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פותח על ידי קלירמאש פתרונות בע"מ -
High fat diet induces hypermethylation of the hypothalamic Pomc promoter and obesity in post-weaning rats
Year:
2013
Source of publication :
Psychoneuroendocrinology
Authors :
מאירי, נעם
;
.
קיסיליוק, טטיאנה
;
.
Volume :
38
Co-Authors:
Marco, A., Faculty of Life Sciences, Bar Ilan University, Ramat-Gan 52900, Israel, Gonda Brain Res Center, Bar Ilan University, Ramat-Gan 52900, Israel
Kisliouk, T., Institute of Animal Science, ARO, The Volcani Center, PO Box 6, Bet Dagan 50250, Israel
Weller, A., Gonda Brain Res Center, Bar Ilan University, Ramat-Gan 52900, Israel, Department of Psychology, Bar Ilan University, Ramat-Gan 52900, Israel
Meiri, N., Institute of Animal Science, ARO, The Volcani Center, PO Box 6, Bet Dagan 50250, Israel
Facilitators :
From page:
2844
To page:
2853
(
Total pages:
10
)
Abstract:
Impaired response of the brain to the leptin signal leads to a persisting dysregulation of food intake and energy balance. High plasma leptin or insulin should activate proopiomelanocortin (POMC), the precursor of the anorexigenic neuropeptide α-melanocyte-stimulating hormone (α-MSH) in the hypothalamic arcuate nucleus (ARC). Nevertheless, in obesity, this signal transduction pathway might be impaired. In this study we investigated whether chronic high fat (HF) diet consumption from post-weaning to adulthood increases CpG methylation of the Pomc promoter. The hypothesis that this would disrupt the essential binding of the transcription factor Sp1 to the Pomc promoter was tested. Male rats were raised from postnatal day 21 till 90 on either HF or standard diet. As a result HF fed rats were significantly heavier, with high leptin and insulin levels in their plasma but almost no changes in ARC mRNA expression levels of Pomc. The Pomc promoter area in the HF-treated rats was found to be hypermethylated. Furthermore, there was a direct correlation in individual rats between CpG methylation at specific sites that affect Sp1 binding and plasma leptin levels and/or body weight. Although, as expected the HF diet resulted in up-regulation of Sp1, the binding of Sp1 to the hypermethylated Pomc promoter was significantly reduced. Therefore, we suggest that hypermethylation on the promoter region of the Pomc gene can emerge at post-lactation periods and interfere with transcription factor binding, thus blocking the effects of high leptin levels, leading to obesity. © 2013 Elsevier Ltd.
Note:
Related Files :
animal experiment
Animals
beta actin
epigenetics
gene expression
Male
obesity
RT-PCR (Real-Time Polymerase Chain Reaction)
עוד תגיות
תוכן קשור
More details
DOI :
10.1016/j.psyneuen.2013.07.011
Article number:
Affiliations:
Database:
סקופוס
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
31219
Last updated date:
02/03/2022 17:27
Creation date:
17/04/2018 01:00
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Scientific Publication
High fat diet induces hypermethylation of the hypothalamic Pomc promoter and obesity in post-weaning rats
38
Marco, A., Faculty of Life Sciences, Bar Ilan University, Ramat-Gan 52900, Israel, Gonda Brain Res Center, Bar Ilan University, Ramat-Gan 52900, Israel
Kisliouk, T., Institute of Animal Science, ARO, The Volcani Center, PO Box 6, Bet Dagan 50250, Israel
Weller, A., Gonda Brain Res Center, Bar Ilan University, Ramat-Gan 52900, Israel, Department of Psychology, Bar Ilan University, Ramat-Gan 52900, Israel
Meiri, N., Institute of Animal Science, ARO, The Volcani Center, PO Box 6, Bet Dagan 50250, Israel
High fat diet induces hypermethylation of the hypothalamic Pomc promoter and obesity in post-weaning rats
Impaired response of the brain to the leptin signal leads to a persisting dysregulation of food intake and energy balance. High plasma leptin or insulin should activate proopiomelanocortin (POMC), the precursor of the anorexigenic neuropeptide α-melanocyte-stimulating hormone (α-MSH) in the hypothalamic arcuate nucleus (ARC). Nevertheless, in obesity, this signal transduction pathway might be impaired. In this study we investigated whether chronic high fat (HF) diet consumption from post-weaning to adulthood increases CpG methylation of the Pomc promoter. The hypothesis that this would disrupt the essential binding of the transcription factor Sp1 to the Pomc promoter was tested. Male rats were raised from postnatal day 21 till 90 on either HF or standard diet. As a result HF fed rats were significantly heavier, with high leptin and insulin levels in their plasma but almost no changes in ARC mRNA expression levels of Pomc. The Pomc promoter area in the HF-treated rats was found to be hypermethylated. Furthermore, there was a direct correlation in individual rats between CpG methylation at specific sites that affect Sp1 binding and plasma leptin levels and/or body weight. Although, as expected the HF diet resulted in up-regulation of Sp1, the binding of Sp1 to the hypermethylated Pomc promoter was significantly reduced. Therefore, we suggest that hypermethylation on the promoter region of the Pomc gene can emerge at post-lactation periods and interfere with transcription factor binding, thus blocking the effects of high leptin levels, leading to obesity. © 2013 Elsevier Ltd.
Scientific Publication
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