Intergenerational inheritance induced by a high-fat diet causes hyperphagia and reduced hypothalamic sensitivity to insulin and leptin in the second-generation of rats
•A high-fat diet causes hyperphagia in second-generation offspring.•A high-fat diet induced intergenerational inheritance in second-generation offspring.•A high-fat diet reduced hypothalamic sensitivity to insulin and leptin of second-generation offspring. The aim was to investigate the intergenerat...
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| Veröffentlicht in: | Nutrition (Burbank, Los Angeles County, Calif.) Los Angeles County, Calif.), 2024-04, Vol.120, p.112333-112333, Article 112333 |
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| container_title | Nutrition (Burbank, Los Angeles County, Calif.) |
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| creator | Maia, Rosana da Conceição Araújo Lima, Taynara Carolina Barbosa, Claudiane Maria Barbosa, Maria Andréa de Queiroz, Karina Barbosa Alzamora, Andréia Carvalho |
| description | •A high-fat diet causes hyperphagia in second-generation offspring.•A high-fat diet induced intergenerational inheritance in second-generation offspring.•A high-fat diet reduced hypothalamic sensitivity to insulin and leptin of second-generation offspring.
The aim was to investigate the intergenerational inheritance induced by a high-fat diet on sensitivity to insulin and leptin in the hypothalamic control of satiety in second-generation offspring, which were fed a control diet.
Progenitor rats were fed a high-fat or a control diet for 59 d until weaning. The first-generation and second-generation offspring were fed the control diet until 90 d of age. Body mass and adiposity index of the progenitors fed the high-fat diet and the second-generation offspring from progenitors fed the high-fat diet were evaluated as were the gene expression of DNA methyltransferase 3a, angiotensin-converting enzyme type 2, angiotensin II type 2 receptor, insulin and leptin signaling pathway (insulin receptor, leptin receptor, insulin receptor substrate 2, protein kinase B, signal transducer and transcriptional activator 3, pro-opiomelanocortin, and neuropeptide Agouti-related protein), superoxide dismutase activity, and the concentration of carbonyl protein and satiety-regulating neuropeptides, pro-opiomelanocortin and neuropeptide Agouti-related protein, in the hypothalamus.
The progenitor group fed a high-fat diet showed increased insulin resistance and reduced insulin-secreting beta-cell function and reduced food intake, without changes in caloric intake. The second-generation offspring from progenitors fed a high-fat diet, compared with second-generation offspring from progenitors fed a control diet group, had decreased insulin-secreting beta-cell function and increased food and caloric intake, insulin resistance, body mass, and adiposity index. Furthermore, second-generation offspring from progenitors fed a high-fat diet had increased DNA methyltransferase 3a, neuropeptide Agouti-related protein, angiotensin II type 1 receptor, and nicotinamide adenine dinucleotide phosphate oxidase p47phox gene expression, superoxide dismutase activity, and neuropeptide Agouti-related protein concentration in the hypothalamus. In addition, there were reduced in gene expression of the insulin receptor, leptin receptor, insulin receptor substrate 2, pro-opiomelanocortin, angiotensin II type 2 receptor, angiotensin-converting enzyme type 2, and angiotensin-(1–7) receptor and pro-opiomelanoc |
| doi_str_mv | 10.1016/j.nut.2023.112333 |
| format | Article |
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The aim was to investigate the intergenerational inheritance induced by a high-fat diet on sensitivity to insulin and leptin in the hypothalamic control of satiety in second-generation offspring, which were fed a control diet.
Progenitor rats were fed a high-fat or a control diet for 59 d until weaning. The first-generation and second-generation offspring were fed the control diet until 90 d of age. Body mass and adiposity index of the progenitors fed the high-fat diet and the second-generation offspring from progenitors fed the high-fat diet were evaluated as were the gene expression of DNA methyltransferase 3a, angiotensin-converting enzyme type 2, angiotensin II type 2 receptor, insulin and leptin signaling pathway (insulin receptor, leptin receptor, insulin receptor substrate 2, protein kinase B, signal transducer and transcriptional activator 3, pro-opiomelanocortin, and neuropeptide Agouti-related protein), superoxide dismutase activity, and the concentration of carbonyl protein and satiety-regulating neuropeptides, pro-opiomelanocortin and neuropeptide Agouti-related protein, in the hypothalamus.
The progenitor group fed a high-fat diet showed increased insulin resistance and reduced insulin-secreting beta-cell function and reduced food intake, without changes in caloric intake. The second-generation offspring from progenitors fed a high-fat diet, compared with second-generation offspring from progenitors fed a control diet group, had decreased insulin-secreting beta-cell function and increased food and caloric intake, insulin resistance, body mass, and adiposity index. Furthermore, second-generation offspring from progenitors fed a high-fat diet had increased DNA methyltransferase 3a, neuropeptide Agouti-related protein, angiotensin II type 1 receptor, and nicotinamide adenine dinucleotide phosphate oxidase p47phox gene expression, superoxide dismutase activity, and neuropeptide Agouti-related protein concentration in the hypothalamus. In addition, there were reduced in gene expression of the insulin receptor, leptin receptor, insulin receptor substrate 2, pro-opiomelanocortin, angiotensin II type 2 receptor, angiotensin-converting enzyme type 2, and angiotensin-(1–7) receptor and pro-opiomelanocortin concentration in the second-generation offspring from progenitors fed the high-fat diet.
Overall, progenitors fed a high-fat diet induced changes in the hypothalamic control of satiety of the second-generation offspring from progenitors fed the high-fat diet through intergenerational inheritance. These changes led to hyperphagia, alterations in the hypothalamic pathways of insulin, and leptin and adiposity index increase, favoring the occurrence of different cardiometabolic disorders in the second-generation offspring from progenitors fed the high-fat diet fed only with the control diet.</description><identifier>ISSN: 0899-9007</identifier><identifier>EISSN: 1873-1244</identifier><identifier>DOI: 10.1016/j.nut.2023.112333</identifier><identifier>PMID: 38271759</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adenine ; Adipose tissue ; Agouti-related protein ; Agouti-Related Protein - metabolism ; AKT protein ; Angiotensin ; Angiotensin II ; Angiotensins - metabolism ; Animals ; Appetite ; Beta cells ; Blood pressure ; Body fat ; Body mass ; Carbohydrates ; Carbonyl compounds ; Carbonyls ; Deoxyribonucleic acid ; Diet ; Diet, High-Fat - adverse effects ; DNA ; DNA methylation ; DNA methyltransferase ; DNA Methyltransferase 3A ; DNA methyltransferase enzymes ; Enzymes ; Epigenetics ; Females ; Food ; Food intake ; Gene expression ; Glucose ; Heredity ; High fat diet ; Homeostasis ; Hyperphagia ; Hyperphagia - complications ; Hypothalamus ; Hypothalamus - metabolism ; Insulin ; Insulin - metabolism ; Insulin and leptin sensitivity ; Insulin Receptor Substrate Proteins - metabolism ; Insulin receptors ; Insulin Resistance ; Intergenerational inheritance ; Kinases ; Leptin - metabolism ; Metabolism ; NAD(P)H oxidase ; NADPH oxidase ; NADPH-diaphorase ; Neuropeptides ; Neuropeptides - metabolism ; Nicotinamide ; Nicotinamide adenine dinucleotide ; Nutrition research ; Obesity - genetics ; Obesity - metabolism ; Offspring ; Peptidyl-dipeptidase A ; Pro-Opiomelanocortin - genetics ; Pro-Opiomelanocortin - metabolism ; Proteins ; Rats ; Rats, Sprague-Dawley ; Receptor, Angiotensin, Type 2 - metabolism ; Receptor, Insulin - genetics ; Receptor, Insulin - metabolism ; Receptors ; Receptors, Leptin - genetics ; Satiety ; Sensitivity ; Signal transduction ; Substrates ; Superoxide dismutase ; Superoxide Dismutase - metabolism ; Weaning</subject><ispartof>Nutrition (Burbank, Los Angeles County, Calif.), 2024-04, Vol.120, p.112333-112333, Article 112333</ispartof><rights>2023 Elsevier Inc.</rights><rights>Copyright © 2023 Elsevier Inc. All rights reserved.</rights><rights>2023. Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c381t-43a3dbce0921c108f51f2498f1fd436cb4d99ae4cb5fc0e5cd1a3d82715d1d13</citedby><cites>FETCH-LOGICAL-c381t-43a3dbce0921c108f51f2498f1fd436cb4d99ae4cb5fc0e5cd1a3d82715d1d13</cites><orcidid>0000-0002-8171-435X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/2928580619?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,3541,27915,27916,45986,64374,64376,64378,72230</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38271759$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Maia, Rosana da Conceição Araújo</creatorcontrib><creatorcontrib>Lima, Taynara Carolina</creatorcontrib><creatorcontrib>Barbosa, Claudiane Maria</creatorcontrib><creatorcontrib>Barbosa, Maria Andréa</creatorcontrib><creatorcontrib>de Queiroz, Karina Barbosa</creatorcontrib><creatorcontrib>Alzamora, Andréia Carvalho</creatorcontrib><title>Intergenerational inheritance induced by a high-fat diet causes hyperphagia and reduced hypothalamic sensitivity to insulin and leptin in the second-generation of rats</title><title>Nutrition (Burbank, Los Angeles County, Calif.)</title><addtitle>Nutrition</addtitle><description>•A high-fat diet causes hyperphagia in second-generation offspring.•A high-fat diet induced intergenerational inheritance in second-generation offspring.•A high-fat diet reduced hypothalamic sensitivity to insulin and leptin of second-generation offspring.
The aim was to investigate the intergenerational inheritance induced by a high-fat diet on sensitivity to insulin and leptin in the hypothalamic control of satiety in second-generation offspring, which were fed a control diet.
Progenitor rats were fed a high-fat or a control diet for 59 d until weaning. The first-generation and second-generation offspring were fed the control diet until 90 d of age. Body mass and adiposity index of the progenitors fed the high-fat diet and the second-generation offspring from progenitors fed the high-fat diet were evaluated as were the gene expression of DNA methyltransferase 3a, angiotensin-converting enzyme type 2, angiotensin II type 2 receptor, insulin and leptin signaling pathway (insulin receptor, leptin receptor, insulin receptor substrate 2, protein kinase B, signal transducer and transcriptional activator 3, pro-opiomelanocortin, and neuropeptide Agouti-related protein), superoxide dismutase activity, and the concentration of carbonyl protein and satiety-regulating neuropeptides, pro-opiomelanocortin and neuropeptide Agouti-related protein, in the hypothalamus.
The progenitor group fed a high-fat diet showed increased insulin resistance and reduced insulin-secreting beta-cell function and reduced food intake, without changes in caloric intake. The second-generation offspring from progenitors fed a high-fat diet, compared with second-generation offspring from progenitors fed a control diet group, had decreased insulin-secreting beta-cell function and increased food and caloric intake, insulin resistance, body mass, and adiposity index. Furthermore, second-generation offspring from progenitors fed a high-fat diet had increased DNA methyltransferase 3a, neuropeptide Agouti-related protein, angiotensin II type 1 receptor, and nicotinamide adenine dinucleotide phosphate oxidase p47phox gene expression, superoxide dismutase activity, and neuropeptide Agouti-related protein concentration in the hypothalamus. In addition, there were reduced in gene expression of the insulin receptor, leptin receptor, insulin receptor substrate 2, pro-opiomelanocortin, angiotensin II type 2 receptor, angiotensin-converting enzyme type 2, and angiotensin-(1–7) receptor and pro-opiomelanocortin concentration in the second-generation offspring from progenitors fed the high-fat diet.
Overall, progenitors fed a high-fat diet induced changes in the hypothalamic control of satiety of the second-generation offspring from progenitors fed the high-fat diet through intergenerational inheritance. These changes led to hyperphagia, alterations in the hypothalamic pathways of insulin, and leptin and adiposity index increase, favoring the occurrence of different cardiometabolic disorders in the second-generation offspring from progenitors fed the high-fat diet fed only with the control diet.</description><subject>Adenine</subject><subject>Adipose tissue</subject><subject>Agouti-related protein</subject><subject>Agouti-Related Protein - metabolism</subject><subject>AKT protein</subject><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Angiotensins - metabolism</subject><subject>Animals</subject><subject>Appetite</subject><subject>Beta cells</subject><subject>Blood pressure</subject><subject>Body fat</subject><subject>Body mass</subject><subject>Carbohydrates</subject><subject>Carbonyl compounds</subject><subject>Carbonyls</subject><subject>Deoxyribonucleic acid</subject><subject>Diet</subject><subject>Diet, High-Fat - adverse effects</subject><subject>DNA</subject><subject>DNA methylation</subject><subject>DNA methyltransferase</subject><subject>DNA Methyltransferase 3A</subject><subject>DNA methyltransferase enzymes</subject><subject>Enzymes</subject><subject>Epigenetics</subject><subject>Females</subject><subject>Food</subject><subject>Food intake</subject><subject>Gene expression</subject><subject>Glucose</subject><subject>Heredity</subject><subject>High fat diet</subject><subject>Homeostasis</subject><subject>Hyperphagia</subject><subject>Hyperphagia - complications</subject><subject>Hypothalamus</subject><subject>Hypothalamus - metabolism</subject><subject>Insulin</subject><subject>Insulin - metabolism</subject><subject>Insulin and leptin sensitivity</subject><subject>Insulin Receptor Substrate Proteins - metabolism</subject><subject>Insulin receptors</subject><subject>Insulin Resistance</subject><subject>Intergenerational inheritance</subject><subject>Kinases</subject><subject>Leptin - metabolism</subject><subject>Metabolism</subject><subject>NAD(P)H oxidase</subject><subject>NADPH oxidase</subject><subject>NADPH-diaphorase</subject><subject>Neuropeptides</subject><subject>Neuropeptides - metabolism</subject><subject>Nicotinamide</subject><subject>Nicotinamide adenine dinucleotide</subject><subject>Nutrition research</subject><subject>Obesity - genetics</subject><subject>Obesity - metabolism</subject><subject>Offspring</subject><subject>Peptidyl-dipeptidase A</subject><subject>Pro-Opiomelanocortin - genetics</subject><subject>Pro-Opiomelanocortin - metabolism</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor, Angiotensin, Type 2 - metabolism</subject><subject>Receptor, Insulin - genetics</subject><subject>Receptor, Insulin - metabolism</subject><subject>Receptors</subject><subject>Receptors, Leptin - genetics</subject><subject>Satiety</subject><subject>Sensitivity</subject><subject>Signal transduction</subject><subject>Substrates</subject><subject>Superoxide dismutase</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Weaning</subject><issn>0899-9007</issn><issn>1873-1244</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kc9q3DAYxEVpSbZpHqCXIuilF2_0Wf4neiqhTQOBXHIXsvR5rcUruZIc2CfKa1YbJy30UBBoEL8ZxAwhH4FtgUFztd-6JW1LVvItQMk5f0M20LW8gLKq3pIN64QoBGPtOXkf454xBqIRZ-Scd2ULbS025OnWJQw7dBhUst6piVo3YrBJOY1Zm0Wjof2RKjra3VgMKlFjMVGtloiRjscZwzyqnVVUOUMDro787tOoJnWwmkZ00Sb7aNORJp9T4zJZ98xPOKcs80kjZlB7Z4q__6F-oFnFD-TdoKaIly_3BXn48f3h-mdxd39ze_3trtC8g1RUXHHTa2SiBA2sG2oYykp0Awym4o3uKyOEwkr39aAZ1tpANpzaqA0Y4Bfkyxo7B_9rwZjkwUaN06Qc-iXKUpSCtU3VNBn9_A-690vIBT5TXd2xBkSmYKV08DEGHOQc7EGFowQmTyPKvcwjytOIch0xez69JC_9Ac0fx-tqGfi6ApibeLQYZNQW817GBtRJGm__E_8btPSw3A</recordid><startdate>202404</startdate><enddate>202404</enddate><creator>Maia, Rosana da Conceição Araújo</creator><creator>Lima, Taynara Carolina</creator><creator>Barbosa, Claudiane Maria</creator><creator>Barbosa, Maria Andréa</creator><creator>de Queiroz, Karina Barbosa</creator><creator>Alzamora, Andréia Carvalho</creator><general>Elsevier Inc</general><general>Elsevier Limited</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>7RQ</scope><scope>7RV</scope><scope>7TS</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88C</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AN0</scope><scope>ASE</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FPQ</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K6X</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M0T</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-8171-435X</orcidid></search><sort><creationdate>202404</creationdate><title>Intergenerational inheritance induced by a high-fat diet causes hyperphagia and reduced hypothalamic sensitivity to insulin and leptin in the second-generation of rats</title><author>Maia, Rosana da Conceição Araújo ; Lima, Taynara Carolina ; Barbosa, Claudiane Maria ; Barbosa, Maria Andréa ; de Queiroz, Karina Barbosa ; Alzamora, Andréia Carvalho</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c381t-43a3dbce0921c108f51f2498f1fd436cb4d99ae4cb5fc0e5cd1a3d82715d1d13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Adenine</topic><topic>Adipose tissue</topic><topic>Agouti-related protein</topic><topic>Agouti-Related Protein - metabolism</topic><topic>AKT protein</topic><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Angiotensins - metabolism</topic><topic>Animals</topic><topic>Appetite</topic><topic>Beta cells</topic><topic>Blood pressure</topic><topic>Body fat</topic><topic>Body mass</topic><topic>Carbohydrates</topic><topic>Carbonyl compounds</topic><topic>Carbonyls</topic><topic>Deoxyribonucleic acid</topic><topic>Diet</topic><topic>Diet, High-Fat - adverse effects</topic><topic>DNA</topic><topic>DNA methylation</topic><topic>DNA methyltransferase</topic><topic>DNA Methyltransferase 3A</topic><topic>DNA methyltransferase enzymes</topic><topic>Enzymes</topic><topic>Epigenetics</topic><topic>Females</topic><topic>Food</topic><topic>Food intake</topic><topic>Gene expression</topic><topic>Glucose</topic><topic>Heredity</topic><topic>High fat diet</topic><topic>Homeostasis</topic><topic>Hyperphagia</topic><topic>Hyperphagia - complications</topic><topic>Hypothalamus</topic><topic>Hypothalamus - metabolism</topic><topic>Insulin</topic><topic>Insulin - metabolism</topic><topic>Insulin and leptin sensitivity</topic><topic>Insulin Receptor Substrate Proteins - metabolism</topic><topic>Insulin receptors</topic><topic>Insulin Resistance</topic><topic>Intergenerational inheritance</topic><topic>Kinases</topic><topic>Leptin - metabolism</topic><topic>Metabolism</topic><topic>NAD(P)H oxidase</topic><topic>NADPH oxidase</topic><topic>NADPH-diaphorase</topic><topic>Neuropeptides</topic><topic>Neuropeptides - metabolism</topic><topic>Nicotinamide</topic><topic>Nicotinamide adenine dinucleotide</topic><topic>Nutrition research</topic><topic>Obesity - genetics</topic><topic>Obesity - metabolism</topic><topic>Offspring</topic><topic>Peptidyl-dipeptidase A</topic><topic>Pro-Opiomelanocortin - genetics</topic><topic>Pro-Opiomelanocortin - metabolism</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor, Angiotensin, Type 2 - metabolism</topic><topic>Receptor, Insulin - 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Academic</collection><jtitle>Nutrition (Burbank, Los Angeles County, Calif.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Maia, Rosana da Conceição Araújo</au><au>Lima, Taynara Carolina</au><au>Barbosa, Claudiane Maria</au><au>Barbosa, Maria Andréa</au><au>de Queiroz, Karina Barbosa</au><au>Alzamora, Andréia Carvalho</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Intergenerational inheritance induced by a high-fat diet causes hyperphagia and reduced hypothalamic sensitivity to insulin and leptin in the second-generation of rats</atitle><jtitle>Nutrition (Burbank, Los Angeles County, Calif.)</jtitle><addtitle>Nutrition</addtitle><date>2024-04</date><risdate>2024</risdate><volume>120</volume><spage>112333</spage><epage>112333</epage><pages>112333-112333</pages><artnum>112333</artnum><issn>0899-9007</issn><eissn>1873-1244</eissn><abstract>•A high-fat diet causes hyperphagia in second-generation offspring.•A high-fat diet induced intergenerational inheritance in second-generation offspring.•A high-fat diet reduced hypothalamic sensitivity to insulin and leptin of second-generation offspring.
The aim was to investigate the intergenerational inheritance induced by a high-fat diet on sensitivity to insulin and leptin in the hypothalamic control of satiety in second-generation offspring, which were fed a control diet.
Progenitor rats were fed a high-fat or a control diet for 59 d until weaning. The first-generation and second-generation offspring were fed the control diet until 90 d of age. Body mass and adiposity index of the progenitors fed the high-fat diet and the second-generation offspring from progenitors fed the high-fat diet were evaluated as were the gene expression of DNA methyltransferase 3a, angiotensin-converting enzyme type 2, angiotensin II type 2 receptor, insulin and leptin signaling pathway (insulin receptor, leptin receptor, insulin receptor substrate 2, protein kinase B, signal transducer and transcriptional activator 3, pro-opiomelanocortin, and neuropeptide Agouti-related protein), superoxide dismutase activity, and the concentration of carbonyl protein and satiety-regulating neuropeptides, pro-opiomelanocortin and neuropeptide Agouti-related protein, in the hypothalamus.
The progenitor group fed a high-fat diet showed increased insulin resistance and reduced insulin-secreting beta-cell function and reduced food intake, without changes in caloric intake. The second-generation offspring from progenitors fed a high-fat diet, compared with second-generation offspring from progenitors fed a control diet group, had decreased insulin-secreting beta-cell function and increased food and caloric intake, insulin resistance, body mass, and adiposity index. Furthermore, second-generation offspring from progenitors fed a high-fat diet had increased DNA methyltransferase 3a, neuropeptide Agouti-related protein, angiotensin II type 1 receptor, and nicotinamide adenine dinucleotide phosphate oxidase p47phox gene expression, superoxide dismutase activity, and neuropeptide Agouti-related protein concentration in the hypothalamus. In addition, there were reduced in gene expression of the insulin receptor, leptin receptor, insulin receptor substrate 2, pro-opiomelanocortin, angiotensin II type 2 receptor, angiotensin-converting enzyme type 2, and angiotensin-(1–7) receptor and pro-opiomelanocortin concentration in the second-generation offspring from progenitors fed the high-fat diet.
Overall, progenitors fed a high-fat diet induced changes in the hypothalamic control of satiety of the second-generation offspring from progenitors fed the high-fat diet through intergenerational inheritance. These changes led to hyperphagia, alterations in the hypothalamic pathways of insulin, and leptin and adiposity index increase, favoring the occurrence of different cardiometabolic disorders in the second-generation offspring from progenitors fed the high-fat diet fed only with the control diet.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>38271759</pmid><doi>10.1016/j.nut.2023.112333</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-8171-435X</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0899-9007 |
| ispartof | Nutrition (Burbank, Los Angeles County, Calif.), 2024-04, Vol.120, p.112333-112333, Article 112333 |
| issn | 0899-9007 1873-1244 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2929076466 |
| source | MEDLINE; Elsevier ScienceDirect Journals Complete; ProQuest Central UK/Ireland |
| subjects | Adenine Adipose tissue Agouti-related protein Agouti-Related Protein - metabolism AKT protein Angiotensin Angiotensin II Angiotensins - metabolism Animals Appetite Beta cells Blood pressure Body fat Body mass Carbohydrates Carbonyl compounds Carbonyls Deoxyribonucleic acid Diet Diet, High-Fat - adverse effects DNA DNA methylation DNA methyltransferase DNA Methyltransferase 3A DNA methyltransferase enzymes Enzymes Epigenetics Females Food Food intake Gene expression Glucose Heredity High fat diet Homeostasis Hyperphagia Hyperphagia - complications Hypothalamus Hypothalamus - metabolism Insulin Insulin - metabolism Insulin and leptin sensitivity Insulin Receptor Substrate Proteins - metabolism Insulin receptors Insulin Resistance Intergenerational inheritance Kinases Leptin - metabolism Metabolism NAD(P)H oxidase NADPH oxidase NADPH-diaphorase Neuropeptides Neuropeptides - metabolism Nicotinamide Nicotinamide adenine dinucleotide Nutrition research Obesity - genetics Obesity - metabolism Offspring Peptidyl-dipeptidase A Pro-Opiomelanocortin - genetics Pro-Opiomelanocortin - metabolism Proteins Rats Rats, Sprague-Dawley Receptor, Angiotensin, Type 2 - metabolism Receptor, Insulin - genetics Receptor, Insulin - metabolism Receptors Receptors, Leptin - genetics Satiety Sensitivity Signal transduction Substrates Superoxide dismutase Superoxide Dismutase - metabolism Weaning |
| title | Intergenerational inheritance induced by a high-fat diet causes hyperphagia and reduced hypothalamic sensitivity to insulin and leptin in the second-generation of rats |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-14T23%3A30%3A51IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Intergenerational%20inheritance%20induced%20by%20a%20high-fat%20diet%20causes%20hyperphagia%20and%20reduced%20hypothalamic%20sensitivity%20to%20insulin%20and%20leptin%20in%20the%20second-generation%20of%20rats&rft.jtitle=Nutrition%20(Burbank,%20Los%20Angeles%20County,%20Calif.)&rft.au=Maia,%20Rosana%20da%20Concei%C3%A7%C3%A3o%20Ara%C3%BAjo&rft.date=2024-04&rft.volume=120&rft.spage=112333&rft.epage=112333&rft.pages=112333-112333&rft.artnum=112333&rft.issn=0899-9007&rft.eissn=1873-1244&rft_id=info:doi/10.1016/j.nut.2023.112333&rft_dat=%3Cproquest_cross%3E2929076466%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2928580619&rft_id=info:pmid/38271759&rft_els_id=S0899900723003611&rfr_iscdi=true |