin the muscle, heart, and adipose tissues. UCP2 gene is also under the control of PPARs even in tissues in which it is the predominantly expressed UCP (eg, the pancreas and liver). This review summarizes the current understanding of the role of PPARs in UCPs gene expression in normal conditions and also in the context of type-2 diabetes or obesity.

scholarly journals Enhancement of the Antiobesity and Antioxidant Effect of Purple Sweet Potato Extracts and Enhancement of the Effects by Fermentation

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 888
Author(s):  
Seul Gi Lee ◽  
Jongbeom Chae ◽  
Dong Se Kim ◽  
Jung-Bok Lee ◽  
Gi-Seok Kwon ◽  
...  
Keyword(s):  
Sweet Potato ◽  
Ipomoea Batatas ◽  
Radical Scavenging ◽  
The Body ◽  
Brown Adipocyte ◽  
Obese Mice ◽  
Adipose Tissues ◽  
White Adipocytes ◽  
Beige Adipocytes ◽  
Purple Sweet Potato

The browning of white adipocytes, which transforms energy-storing white adipocytes to heat-producing beige adipocytes, is considered a strategy against metabolic diseases. Several dietary compounds, such as anthocyanins, flavonoids, and phenolic acids, induce a brown adipocyte-like phenotype in white adipocytes. In this study, we demonstrated that purple sweet potato (Ipomoea batatas) extract (PSP) exhibited potent radical scavenging activity. In addition, PSP was found to contain large amounts of phenolic, flavonoid, and anthocyanin compounds; the amount of these compounds was affected by fermentation. Functionally, PSP-induced adipose browning in high-fat-diet (HFD)-induced obese mice. The administration of PSP significantly suppressed the body weight gain and abnormal expansion of white adipose tissues in the obese mice. The expression of adipose browning-related genes was higher in the inguinal white adipose tissues from the PSP-treated mice than those in the HFD-fed mice. Moreover, PSP-treated 3T3-L1 adipocytes formed multilocular lipid droplets, similar to those formed in the 3T3-L1 adipocytes treated with a browning induction cocktail. The PSP-treated cells had an increased expression level of mitochondria and lipolysis-related genes. The browning effects of PSP were enhanced by fermentation with Lactobacillus. This study, to our knowledge, is the first to identify a new mechanism to increase the antiobesity effects of PSP by inducing adipocyte browning of adipocytes.

scholarly journals PSIX-33 Docosahexaenoic Acid (DHA) but not Eicosapentaenoic Acid (EPA) induces the trans-differentiation of C2C12 into white-like adipocytes phenotype

2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 309-310
Author(s):  
Yan Huang ◽  
Saeed Ghnaimawi ◽  
Yongjie Wang ◽  
Shilei Zhang ◽  
Jamie Baum
Keyword(s):  
Mitochondrial Biogenesis ◽  
Cultured Cells ◽  
Adipogenic Differentiation ◽  
The Body ◽  
C2c12 Cells ◽  
Brown Adipocyte ◽  
Marker Genes ◽  
Induction Medium ◽  
Spare Capacity ◽  
Epa And Dha

Abstract Muscle-derived stem cells (MDSCs, or myoblasts) play an important role in myotubes regeneration. However, these cells can differentiate into adipocytes once exposed to EPA and DHA, which are highly suggested during pregnancy. The objective of this study aims at determining the effect of isolated EPA and DHA on C2C12 cells undergoing white and brown adipogenic differentiation. Confluent cultured cells were treated with white and brown adipocyte induction medium (WIM and BIM respectively) with 50µM EPA and 50µM DHA separately. DHA treated groups differentiated into white-like adipocyte by down-regulating the expression of myogenic genes such as MyoD, MyoG, and Mrf4; but promoted white adipocyte marker genes(P < 0.05). Moreover, cells treated with WIM and DHA exhibited a decrease in mitochondrial biogenesis through suppressing PGC1a and TFAM expression (P < 0.05). Also, DHA promoted the expression of lipolysis regulating genes. DHA impaired C2C12 cells browning through reducing the mitochondrial biogenesis by significantly suppressing the expression of COX7a1, PGC1a, and UCP3 genes (P < 0.05). DHA treated groups showed an increased accumulation of lipid droplets and suppressed maximal mitochondrial respiration and spare capacity. EPA treatment reduced myogenesis regulating genes (P < 0.05) but did not affect adipogenic genes (P >0.05). Likewise, EPA suppressed the expression of WAT signature genes (P < 0.05), indicating its antagonism to DHA. EPA and WIM treatment suppressed the expression of TFAM and PGC1a, but did not affect PGC1a protein level. Although mitochondrial biogenic gene expression was reduced in EPA and BIDM treated group, no changes in mitochondrial function were observed. EPA supplementation did not affect the differential route of C2C12 into brown adipocytes. To conclude, EPA and DHA may similarly affect the integrity of muscle tissue, but DHA is a potent adipogenic and lipogenic factor that can change the metabolic profile of the body by increasing intramuscular fat.

scholarly journals Genome-wide discovery of G-quadruplexes in barley

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
H. Busra Cagirici ◽  
Hikmet Budak ◽  
Taner Z. Sen
Keyword(s):  
Transcription Initiation ◽  
Large Window ◽  
First Intron ◽  
Domain Sequence ◽  
Genome Wide ◽  
Square Planar ◽  
Peak Points ◽  
Molecular Functions ◽  
Nucleic Acid Structures ◽  
Provided Examples

AbstractG-quadruplexes (G4s) are four-stranded nucleic acid structures with closely spaced guanine bases forming square planar G-quartets. Aberrant formation of G4 structures has been associated with genomic instability. However, most plant species are lacking comprehensive studies of G4 motifs. In this study, genome-wide identification of G4 motifs in barley was performed, followed by a comparison of genomic distribution and molecular functions to other monocot species, such as wheat, maize, and rice. Similar to the reports on human and some plants like wheat, G4 motifs peaked around the 5′ untranslated region (5′ UTR), the first coding domain sequence, and the first intron start sites on antisense strands. Our comparative analyses in human, Arabidopsis, maize, rice, and sorghum demonstrated that the peak points could be erroneously merged into a single peak when large window sizes are used. We also showed that the G4 distributions around genic regions are relatively similar in the species studied, except in the case of Arabidopsis. G4 containing genes in monocots showed conserved molecular functions for transcription initiation and hydrolase activity. Additionally, we provided examples of imperfect G4 motifs.

scholarly journals Future Prospects of Gene Therapy for Friedreich’s Ataxia

2021 ◽  
Vol 22 (4) ◽  
pp. 1815 ◽  
Author(s):  
Gabriel Ocana-Santero ◽  
Javier Díaz-Nido ◽  
Saúl Herranz-Martín
Keyword(s):  
Gene Therapy ◽  
Viral Vectors ◽  
Autosomal Recessive ◽  
State Of The Art ◽  
Friedreich’S Ataxia ◽  
Friedreich's Ataxia ◽  
First Intron ◽  
Progressive Neurodegeneration ◽  
Feasible Solutions ◽  
Neurogenetic Disease

Friedreich’s ataxia is an autosomal recessive neurogenetic disease that is mainly associated with atrophy of the spinal cord and progressive neurodegeneration in the cerebellum. The disease is caused by a GAA-expansion in the first intron of the frataxin gene leading to a decreased level of frataxin protein, which results in mitochondrial dysfunction. Currently, there is no effective treatment to delay neurodegeneration in Friedreich’s ataxia. A plausible therapeutic approach is gene therapy. Indeed, Friedreich’s ataxia mouse models have been treated with viral vectors en-coding for either FXN or neurotrophins, such as brain-derived neurotrophic factor showing promising results. Thus, gene therapy is increasingly consolidating as one of the most promising therapies. However, several hurdles have to be overcome, including immunotoxicity and pheno-toxicity. We review the state of the art of gene therapy in Friedreich’s ataxia, addressing the main challenges and the most feasible solutions for them.

scholarly journals Identification of an enhancer sequence within the first intron required for cartilage-specific transcription of the α2(XI) collagen gene. VOLUME 275 (2000) PAGES 12712-12718

2009 ◽  
Vol 284 (17) ◽  
pp. 11748.2-11748 ◽  
Author(s):  
Ying Liu ◽  
Haochuan Li ◽  
Kazuhiro Tanaka ◽  
Noriyuki Tsumaki ◽  
Yoshihiko Yamada
Keyword(s):  
Collagen Gene ◽  
Enhancer Sequence ◽  
First Intron

scholarly journals Mitochondrial Group II Introns, Cytochrome c Oxidase, and Senescence in Podospora anserina

1999 ◽  
Vol 19 (6) ◽  
pp. 4093-4100 ◽  
Author(s):  
Odile Begel ◽  
Jocelyne Boulay ◽  
Beatrice Albert ◽  
Eric Dufour ◽  
Annie Sainsard-Chanet
Keyword(s):  
Life Span ◽  
Integration Site ◽  
Group Ii Intron ◽  
Podospora Anserina ◽  
Wild Type ◽  
First Intron ◽  
Limited Life ◽  
Related Group ◽  
Group Ii ◽  
Mitochondrial Chromosome

ABSTRACT Podospora anserina is a filamentous fungus with a limited life span. It expresses a degenerative syndrome called senescence, which is always associated with the accumulation of circular molecules (senDNAs) containing specific regions of the mitochondrial chromosome. A mobile group II intron (α) has been thought to play a prominent role in this syndrome. Intron α is the first intron of the cytochrome c oxidase subunit I gene (COX1). Mitochondrial mutants that escape the senescence process are missing this intron, as well as the first exon of theCOX1 gene. We describe here the first mutant of P. anserina that has the α sequence precisely deleted and whose cytochrome c oxidase activity is identical to that of wild-type cells. The integration site of the intron is slightly modified, and this change prevents efficient homing of intron α. We show here that this mutant displays a senescence syndrome similar to that of the wild type and that its life span is increased about twofold. The introduction of a related group II intron into the mitochondrial genome of the mutant does not restore the wild-type life span. These data clearly demonstrate that intron α is not the specific senescence factor but rather an accelerator or amplifier of the senescence process. They emphasize the role that intron α plays in the instability of the mitochondrial chromosome and the link between this instability and longevity. Our results strongly support the idea that in Podospora, “immortality” can be acquired not by the absence of intron α but rather by the lack of active cytochromec oxidase.

Growth factor regulation of uncoupling protein-1 mRNA expression in brown adipocytes

2002 ◽  
Vol 282 (1) ◽  
pp. C105-C112 ◽  
Author(s):  
Bibian García ◽  
Maria-Jesús Obregón
Keyword(s):  
Growth Factor ◽  
Adipocyte Differentiation ◽  
Uncoupling Protein ◽  
Brown Adipocyte ◽  
Mrna Levels ◽  
Uncoupling Protein 1 ◽  
Brown Adipocytes ◽  
Proliferation And Differentiation ◽  
Epidermal Growth ◽  
Continuous Presence

To study the effect of the mitogens epidermal growth factor (EGF), acidic and basic fibroblast growth factors (aFGF and bFGF), and vasopressin on brown adipocyte differentiation, we analyzed the expression of uncoupling protein-1 (UCP-1) mRNA. Quiescent brown preadipocytes express high levels of UCP-1 mRNA in response to triiodothyronine (T3) and norepinephrine (NE). The addition of serum or the mitogenic condition aFGF + vasopressin + NE or EGF + vasopressin + NE decreases UCP-1 mRNA. A second addition of mitogens further decreases UCP-1 mRNA. Treatment with aFGF or bFGF alone increases UCP-1 mRNA, whereas the addition of EGF or vasopressin dramatically reduces UCP-1 mRNA levels. The continuous presence of T3 increases UCP-1 mRNA levels in cells treated with EGF, aFGF, or bFGF. The effect of T3 on the stimulation of DNA synthesis also was tested. T3 inhibits the mitogenic activity of aFGF and bFGF. In conclusion, mitogens like aFGF or bFGF allow brown adipocyte differentiation, whereas EGF and vasopressin inhibit the differentiation process. T3 behaves as an important hormone that regulates both brown adipocyte proliferation and differentiation.

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