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Impact of maternal high fat diet on hypothalamic transcriptome in neonatal Sprague Dawley rats
Maternal consumption of a high fat diet during early development has been shown to impact the formation of hypothalamic neurocircuitry, thereby contributing to imbalances in appetite and energy homeostasis and increasing the risk of obesity in subsequent generations. Early in postnatal life, the neu...
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description | Maternal consumption of a high fat diet during early development has been shown to impact the formation of hypothalamic neurocircuitry, thereby contributing to imbalances in appetite and energy homeostasis and increasing the risk of obesity in subsequent generations. Early in postnatal life, the neuronal projections responsible for energy homeostasis develop in response to appetite-related peptides such as leptin. To date, no study characterises the genome-wide transcriptional changes that occur in response to exposure to high fat diet during this critical window. We explored the effects of maternal high fat diet consumption on hypothalamic gene expression in Sprague Dawley rat offspring at postnatal day 10. RNA-sequencing enabled discovery of differentially expressed genes between offspring of dams fed a high fat diet and offspring of control diet fed dams. Female high fat diet offspring displayed altered expression of 86 genes (adjusted P-value |
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Early in postnatal life, the neuronal projections responsible for energy homeostasis develop in response to appetite-related peptides such as leptin. To date, no study characterises the genome-wide transcriptional changes that occur in response to exposure to high fat diet during this critical window. We explored the effects of maternal high fat diet consumption on hypothalamic gene expression in Sprague Dawley rat offspring at postnatal day 10. RNA-sequencing enabled discovery of differentially expressed genes between offspring of dams fed a high fat diet and offspring of control diet fed dams. Female high fat diet offspring displayed altered expression of 86 genes (adjusted P-value<0.05), including genes coding for proteins of the extra cellular matrix, particularly Collagen 1a1 (Col1a1), Col1a2, Col3a1, and the imprinted Insulin-like growth factor 2 (Igf2) gene. Male high fat diet offspring showed significant changes in collagen genes (Col1a1 and Col3a1) and significant upregulation of two genes involved in regulation of dopamine availability in the brain, tyrosine hydroxylase (Th) and dopamine reuptake transporter Slc6a3 (also known as Dat1). Transcriptional changes were accompanied by increased body weight, body fat and body length in the high fat diet offspring, as well as altered blood glucose and plasma leptin. Transcriptional changes identified in the hypothalamus of offspring of high fat diet mothers could alter neuronal projection formation during early development leading to abnormalities in the neuronal circuitry controlling appetite in later life, hence priming offspring to the development of obesity.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0189492</identifier><identifier>PMID: 29240779</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Abnormalities ; Animals ; Animals, Newborn ; Appetite ; Biology and Life Sciences ; Blood glucose ; Body fat ; Body length ; Body weight ; Brain ; Circuits ; Coding ; Collagen ; Collagen (type I) ; Dams ; Diet ; Diet, High-Fat ; DNA methylation ; Dopamine ; Dopamine transporter ; Energy balance ; Female ; Food ; Gene expression ; Gene regulation ; Gene sequencing ; Genes ; Genomes ; Health aspects ; High fat diet ; Homeostasis ; Hydroxylase ; Hypothalamus ; Hypothalamus - metabolism ; Insulin ; Insulin-like growth factor II ; Insulin-like growth factors ; Laboratory rats ; Leptin ; Medicine ; Medicine and Health Sciences ; Neonates ; Neural coding ; Neurons ; Neuropeptides ; Neurosciences ; Newborn babies ; Nutrition ; Obesity ; Offspring ; Peptides ; Phenotype ; Pregnancy ; Priming ; Proteins ; Rats ; Rats, Sprague-Dawley ; Research and analysis methods ; Ribonucleic acid ; RNA ; Rodents ; Stem cells ; Transcription ; Transcriptome ; Tyrosine</subject><ispartof>PloS one, 2017-12, Vol.12 (12), p.e0189492-e0189492</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Barrand et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2017 Barrand et al 2017 Barrand et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-d2dd83174831a292cf41eff894c22bd075ec4a46bb5163883936224b0711ab6d3</citedby><cites>FETCH-LOGICAL-c692t-d2dd83174831a292cf41eff894c22bd075ec4a46bb5163883936224b0711ab6d3</cites><orcidid>0000-0001-5642-5196</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1977209962/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1977209962?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,883,25736,27907,27908,36995,36996,44573,53774,53776,74877</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29240779$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Aguila, Marcia B.</contributor><creatorcontrib>Barrand, Sanna</creatorcontrib><creatorcontrib>Crowley, Tamsyn M</creatorcontrib><creatorcontrib>Wood-Bradley, Ryan J</creatorcontrib><creatorcontrib>De Jong, Kirstie A</creatorcontrib><creatorcontrib>Armitage, James A</creatorcontrib><title>Impact of maternal high fat diet on hypothalamic transcriptome in neonatal Sprague Dawley rats</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Maternal consumption of a high fat diet during early development has been shown to impact the formation of hypothalamic neurocircuitry, thereby contributing to imbalances in appetite and energy homeostasis and increasing the risk of obesity in subsequent generations. Early in postnatal life, the neuronal projections responsible for energy homeostasis develop in response to appetite-related peptides such as leptin. To date, no study characterises the genome-wide transcriptional changes that occur in response to exposure to high fat diet during this critical window. We explored the effects of maternal high fat diet consumption on hypothalamic gene expression in Sprague Dawley rat offspring at postnatal day 10. RNA-sequencing enabled discovery of differentially expressed genes between offspring of dams fed a high fat diet and offspring of control diet fed dams. Female high fat diet offspring displayed altered expression of 86 genes (adjusted P-value<0.05), including genes coding for proteins of the extra cellular matrix, particularly Collagen 1a1 (Col1a1), Col1a2, Col3a1, and the imprinted Insulin-like growth factor 2 (Igf2) gene. Male high fat diet offspring showed significant changes in collagen genes (Col1a1 and Col3a1) and significant upregulation of two genes involved in regulation of dopamine availability in the brain, tyrosine hydroxylase (Th) and dopamine reuptake transporter Slc6a3 (also known as Dat1). Transcriptional changes were accompanied by increased body weight, body fat and body length in the high fat diet offspring, as well as altered blood glucose and plasma leptin. Transcriptional changes identified in the hypothalamus of offspring of high fat diet mothers could alter neuronal projection formation during early development leading to abnormalities in the neuronal circuitry controlling appetite in later life, hence priming offspring to the development of obesity.</description><subject>Abnormalities</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Appetite</subject><subject>Biology and Life Sciences</subject><subject>Blood glucose</subject><subject>Body fat</subject><subject>Body length</subject><subject>Body weight</subject><subject>Brain</subject><subject>Circuits</subject><subject>Coding</subject><subject>Collagen</subject><subject>Collagen (type I)</subject><subject>Dams</subject><subject>Diet</subject><subject>Diet, High-Fat</subject><subject>DNA methylation</subject><subject>Dopamine</subject><subject>Dopamine transporter</subject><subject>Energy balance</subject><subject>Female</subject><subject>Food</subject><subject>Gene expression</subject><subject>Gene regulation</subject><subject>Gene sequencing</subject><subject>Genes</subject><subject>Genomes</subject><subject>Health aspects</subject><subject>High fat diet</subject><subject>Homeostasis</subject><subject>Hydroxylase</subject><subject>Hypothalamus</subject><subject>Hypothalamus - metabolism</subject><subject>Insulin</subject><subject>Insulin-like growth factor II</subject><subject>Insulin-like growth factors</subject><subject>Laboratory rats</subject><subject>Leptin</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Neonates</subject><subject>Neural coding</subject><subject>Neurons</subject><subject>Neuropeptides</subject><subject>Neurosciences</subject><subject>Newborn babies</subject><subject>Nutrition</subject><subject>Obesity</subject><subject>Offspring</subject><subject>Peptides</subject><subject>Phenotype</subject><subject>Pregnancy</subject><subject>Priming</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Research and analysis methods</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Rodents</subject><subject>Stem 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of maternal high fat diet on hypothalamic transcriptome in neonatal Sprague Dawley rats</title><author>Barrand, Sanna ; Crowley, Tamsyn M ; Wood-Bradley, Ryan J ; De Jong, Kirstie A ; Armitage, James A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-d2dd83174831a292cf41eff894c22bd075ec4a46bb5163883936224b0711ab6d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Abnormalities</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Appetite</topic><topic>Biology and Life Sciences</topic><topic>Blood glucose</topic><topic>Body fat</topic><topic>Body length</topic><topic>Body weight</topic><topic>Brain</topic><topic>Circuits</topic><topic>Coding</topic><topic>Collagen</topic><topic>Collagen (type I)</topic><topic>Dams</topic><topic>Diet</topic><topic>Diet, High-Fat</topic><topic>DNA methylation</topic><topic>Dopamine</topic><topic>Dopamine 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consumption of a high fat diet during early development has been shown to impact the formation of hypothalamic neurocircuitry, thereby contributing to imbalances in appetite and energy homeostasis and increasing the risk of obesity in subsequent generations. Early in postnatal life, the neuronal projections responsible for energy homeostasis develop in response to appetite-related peptides such as leptin. To date, no study characterises the genome-wide transcriptional changes that occur in response to exposure to high fat diet during this critical window. We explored the effects of maternal high fat diet consumption on hypothalamic gene expression in Sprague Dawley rat offspring at postnatal day 10. RNA-sequencing enabled discovery of differentially expressed genes between offspring of dams fed a high fat diet and offspring of control diet fed dams. Female high fat diet offspring displayed altered expression of 86 genes (adjusted P-value<0.05), including genes coding for proteins of the extra cellular matrix, particularly Collagen 1a1 (Col1a1), Col1a2, Col3a1, and the imprinted Insulin-like growth factor 2 (Igf2) gene. Male high fat diet offspring showed significant changes in collagen genes (Col1a1 and Col3a1) and significant upregulation of two genes involved in regulation of dopamine availability in the brain, tyrosine hydroxylase (Th) and dopamine reuptake transporter Slc6a3 (also known as Dat1). Transcriptional changes were accompanied by increased body weight, body fat and body length in the high fat diet offspring, as well as altered blood glucose and plasma leptin. Transcriptional changes identified in the hypothalamus of offspring of high fat diet mothers could alter neuronal projection formation during early development leading to abnormalities in the neuronal circuitry controlling appetite in later life, hence priming offspring to the development of obesity.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>29240779</pmid><doi>10.1371/journal.pone.0189492</doi><tpages>e0189492</tpages><orcidid>https://orcid.org/0000-0001-5642-5196</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Abnormalities Animals Animals, Newborn Appetite Biology and Life Sciences Blood glucose Body fat Body length Body weight Brain Circuits Coding Collagen Collagen (type I) Dams Diet Diet, High-Fat DNA methylation Dopamine Dopamine transporter Energy balance Female Food Gene expression Gene regulation Gene sequencing Genes Genomes Health aspects High fat diet Homeostasis Hydroxylase Hypothalamus Hypothalamus - metabolism Insulin Insulin-like growth factor II Insulin-like growth factors Laboratory rats Leptin Medicine Medicine and Health Sciences Neonates Neural coding Neurons Neuropeptides Neurosciences Newborn babies Nutrition Obesity Offspring Peptides Phenotype Pregnancy Priming Proteins Rats Rats, Sprague-Dawley Research and analysis methods Ribonucleic acid RNA Rodents Stem cells Transcription Transcriptome Tyrosine |
title | Impact of maternal high fat diet on hypothalamic transcriptome in neonatal Sprague Dawley rats |
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