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Prenatal Bisphenol a Exposure and Postnatal Trans Fat Diet Alter Small Intestinal Morphology and Its Global DNA Methylation in Male Sprague-Dawley Rats, Leading to Obesity Development
In this study, we aimed to determine whether a postnatal trans fat diet (TFD) could aggravate prenatal bisphenol A (BPA) exposure effects on offspring’s small intestine and adulthood obesity, due to the relatively sparse findings on how the interaction between these two variables interrupt the small...
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Published in: | Nutrients 2022-06, Vol.14 (12), p.2382 |
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description | In this study, we aimed to determine whether a postnatal trans fat diet (TFD) could aggravate prenatal bisphenol A (BPA) exposure effects on offspring’s small intestine and adulthood obesity, due to the relatively sparse findings on how the interaction between these two variables interrupt the small intestinal cells. Twelve pregnant rats were administered with either unspiked drinking water (control; CTL) or BPA-spiked drinking water throughout pregnancy. Twelve weaned pups from each pregnancy group were then given either a normal diet (ND) or TFD from postnatal week (PNW) 3 until PNW14, divided into control offspring on normal diet (CTL-ND), BPA-exposed offspring on normal diet (BPA-ND), control offspring on trans fat diet (CTL-TFD), and BPA offspring on trans fat diet (BPA-TFD) groups. Body weight (BW), waist circumference, and food and water intake were measured weekly in offspring. At PNW14, small intestines were collected for global DNA methylation and histological analyses. Marked differences in BW were observed starting at PNW9 in BPA-TFD (389.5 ± 10.0 g; p < 0.05) relative to CTL-ND (339.0 ± 7.2 g), which persisted until PNW13 (505.0 ± 15.6 g). In contrast, water and food intake between offspring were significantly different (p < 0.01−0.05) at earlier ages only (PNW4−6 and PNW7−9, respectively). Furthermore, substantial differences in the general parameters of the intestinal structures were exclusive to ileum crypt length alone, whereby both BPA-ND (150.5 ± 5.1 μm; p < 0.001), and BPA-TFD (130.3 ± 9.9 μm; p < 0.05) were significantly longer than CTL-ND (96.8 ± 8.9 μm). Moreover, BPA-ND (2.898 ± 0.147%; p < 0.05) demonstrated global small intestinal hypermethylation when compared to CTL-ND and CTL-TFD (1.973 ± 0.232% and 1.913 ± 0.256%, respectively). Prenatal BPA exposure may significantly affect offspring’s physiological parameters and intestinal function. Additionally, our data suggest that there might be compensatory responses to postnatal TFD in the combined BPA prenatal group (BPA-TFD). |
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Twelve pregnant rats were administered with either unspiked drinking water (control; CTL) or BPA-spiked drinking water throughout pregnancy. Twelve weaned pups from each pregnancy group were then given either a normal diet (ND) or TFD from postnatal week (PNW) 3 until PNW14, divided into control offspring on normal diet (CTL-ND), BPA-exposed offspring on normal diet (BPA-ND), control offspring on trans fat diet (CTL-TFD), and BPA offspring on trans fat diet (BPA-TFD) groups. Body weight (BW), waist circumference, and food and water intake were measured weekly in offspring. At PNW14, small intestines were collected for global DNA methylation and histological analyses. Marked differences in BW were observed starting at PNW9 in BPA-TFD (389.5 ± 10.0 g; p < 0.05) relative to CTL-ND (339.0 ± 7.2 g), which persisted until PNW13 (505.0 ± 15.6 g). In contrast, water and food intake between offspring were significantly different (p < 0.01−0.05) at earlier ages only (PNW4−6 and PNW7−9, respectively). Furthermore, substantial differences in the general parameters of the intestinal structures were exclusive to ileum crypt length alone, whereby both BPA-ND (150.5 ± 5.1 μm; p < 0.001), and BPA-TFD (130.3 ± 9.9 μm; p < 0.05) were significantly longer than CTL-ND (96.8 ± 8.9 μm). Moreover, BPA-ND (2.898 ± 0.147%; p < 0.05) demonstrated global small intestinal hypermethylation when compared to CTL-ND and CTL-TFD (1.973 ± 0.232% and 1.913 ± 0.256%, respectively). Prenatal BPA exposure may significantly affect offspring’s physiological parameters and intestinal function. Additionally, our data suggest that there might be compensatory responses to postnatal TFD in the combined BPA prenatal group (BPA-TFD).</description><identifier>ISSN: 2072-6643</identifier><identifier>EISSN: 2072-6643</identifier><identifier>DOI: 10.3390/nu14122382</identifier><identifier>PMID: 35745112</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Adult ; Adults ; Animals ; Benzhydryl Compounds ; Bisphenol A ; Body Weight ; Cytotoxicity ; Development and progression ; Diet ; DNA Methylation ; Drinking Water ; Exposure ; Female ; Food ; Food intake ; Health aspects ; Humans ; Hypotheses ; Ileum ; Image retrieval ; Intestine ; Intestine, Small ; Lymphocytes T ; Male ; Metabolism ; Methylation ; Morphology ; Obesity ; Obesity - genetics ; Offspring ; Permeability ; Phenols ; Physiology ; Pregnancy ; Prenatal experience ; Prenatal Exposure Delayed Effects - genetics ; Puerperium ; Rats ; Rats, Sprague-Dawley ; Risk factors ; Small intestine ; Trans fats ; Trans Fatty Acids ; Water intake ; Water intakes</subject><ispartof>Nutrients, 2022-06, Vol.14 (12), p.2382</ispartof><rights>COPYRIGHT 2022 MDPI AG</rights><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c473t-a94c40fcf0a77d972daf08f5f544cc6b7ab97a73ca93f6422010a8d28909a94f3</citedby><cites>FETCH-LOGICAL-c473t-a94c40fcf0a77d972daf08f5f544cc6b7ab97a73ca93f6422010a8d28909a94f3</cites><orcidid>0000-0002-1671-4839 ; 0000-0003-1057-7850</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2679794061/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2679794061?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,25732,27903,27904,36991,44569,53769,53771,74872</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35745112$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zulkifli, Sarah</creatorcontrib><creatorcontrib>Mohd Nor, Noor Shafina</creatorcontrib><creatorcontrib>Sheikh Abdul Kadir, Siti Hamimah</creatorcontrib><creatorcontrib>Mohd Ranai, Norashikin</creatorcontrib><creatorcontrib>Mohd Kornain, Noor Kaslina</creatorcontrib><creatorcontrib>Wan Mohd Zain, Wan Nor I'zzah</creatorcontrib><creatorcontrib>Abdul Aziz, Mardiana</creatorcontrib><title>Prenatal Bisphenol a Exposure and Postnatal Trans Fat Diet Alter Small Intestinal Morphology and Its Global DNA Methylation in Male Sprague-Dawley Rats, Leading to Obesity Development</title><title>Nutrients</title><addtitle>Nutrients</addtitle><description>In this study, we aimed to determine whether a postnatal trans fat diet (TFD) could aggravate prenatal bisphenol A (BPA) exposure effects on offspring’s small intestine and adulthood obesity, due to the relatively sparse findings on how the interaction between these two variables interrupt the small intestinal cells. Twelve pregnant rats were administered with either unspiked drinking water (control; CTL) or BPA-spiked drinking water throughout pregnancy. Twelve weaned pups from each pregnancy group were then given either a normal diet (ND) or TFD from postnatal week (PNW) 3 until PNW14, divided into control offspring on normal diet (CTL-ND), BPA-exposed offspring on normal diet (BPA-ND), control offspring on trans fat diet (CTL-TFD), and BPA offspring on trans fat diet (BPA-TFD) groups. Body weight (BW), waist circumference, and food and water intake were measured weekly in offspring. At PNW14, small intestines were collected for global DNA methylation and histological analyses. Marked differences in BW were observed starting at PNW9 in BPA-TFD (389.5 ± 10.0 g; p < 0.05) relative to CTL-ND (339.0 ± 7.2 g), which persisted until PNW13 (505.0 ± 15.6 g). In contrast, water and food intake between offspring were significantly different (p < 0.01−0.05) at earlier ages only (PNW4−6 and PNW7−9, respectively). Furthermore, substantial differences in the general parameters of the intestinal structures were exclusive to ileum crypt length alone, whereby both BPA-ND (150.5 ± 5.1 μm; p < 0.001), and BPA-TFD (130.3 ± 9.9 μm; p < 0.05) were significantly longer than CTL-ND (96.8 ± 8.9 μm). Moreover, BPA-ND (2.898 ± 0.147%; p < 0.05) demonstrated global small intestinal hypermethylation when compared to CTL-ND and CTL-TFD (1.973 ± 0.232% and 1.913 ± 0.256%, respectively). Prenatal BPA exposure may significantly affect offspring’s physiological parameters and intestinal function. Additionally, our data suggest that there might be compensatory responses to postnatal TFD in the combined BPA prenatal group (BPA-TFD).</description><subject>Adult</subject><subject>Adults</subject><subject>Animals</subject><subject>Benzhydryl Compounds</subject><subject>Bisphenol A</subject><subject>Body Weight</subject><subject>Cytotoxicity</subject><subject>Development and progression</subject><subject>Diet</subject><subject>DNA Methylation</subject><subject>Drinking Water</subject><subject>Exposure</subject><subject>Female</subject><subject>Food</subject><subject>Food intake</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Ileum</subject><subject>Image retrieval</subject><subject>Intestine</subject><subject>Intestine, Small</subject><subject>Lymphocytes T</subject><subject>Male</subject><subject>Metabolism</subject><subject>Methylation</subject><subject>Morphology</subject><subject>Obesity</subject><subject>Obesity - genetics</subject><subject>Offspring</subject><subject>Permeability</subject><subject>Phenols</subject><subject>Physiology</subject><subject>Pregnancy</subject><subject>Prenatal experience</subject><subject>Prenatal Exposure Delayed Effects - genetics</subject><subject>Puerperium</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Risk factors</subject><subject>Small intestine</subject><subject>Trans fats</subject><subject>Trans Fatty Acids</subject><subject>Water intake</subject><subject>Water intakes</subject><issn>2072-6643</issn><issn>2072-6643</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNptktFuFCEUhidGY5vaGx_AkHhnnMoAOww3Jmu3rZvs2sbWa3KWYXZpGBiBqe6T-XpSt9ZtIlxAON__A39OUbyu8AmlAn9wY8UqQmhDnhWHBHNS1jWjz_f2B8VxjLf4fnDMa_qyOKATziZVRQ6LX1dBO0hg0ScTh4123iJAZz8HH8egEbgWXfmYdshNABfROSQ0MzqhqU06oOserEVzl3RMxmVq6cOw8davt3_k8xTRhfWrXJl9maKlTputhWS8Q8ahJViNrocA61GXM_hh9RZ9hRTfo4WG1rg1Sh5drnQ0aYtm-k5bP_TapVfFiw5s1McP61Hx7fzs5vRzubi8mJ9OF6VinKYSBFMMd6rDwHkrOGmhw0036SaMKVWvOKwEB04VCNrVjBBcYWha0ggssrajR8XHne8wrnrdqnx1ACuHYHoIW-nByKcVZzZy7e-kIBQ3kyobvH0wCP77mDOSt34MOacoSc0FFwzXe9Q65yGN63w2U72JSk45EYxw1uBMnfyHyrPVvVHe6c7k8yeCdzuBCj7GoLvHh1dY3reP_Nc-GX6z_9VH9G-z0N-be8E7</recordid><startdate>20220608</startdate><enddate>20220608</enddate><creator>Zulkifli, Sarah</creator><creator>Mohd Nor, Noor Shafina</creator><creator>Sheikh Abdul Kadir, Siti Hamimah</creator><creator>Mohd Ranai, Norashikin</creator><creator>Mohd Kornain, Noor Kaslina</creator><creator>Wan Mohd Zain, Wan Nor I'zzah</creator><creator>Abdul Aziz, Mardiana</creator><general>MDPI AG</general><general>MDPI</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-1671-4839</orcidid><orcidid>https://orcid.org/0000-0003-1057-7850</orcidid></search><sort><creationdate>20220608</creationdate><title>Prenatal Bisphenol a Exposure and Postnatal Trans Fat Diet Alter Small Intestinal Morphology and Its Global DNA Methylation in Male Sprague-Dawley Rats, Leading to Obesity Development</title><author>Zulkifli, Sarah ; Mohd Nor, Noor Shafina ; Sheikh Abdul Kadir, Siti Hamimah ; Mohd Ranai, Norashikin ; Mohd Kornain, Noor Kaslina ; Wan Mohd Zain, Wan Nor I'zzah ; Abdul Aziz, Mardiana</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c473t-a94c40fcf0a77d972daf08f5f544cc6b7ab97a73ca93f6422010a8d28909a94f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Adult</topic><topic>Adults</topic><topic>Animals</topic><topic>Benzhydryl Compounds</topic><topic>Bisphenol A</topic><topic>Body Weight</topic><topic>Cytotoxicity</topic><topic>Development and progression</topic><topic>Diet</topic><topic>DNA Methylation</topic><topic>Drinking Water</topic><topic>Exposure</topic><topic>Female</topic><topic>Food</topic><topic>Food intake</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Hypotheses</topic><topic>Ileum</topic><topic>Image retrieval</topic><topic>Intestine</topic><topic>Intestine, Small</topic><topic>Lymphocytes T</topic><topic>Male</topic><topic>Metabolism</topic><topic>Methylation</topic><topic>Morphology</topic><topic>Obesity</topic><topic>Obesity - genetics</topic><topic>Offspring</topic><topic>Permeability</topic><topic>Phenols</topic><topic>Physiology</topic><topic>Pregnancy</topic><topic>Prenatal experience</topic><topic>Prenatal Exposure Delayed Effects - genetics</topic><topic>Puerperium</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Risk factors</topic><topic>Small intestine</topic><topic>Trans fats</topic><topic>Trans Fatty Acids</topic><topic>Water intake</topic><topic>Water intakes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zulkifli, Sarah</creatorcontrib><creatorcontrib>Mohd Nor, Noor Shafina</creatorcontrib><creatorcontrib>Sheikh Abdul Kadir, Siti Hamimah</creatorcontrib><creatorcontrib>Mohd Ranai, Norashikin</creatorcontrib><creatorcontrib>Mohd Kornain, Noor Kaslina</creatorcontrib><creatorcontrib>Wan Mohd Zain, Wan Nor I'zzah</creatorcontrib><creatorcontrib>Abdul Aziz, Mardiana</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Physical Education Index</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Publicly Available Content (ProQuest)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nutrients</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zulkifli, Sarah</au><au>Mohd Nor, Noor Shafina</au><au>Sheikh Abdul Kadir, Siti Hamimah</au><au>Mohd Ranai, Norashikin</au><au>Mohd Kornain, Noor Kaslina</au><au>Wan Mohd Zain, Wan Nor I'zzah</au><au>Abdul Aziz, Mardiana</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prenatal Bisphenol a Exposure and Postnatal Trans Fat Diet Alter Small Intestinal Morphology and Its Global DNA Methylation in Male Sprague-Dawley Rats, Leading to Obesity Development</atitle><jtitle>Nutrients</jtitle><addtitle>Nutrients</addtitle><date>2022-06-08</date><risdate>2022</risdate><volume>14</volume><issue>12</issue><spage>2382</spage><pages>2382-</pages><issn>2072-6643</issn><eissn>2072-6643</eissn><abstract>In this study, we aimed to determine whether a postnatal trans fat diet (TFD) could aggravate prenatal bisphenol A (BPA) exposure effects on offspring’s small intestine and adulthood obesity, due to the relatively sparse findings on how the interaction between these two variables interrupt the small intestinal cells. Twelve pregnant rats were administered with either unspiked drinking water (control; CTL) or BPA-spiked drinking water throughout pregnancy. Twelve weaned pups from each pregnancy group were then given either a normal diet (ND) or TFD from postnatal week (PNW) 3 until PNW14, divided into control offspring on normal diet (CTL-ND), BPA-exposed offspring on normal diet (BPA-ND), control offspring on trans fat diet (CTL-TFD), and BPA offspring on trans fat diet (BPA-TFD) groups. Body weight (BW), waist circumference, and food and water intake were measured weekly in offspring. At PNW14, small intestines were collected for global DNA methylation and histological analyses. Marked differences in BW were observed starting at PNW9 in BPA-TFD (389.5 ± 10.0 g; p < 0.05) relative to CTL-ND (339.0 ± 7.2 g), which persisted until PNW13 (505.0 ± 15.6 g). In contrast, water and food intake between offspring were significantly different (p < 0.01−0.05) at earlier ages only (PNW4−6 and PNW7−9, respectively). Furthermore, substantial differences in the general parameters of the intestinal structures were exclusive to ileum crypt length alone, whereby both BPA-ND (150.5 ± 5.1 μm; p < 0.001), and BPA-TFD (130.3 ± 9.9 μm; p < 0.05) were significantly longer than CTL-ND (96.8 ± 8.9 μm). Moreover, BPA-ND (2.898 ± 0.147%; p < 0.05) demonstrated global small intestinal hypermethylation when compared to CTL-ND and CTL-TFD (1.973 ± 0.232% and 1.913 ± 0.256%, respectively). Prenatal BPA exposure may significantly affect offspring’s physiological parameters and intestinal function. Additionally, our data suggest that there might be compensatory responses to postnatal TFD in the combined BPA prenatal group (BPA-TFD).</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>35745112</pmid><doi>10.3390/nu14122382</doi><orcidid>https://orcid.org/0000-0002-1671-4839</orcidid><orcidid>https://orcid.org/0000-0003-1057-7850</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Adult Adults Animals Benzhydryl Compounds Bisphenol A Body Weight Cytotoxicity Development and progression Diet DNA Methylation Drinking Water Exposure Female Food Food intake Health aspects Humans Hypotheses Ileum Image retrieval Intestine Intestine, Small Lymphocytes T Male Metabolism Methylation Morphology Obesity Obesity - genetics Offspring Permeability Phenols Physiology Pregnancy Prenatal experience Prenatal Exposure Delayed Effects - genetics Puerperium Rats Rats, Sprague-Dawley Risk factors Small intestine Trans fats Trans Fatty Acids Water intake Water intakes |
title | Prenatal Bisphenol a Exposure and Postnatal Trans Fat Diet Alter Small Intestinal Morphology and Its Global DNA Methylation in Male Sprague-Dawley Rats, Leading to Obesity Development |
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