Chicken leptin gene
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ABSTRACT:
PROVIDER: PRJEB22486 | ENA |
REPOSITORIES: ENA
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Project description:Obesity induces profound transcriptome changes in adipocytes; recent evidence suggests that lncRNAs play key roles in this process. Here, we performed a comprehensive transcriptome study by RNA-Seq in adipocytes isolated from interscapular brown, inguinal and epididymal white adipose tissues in diet-induced obese mice. Our analysis reveals a set of obesity-dysregulated lncRNAs, many of which exhibit dynamic changes in fed vs. fasted state, potentially serving as novel molecular markers reflecting adipose energy status. Among the most prominent ones is Lnc-leptin, an lncRNA transcribed from an enhancer region upstream of Leptin. Expression of Lnc-leptin is sensitive to insulin and closely correlates to Leptin expression across diverse pathophysiological conditions. Functionally, induction of Lnc-leptin is essential for adipogenesis, and its presence is required for a loop formation between exon2 of Lnc-leptin and promoter of Leptin in mature adipocytes and the maintenance of Leptin expression in vitro and in vivo. Our study establishes Lnc-leptin as a new regulator of Leptin.
2018-04-19 | GSE113315 | GEO
Project description:Here we provided the first single-base resolution DNA methylatome in chicken lungs by whole-genome bisulfite sequencing (MethylC-seq). In addition, two genetically distinct highly inbred chicken lines, Leghorn and Fayoumi, were used to examine how DNA methylation regulates mRNA gene expression between two lines. The methylation profile demonstrated that methylcytosines in the chicken were more likely to occur in CG dinucleotides than in non-CG sites. DNA methylation in the gene body region, especially in the internal exons, was higher than in the 5’ and 3’ flanking regions of genes.Differentially methylated region (DMR) analysis indicated widespread differences between the Leghorn and Fayoumi lines. Of particular interest, many identified DMR-associated genes were significantly enriched in immune-related groups, which indicate that DNA methylation may regulate host immune response to pathogen infection in chickens as these two genetic lines have demonstrated differential resistance to a few pathogens. This work establishes a comprehensive and precise DNA methylation pattern in chickens and lays a solid foundation for future studies on epigenetic modifications related to poultry growth, disease, and development.
2015-06-28 | GSE56975 | GEO
Project description:Leptin monotherapy (i.e. without the use of administered insulin and/or any other molecule) corrects ID-induced metabolic aberrancies and promotes survival of insulin deficient rodents. These results generated great interest in the possibility of treating insulin deficient patients with leptin and/or molecule(s) underlying its beneficial effects. Hence, with the goal of identifying circulating molecule(s) underlying the advantageous effect of leptin we performed quantitative proteomic analysis of plasma and identified S100A9 as a putative peripheral mediator of leptin action. Here, to identify circulating molecule(s) underlying the advantageous effect of leptin we compared the results obtained by quantitative proteomic analysis of plasma between 2 groups of mice: streptozotocin (STZ)-treated mice that underwent intracerebroventricular (icv) leptin treatment for 12 days (STZ-Leptin) and ii) STZ-treated mice that underwent icv leptin treatment for 10 days and were withdrawn from leptin treatment for the following two days (STZ-Leptin-STOP). STZ treatment led to a massive loss of pancreatic insulin-producing β-cells, diminished pancreatic Proinsulin mRNA level, and caused severe insulinopenia, and hyperglycemia. icv leptin administration normalized hyperglycemia. However, two days after leptin delivery was halted hyperglycemia reappeared. We hypothesized that change in plasmatic protein(s) content could underlie re-emergence of hyperglycemia following decrease of leptin action.
2019-07-12 | PXD013466 | Pride
Project description:Population based studies have established that androgen deficiency in males correlates with type 2 diabetes, visceral adiposity, and metabolic syndrome. Androgen therapy has been investigated as a possible treatment regime to combat these disorders. However, the molecular mechanism of androgen effects on these diseases still remain poorly understood. The zucker diabetic fatty (ZDF) rat, containing a mutation in the leptin receptor, is a well-investigated model of obesity and type 2 diabetes. Male rats are characterized as androgen deficient and spontaneously develop obese, hyperlipidemia, hyperglycemia and hyperinsulinemia. In this study, we used ZDF male rats as a model of metabolic syndrome to investigate the effects of testosterone administration on the development of the metabolic conditions. Methods: Male ZDF rats at six week of age were randomly divided into two groups and administered testosterone undecanoate(TU) or vehicle alone every three days for three weeks. After three weeks, overnight fasted blood glucose and insulin concentrations were significantly higher and glucose tolerance and insulin sensitivity were impaired in TU treated ZDF rats compared to vehicle controls. Moreover, increased serum triglycerides and VLDL were observed in TU treated rats. To further explore the observed metabolic changes in TU treated ZDF rats, whole-genome microarray analysis were performed on isolated liver mRNA. Results: Array analysis revealed that many hepatic lipogenic genes were increased in male ZDF rat livers treated with TU. Interestingly, SREBP-1c, a key transcriptional activator of lipogenic genes and PGC-1 , an activator of SREBP-1c were induced while small heterodimer partner, a transcriptional inhibitor of lipogenic genes was suppressed by TU treatment. Exploring signaling pathways for these effects, we observed that the hepatic activated forms of STAT3 and AMPK, two known inhibitors of hepatic lipogenesis, were decreased in TU treated rat. Moreover, we observed that DHT could block the induction of STAT3 and AMPK phosphorylation in treated primary human hepatocytes. Preliminarily, in the leptin receptor positive zucker diabetic lean male rats, we observed that TU treatment has an oppose effect on the hepatic lipogenic genes, suggesting that hepatic leptin signaling may influence androgen signaling. Further insight into the relationship between androgen deficiency and the leptin system may help improve treatment of the metabolic syndrome. Population based studies have established that androgen deficiency in males correlates with type 2 diabetes, visceral adiposity, and metabolic syndrome. Androgen therapy has been investigated as a possible treatment regime to combat these disorders. However, the molecular mechanism of androgen effects on these diseases still remain poorly understood. The zucker diabetic fatty (ZDF) rat, containing a mutation in the leptin receptor, is a well-investigated model of obesity and type 2 diabetes. Male rats are characterized as androgen deficient and spontaneously develop obese, hyperlipidemia, hyperglycemia and hyperinsulinemia. In this study, we used ZDF male rats as a model of metabolic syndrome to investigate the effects of testosterone administration on the development of the metabolic conditions. Two-condition experiment. (1) lean ZDF rats (control) vs. lean ZDF rats (testosterone treated). (2) obese ZDF rats (control) vs. obese ZDF rats (testosterone treated). Biological replicates: 4 control replicates, 4 treated replicates.
2012-09-02 | E-GEOD-23941 | biostudies-arrayexpress
Project description:Here we provided the first single-base resolution DNA methylatome in chicken lungs by whole-genome bisulfite sequencing (MethylC-seq). In addition, two genetically distinct highly inbred chicken lines, Leghorn and Fayoumi, were used to examine how DNA methylation regulates mRNA gene expression between two lines. The methylation profile demonstrated that methylcytosines in the chicken were more likely to occur in CG dinucleotides than in non-CG sites. DNA methylation in the gene body region, especially in the internal exons, was higher than in the 5’ and 3’ flanking regions of genes.Differentially methylated region (DMR) analysis indicated widespread differences between the Leghorn and Fayoumi lines. Of particular interest, many identified DMR-associated genes were significantly enriched in immune-related groups, which indicate that DNA methylation may regulate host immune response to pathogen infection in chickens as these two genetic lines have demonstrated differential resistance to a few pathogens. This work establishes a comprehensive and precise DNA methylation pattern in chickens and lays a solid foundation for future studies on epigenetic modifications related to poultry growth, disease, and development. DNA methylation profiles of two highly inbred chicken lines, Leghorn and Fayoumi,which were generated by deep sequencing, using Illumina GAII
2015-06-28 | E-GEOD-56975 | biostudies-arrayexpress
Project description:Four weeks old male broilers, fed ad libitum or fasted for 16h or 48h were used to describe the evolution of global gene expression profiles in chicken liver during a 48h fasting period using a chicken 20K oligo array. Among the 20460 oligos on the microarray, 13057 were identified as aligning with a unique coding region of the 2.1 Washington University assembly of the chicken sequence genome. So the statistical analyses were performed on this 13057 gene set. A total number of 2062 differentially expressed genes were identified. The number of genes differentially expressed after 48h of fasting compared to the Fed state was 4-fold higher than after 16h of fasting. Analysis was focused on 1162 genes selected among these 2062 genes for which a human ortholog could be identified, thus allowing functional information collect. Quantitative real-time polymerase chain reaction (qRT-PCR) validated our results. Keywords: Chicken fasted, transcriptional profiling, differentially expressed genes
2008-05-06 | GSE11290 | GEO
Project description:Population based studies have established that androgen deficiency in males correlates with type 2 diabetes, visceral adiposity, and metabolic syndrome. Androgen therapy has been investigated as a possible treatment regime to combat these disorders. However, the molecular mechanism of androgen effects on these diseases still remain poorly understood. The zucker diabetic fatty (ZDF) rat, containing a mutation in the leptin receptor, is a well-investigated model of obesity and type 2 diabetes. Male rats are characterized as androgen deficient and spontaneously develop obese, hyperlipidemia, hyperglycemia and hyperinsulinemia. In this study, we used ZDF male rats as a model of metabolic syndrome to investigate the effects of testosterone administration on the development of the metabolic conditions. Methods: Male ZDF rats at six week of age were randomly divided into two groups and administered testosterone undecanoate(TU) or vehicle alone every three days for three weeks. After three weeks, overnight fasted blood glucose and insulin concentrations were significantly higher and glucose tolerance and insulin sensitivity were impaired in TU treated ZDF rats compared to vehicle controls. Moreover, increased serum triglycerides and VLDL were observed in TU treated rats. To further explore the observed metabolic changes in TU treated ZDF rats, whole-genome microarray analysis were performed on isolated liver mRNA. Results: Array analysis revealed that many hepatic lipogenic genes were increased in male ZDF rat livers treated with TU. Interestingly, SREBP-1c, a key transcriptional activator of lipogenic genes and PGC-1 , an activator of SREBP-1c were induced while small heterodimer partner, a transcriptional inhibitor of lipogenic genes was suppressed by TU treatment. Exploring signaling pathways for these effects, we observed that the hepatic activated forms of STAT3 and AMPK, two known inhibitors of hepatic lipogenesis, were decreased in TU treated rat. Moreover, we observed that DHT could block the induction of STAT3 and AMPK phosphorylation in treated primary human hepatocytes. Preliminarily, in the leptin receptor positive zucker diabetic lean male rats, we observed that TU treatment has an oppose effect on the hepatic lipogenic genes, suggesting that hepatic leptin signaling may influence androgen signaling. Further insight into the relationship between androgen deficiency and the leptin system may help improve treatment of the metabolic syndrome. Population based studies have established that androgen deficiency in males correlates with type 2 diabetes, visceral adiposity, and metabolic syndrome. Androgen therapy has been investigated as a possible treatment regime to combat these disorders. However, the molecular mechanism of androgen effects on these diseases still remain poorly understood. The zucker diabetic fatty (ZDF) rat, containing a mutation in the leptin receptor, is a well-investigated model of obesity and type 2 diabetes. Male rats are characterized as androgen deficient and spontaneously develop obese, hyperlipidemia, hyperglycemia and hyperinsulinemia. In this study, we used ZDF male rats as a model of metabolic syndrome to investigate the effects of testosterone administration on the development of the metabolic conditions.
2012-09-02 | GSE23941 | GEO
Project description:We have performed a comparison of global patterns of gene expression between two bird species, the chicken and zebra finch, especially with regard to sex bias of autosomal vs. Z chromosome genes, dosage compensation and evolution of sex bias. Both species appear to lack a Z chromosome-wide mechanism of dosage compensation, because both have a similar pattern of significantly higher expression of Z genes in males relative to females. Unlike the chicken Z chromosome, which has female-specific expression of the non-coding RNA MHM (male hypermethylated), and acetylation of histone 4 lysine 16 (H4K16) near MHM, the zebra finch Z chromosome appears to lack the MHM sequence and acetylation of H4K16. The zebra finch also does not show the reduced male to female (M:F) ratio of gene expression near MHM similar to that found in the chicken. Although the M:F ratios of Z chromosome gene expression are similar across tissues and ages within each species, they differ between the two species. Z genes showing the greatest species difference in M:F ratio were concentrated near the MHM region of the chicken Z chromosome. The current study shows that the zebra finch differs from the chicken because it lacks a specialized region of greater dosage compensation along the Z chromosome, and shows dosage compensation for a different set of Z genes than the chicken. These patterns suggest that different avian taxa may have evolved specific compensatory mechanisms.
2010-02-11 | GSE20035 | GEO
Project description:Adaptation to hypoxia is a complicated and important physiological course for organisms, but the genetic mechanism underlying the adaptation is not fully understood yet. Tibetan Chicken (T), an indigenous chicken breed in China which inhabit in high areas with an altitude above 2,900 meters. Shouguang Chicken(S) and Dwarf Recessive White Chicken (DRW), two lowland chicken breeds, were used as control groups. The heart was the first functional organ to develop during the embryonic development. Furthermore, the heart is an efficient energy converter utilizing the most appropriate fuel for a given environment. Therefore, GeneChip® Chicken Genome Array was employed to identify the differentially expressed genes in embryonic hearts of Tibetan Chicken and two lowland chicken breeds in both hypoxic and normoxic incubating environments with a genome wide profile. Keywords: stress response
2009-09-05 | GSE12675 | GEO
Project description:Leptin, a hormone produced primarily by adipose tissue, plays a role in both energy homeostasis and reproduction, and is required in early pregnancy. Leptin stimulates metalloproteinase activity in cultured human trophoblast and stimulates invasiveness of cultured mouse trophoblast. The goal of the present study was to examine molecular mechanisms of this function in primary cultures of mouse trophoblast. Leptin was found to stimulate the phosphorylation of MEK, but not STAT3.. It also increased levels of the protein SOCS3. The ability of leptin to stimulate metalloproteinase activity was blocked by the MEK inhibitor PD98059, but also by the vehicle inhibitor DMSO. Microarray analysis revealed that leptin stimulated some genes associated with cell motility, such as Stmn1. In addition, leptin appeared to inhibit changes in gene expression associated with terminal differentiation of trophoblast giant cells, including inhibition of members of the TGFÃ signaling pathway and of genes associated with endoreduplication. However, feulgen staining revealed a loss of cells with low ploidy. We conclude that leptin may be promoting trophoblast invasion by maintaining cells in an intermediate stage of differentiation. Keywords: time course, response to hormone treatment, primary cell culture The experiments were performed on primary cultures of mouse trophoblast cells which were isolated from placentas on day 10 of pregnancy. There were two treatments: control (serum-free medium) and recombinant mouse leptin (50 ng/mL). RNA was collected at two time points, 1 hour and 24 hours, for the controls. RNA was collected at three time points after leptin treatment: 1 hour, 6 hours, and 24 hours. Thus, there were 5 samples for each experiment. The experiment was repeated four times, for a total of 20 arrays.
2010-10-08 | E-GEOD-10297 | biostudies-arrayexpress