Perinatal elevation of hypothalamic insulin, acquired malformation of hypothalamic galaninergic neurons, and syndrome X-like alterations in adulthood of neonatally overfed rats
Overnutrition during critical developmental periods is suggested to be a risk factor for obesity and associated metabolic disorders in later life. Underlying mechanisms are unknown. Neuropeptides are essentially involved in the central nervous regulation of body weight. For instance, hypothalamic ga...
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Veröffentlicht in: | Brain research 1999-07, Vol.836 (1), p.146-155 |
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description | Overnutrition during critical developmental periods is suggested to be a risk factor for obesity and associated metabolic disorders in later life. Underlying mechanisms are unknown. Neuropeptides are essentially involved in the central nervous regulation of body weight. For instance, hypothalamic galanin (GAL) is a stimulator of food intake and body weight gain. To investigate long-term consequences of early postnatal overfeeding, the normal litter size of Wistar rats (
n=10; controls) was reduced from day 3 to day 21 of life to only 3 pups per mother (small litters, SL; overnutrition). Throughout life, SL rats displayed hyperphagia (
p |
doi_str_mv | 10.1016/S0006-8993(99)01662-5 |
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n=10; controls) was reduced from day 3 to day 21 of life to only 3 pups per mother (small litters, SL; overnutrition). Throughout life, SL rats displayed hyperphagia (
p<0.01), overweight (
p<0.0001), hyperinsulinemia (
p<0.01), impaired glucose tolerance (
p<0.001), elevated triglycerides (
p<0.001), and an increased systolic blood pressure (
p<0.05). In adulthood, an increase of GAL-neurons in the arcuate hypothalamic nucleus (ARC) was found (
p<0.001), positively correlated to body weight (
p<0.001). A second experiment revealed hyperinsulinemia (
p<0.001) and increased hypothalamic insulin levels (
p<0.05) in SL rats during early postnatal life. Already on day 21 of life, i.e., at the end of the critical hypothalamic differentiation period, in SL rats the number of GAL-neurons was increased in the ARC (
p<0.001), showing a positive correlation to body weight and insulin (
p<0.05). In conclusion, neonatally acquired persisting malformation of hypothalamic galaninergic neurons, induced by early overfeeding and hyperinsulinism, might promote the development of overweight and syndrome X-like alterations during life.]]></description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/S0006-8993(99)01662-5</identifier><identifier>PMID: 10415413</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>London: Elsevier B.V</publisher><subject>Animals ; Animals, Newborn ; Biological and medical sciences ; Body Weight - physiology ; Cell Differentiation - physiology ; Early overnutrition ; Feeding Behavior - physiology ; Female ; Galanin ; Galanin - analysis ; Hypothalamus ; Hypothalamus - cytology ; Hypothalamus - growth & development ; Hypothalamus - metabolism ; Insulin ; Insulin - metabolism ; Medical sciences ; Metabolic diseases ; Microvascular Angina - metabolism ; Microvascular Angina - pathology ; Neurons - chemistry ; Neurons - ultrastructure ; Obesity ; Obesity - metabolism ; Obesity - pathology ; Obesity - physiopathology ; Rats ; Rats, Wistar ; Syndrome X ; Weaning</subject><ispartof>Brain research, 1999-07, Vol.836 (1), p.146-155</ispartof><rights>1999 Elsevier Science B.V.</rights><rights>1999 INIST-CNRS</rights><rights>Copyright 1999 Elsevier Science B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c539t-c7d7c5d81d11ad0e8ebb1c31c2d8ef2192ac43a33946f44a19f3701f32503e663</citedby><cites>FETCH-LOGICAL-c539t-c7d7c5d81d11ad0e8ebb1c31c2d8ef2192ac43a33946f44a19f3701f32503e663</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0006-8993(99)01662-5$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1913558$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10415413$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Plagemann, Andreas</creatorcontrib><creatorcontrib>Harder, Thomas</creatorcontrib><creatorcontrib>Rake, Annett</creatorcontrib><creatorcontrib>Voits, Mechthild</creatorcontrib><creatorcontrib>Fink, Heidrun</creatorcontrib><creatorcontrib>Rohde, Wolfgang</creatorcontrib><creatorcontrib>Dörner, Günter</creatorcontrib><title>Perinatal elevation of hypothalamic insulin, acquired malformation of hypothalamic galaninergic neurons, and syndrome X-like alterations in adulthood of neonatally overfed rats</title><title>Brain research</title><addtitle>Brain Res</addtitle><description><![CDATA[Overnutrition during critical developmental periods is suggested to be a risk factor for obesity and associated metabolic disorders in later life. Underlying mechanisms are unknown. Neuropeptides are essentially involved in the central nervous regulation of body weight. For instance, hypothalamic galanin (GAL) is a stimulator of food intake and body weight gain. To investigate long-term consequences of early postnatal overfeeding, the normal litter size of Wistar rats (
n=10; controls) was reduced from day 3 to day 21 of life to only 3 pups per mother (small litters, SL; overnutrition). Throughout life, SL rats displayed hyperphagia (
p<0.01), overweight (
p<0.0001), hyperinsulinemia (
p<0.01), impaired glucose tolerance (
p<0.001), elevated triglycerides (
p<0.001), and an increased systolic blood pressure (
p<0.05). In adulthood, an increase of GAL-neurons in the arcuate hypothalamic nucleus (ARC) was found (
p<0.001), positively correlated to body weight (
p<0.001). A second experiment revealed hyperinsulinemia (
p<0.001) and increased hypothalamic insulin levels (
p<0.05) in SL rats during early postnatal life. Already on day 21 of life, i.e., at the end of the critical hypothalamic differentiation period, in SL rats the number of GAL-neurons was increased in the ARC (
p<0.001), showing a positive correlation to body weight and insulin (
p<0.05). In conclusion, neonatally acquired persisting malformation of hypothalamic galaninergic neurons, induced by early overfeeding and hyperinsulinism, might promote the development of overweight and syndrome X-like alterations during life.]]></description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Biological and medical sciences</subject><subject>Body Weight - physiology</subject><subject>Cell Differentiation - physiology</subject><subject>Early overnutrition</subject><subject>Feeding Behavior - physiology</subject><subject>Female</subject><subject>Galanin</subject><subject>Galanin - analysis</subject><subject>Hypothalamus</subject><subject>Hypothalamus - cytology</subject><subject>Hypothalamus - growth & development</subject><subject>Hypothalamus - metabolism</subject><subject>Insulin</subject><subject>Insulin - metabolism</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Microvascular Angina - metabolism</subject><subject>Microvascular Angina - pathology</subject><subject>Neurons - chemistry</subject><subject>Neurons - ultrastructure</subject><subject>Obesity</subject><subject>Obesity - metabolism</subject><subject>Obesity - pathology</subject><subject>Obesity - physiopathology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Syndrome X</subject><subject>Weaning</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkVtrFDEUgIModq3-BCUPIgqO5kzmlqciRW2hoKCCbyGbnHSjmWSbzCzsv-pPNHuh-iD06XDCdy45HyHPgb0DBt37b4yxrhqE4K-FeFNeurpqH5AFDH1ddXXDHpLFHXJCnuT8q6ScC_aYnABroG2AL8jtV0wuqEl5ih43anIx0GjparuO00p5NTpNXcizd-EtVfpmdgkNHZW3MY3_x69LDC5gui5JwDnFkEttMDRvg0lxRPqz8u43UuUnTPsmuQyhysx-WsVodi0Dxv1efkvjBpMtUwuan5JHVvmMz47xlPz49PH7-UV19eXz5fmHq0q3XEyV7k2vWzOAAVCG4YDLJWgOujYD2hpErXTDVblH09mmUSAs7xlYXreMY9fxU_Lq0Hed4s2MeZKjyxp9-RrGOctOCBi6ctD7QOg5AK93YHsAdYo5J7Ryndyo0lYCkzuncu9U7oRJIeTeqWxL3YvjgHk5ovmn6iCxAC-PgMq6iEkqaJf_cgJ42w4FOztgWM62cZhk1g6DRlOU6kma6O7Z5A8xRsKL</recordid><startdate>19990731</startdate><enddate>19990731</enddate><creator>Plagemann, Andreas</creator><creator>Harder, Thomas</creator><creator>Rake, Annett</creator><creator>Voits, Mechthild</creator><creator>Fink, Heidrun</creator><creator>Rohde, Wolfgang</creator><creator>Dörner, Günter</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><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>7TK</scope><scope>7X8</scope></search><sort><creationdate>19990731</creationdate><title>Perinatal elevation of hypothalamic insulin, acquired malformation of hypothalamic galaninergic neurons, and syndrome X-like alterations in adulthood of neonatally overfed rats</title><author>Plagemann, Andreas ; Harder, Thomas ; Rake, Annett ; Voits, Mechthild ; Fink, Heidrun ; Rohde, Wolfgang ; Dörner, Günter</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c539t-c7d7c5d81d11ad0e8ebb1c31c2d8ef2192ac43a33946f44a19f3701f32503e663</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Biological and medical sciences</topic><topic>Body Weight - physiology</topic><topic>Cell Differentiation - physiology</topic><topic>Early overnutrition</topic><topic>Feeding Behavior - physiology</topic><topic>Female</topic><topic>Galanin</topic><topic>Galanin - analysis</topic><topic>Hypothalamus</topic><topic>Hypothalamus - cytology</topic><topic>Hypothalamus - growth & development</topic><topic>Hypothalamus - metabolism</topic><topic>Insulin</topic><topic>Insulin - metabolism</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Microvascular Angina - metabolism</topic><topic>Microvascular Angina - pathology</topic><topic>Neurons - chemistry</topic><topic>Neurons - ultrastructure</topic><topic>Obesity</topic><topic>Obesity - metabolism</topic><topic>Obesity - pathology</topic><topic>Obesity - physiopathology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Syndrome X</topic><topic>Weaning</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Plagemann, Andreas</creatorcontrib><creatorcontrib>Harder, Thomas</creatorcontrib><creatorcontrib>Rake, Annett</creatorcontrib><creatorcontrib>Voits, Mechthild</creatorcontrib><creatorcontrib>Fink, Heidrun</creatorcontrib><creatorcontrib>Rohde, Wolfgang</creatorcontrib><creatorcontrib>Dörner, Günter</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Plagemann, Andreas</au><au>Harder, Thomas</au><au>Rake, Annett</au><au>Voits, Mechthild</au><au>Fink, Heidrun</au><au>Rohde, Wolfgang</au><au>Dörner, Günter</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Perinatal elevation of hypothalamic insulin, acquired malformation of hypothalamic galaninergic neurons, and syndrome X-like alterations in adulthood of neonatally overfed rats</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>1999-07-31</date><risdate>1999</risdate><volume>836</volume><issue>1</issue><spage>146</spage><epage>155</epage><pages>146-155</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract><![CDATA[Overnutrition during critical developmental periods is suggested to be a risk factor for obesity and associated metabolic disorders in later life. Underlying mechanisms are unknown. Neuropeptides are essentially involved in the central nervous regulation of body weight. For instance, hypothalamic galanin (GAL) is a stimulator of food intake and body weight gain. To investigate long-term consequences of early postnatal overfeeding, the normal litter size of Wistar rats (
n=10; controls) was reduced from day 3 to day 21 of life to only 3 pups per mother (small litters, SL; overnutrition). Throughout life, SL rats displayed hyperphagia (
p<0.01), overweight (
p<0.0001), hyperinsulinemia (
p<0.01), impaired glucose tolerance (
p<0.001), elevated triglycerides (
p<0.001), and an increased systolic blood pressure (
p<0.05). In adulthood, an increase of GAL-neurons in the arcuate hypothalamic nucleus (ARC) was found (
p<0.001), positively correlated to body weight (
p<0.001). A second experiment revealed hyperinsulinemia (
p<0.001) and increased hypothalamic insulin levels (
p<0.05) in SL rats during early postnatal life. Already on day 21 of life, i.e., at the end of the critical hypothalamic differentiation period, in SL rats the number of GAL-neurons was increased in the ARC (
p<0.001), showing a positive correlation to body weight and insulin (
p<0.05). In conclusion, neonatally acquired persisting malformation of hypothalamic galaninergic neurons, induced by early overfeeding and hyperinsulinism, might promote the development of overweight and syndrome X-like alterations during life.]]></abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier B.V</pub><pmid>10415413</pmid><doi>10.1016/S0006-8993(99)01662-5</doi><tpages>10</tpages></addata></record> |
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subjects | Animals Animals, Newborn Biological and medical sciences Body Weight - physiology Cell Differentiation - physiology Early overnutrition Feeding Behavior - physiology Female Galanin Galanin - analysis Hypothalamus Hypothalamus - cytology Hypothalamus - growth & development Hypothalamus - metabolism Insulin Insulin - metabolism Medical sciences Metabolic diseases Microvascular Angina - metabolism Microvascular Angina - pathology Neurons - chemistry Neurons - ultrastructure Obesity Obesity - metabolism Obesity - pathology Obesity - physiopathology Rats Rats, Wistar Syndrome X Weaning |
title | Perinatal elevation of hypothalamic insulin, acquired malformation of hypothalamic galaninergic neurons, and syndrome X-like alterations in adulthood of neonatally overfed rats |
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