Cholecystokinin-8S levels in discrete hypothalamic nuclei of weanling rats exposed to maternal protein malnutrition
Perinatal malnutrition and growth retardation at birth are suggested to be important risk factors for the development of overweight and syndrome X in later life. Underlying mechanisms are unknown. Body weight and food intake are regulated, e.g. by hypothalamic neuropeptidergic systems which are thou...
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| Veröffentlicht in: | Regulatory peptides 1999-12, Vol.85 (2), p.109-113 |
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| creator | Plagemann, Andreas Rittel, Fanny Waas, Thomas Harder, Thomas Rohde, Wolfgang |
| description | Perinatal malnutrition and growth retardation at birth are suggested to be important risk factors for the development of overweight and syndrome X in later life. Underlying mechanisms are unknown. Body weight and food intake are regulated, e.g. by hypothalamic neuropeptidergic systems which are thought to be highly vulnerable to persisting malorganization due to perinatal malnutrition. To investigate possible consequences for hypothalamic cholecystokinin-8S (CCK-8S) in the offspring, pregnant Wistar rats were fed an 8% protein diet during pregnancy and lactation (low-protein group; LP) while control mothers (CO) received a 17% protein isocaloric standard diet. LP offspring displayed underweight at birth (
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| doi_str_mv | 10.1016/S0167-0115(99)00085-3 |
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P<0.05) and during suckling (
P<0.001), while leptin levels were not altered. At weaning, under basal conditions CCK-8S was decreased in LP offspring in the paraventricular hypothalamic nucleus and arcuate hypothalamic nucleus (
P<0.05), as well as in the dorsomedial hypothalamic nucleus, lateral hypothalamic area and ventromedial hypothalamic nucleus (
P<0.01). In summary, these data indicate (1) an inhibition of the satiety peptide CCK-8S in main regulators of body weight and food intake in low-protein malnourished newborn rats; (2) no direct relationship of hypothalamic CCK-8S to circulating leptin at this age; and (3) no neurochemical signs of hypothalamic CCKergic dysregulation in this animal model at the age of weaning.</description><identifier>ISSN: 0167-0115</identifier><identifier>EISSN: 1873-1686</identifier><identifier>DOI: 10.1016/S0167-0115(99)00085-3</identifier><identifier>PMID: 10651064</identifier><identifier>CODEN: REPPDY</identifier><language>eng</language><publisher>Shannon: Elsevier B.V</publisher><subject>Animals ; Animals, Newborn ; Biological and medical sciences ; Birth Weight ; Body Weight ; Cholecystokinin-8S ; Dietary Proteins - administration & dosage ; Disease Models, Animal ; Eating ; Female ; Hypothalamus ; Hypothalamus - metabolism ; Insulin Resistance ; Leptin ; Male ; Maternal malnutrition ; Maternal-Fetal Exchange ; Medical sciences ; Metabolic diseases ; Nutrition Disorders - complications ; Nutrition Disorders - metabolism ; Obesity - etiology ; Offspring ; Other nutritional diseases (malnutrition, nutritional and vitamin deficiencies...) ; Pregnancy ; Pregnancy Complications - metabolism ; Rat ; Rats ; Rats, Wistar ; Sincalide - analogs & derivatives ; Sincalide - metabolism</subject><ispartof>Regulatory peptides, 1999-12, Vol.85 (2), p.109-113</ispartof><rights>1999 Elsevier Science B.V.</rights><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-3ddd0c748a2aea32ef9e33987ad84be72ec70e4ad6ce7bb0d1d340e493c5f0e53</citedby><cites>FETCH-LOGICAL-c390t-3ddd0c748a2aea32ef9e33987ad84be72ec70e4ad6ce7bb0d1d340e493c5f0e53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0167-0115(99)00085-3$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1234575$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10651064$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Plagemann, Andreas</creatorcontrib><creatorcontrib>Rittel, Fanny</creatorcontrib><creatorcontrib>Waas, Thomas</creatorcontrib><creatorcontrib>Harder, Thomas</creatorcontrib><creatorcontrib>Rohde, Wolfgang</creatorcontrib><title>Cholecystokinin-8S levels in discrete hypothalamic nuclei of weanling rats exposed to maternal protein malnutrition</title><title>Regulatory peptides</title><addtitle>Regul Pept</addtitle><description>Perinatal malnutrition and growth retardation at birth are suggested to be important risk factors for the development of overweight and syndrome X in later life. Underlying mechanisms are unknown. Body weight and food intake are regulated, e.g. by hypothalamic neuropeptidergic systems which are thought to be highly vulnerable to persisting malorganization due to perinatal malnutrition. To investigate possible consequences for hypothalamic cholecystokinin-8S (CCK-8S) in the offspring, pregnant Wistar rats were fed an 8% protein diet during pregnancy and lactation (low-protein group; LP) while control mothers (CO) received a 17% protein isocaloric standard diet. LP offspring displayed underweight at birth (
P<0.05) and during suckling (
P<0.001), while leptin levels were not altered. At weaning, under basal conditions CCK-8S was decreased in LP offspring in the paraventricular hypothalamic nucleus and arcuate hypothalamic nucleus (
P<0.05), as well as in the dorsomedial hypothalamic nucleus, lateral hypothalamic area and ventromedial hypothalamic nucleus (
P<0.01). In summary, these data indicate (1) an inhibition of the satiety peptide CCK-8S in main regulators of body weight and food intake in low-protein malnourished newborn rats; (2) no direct relationship of hypothalamic CCK-8S to circulating leptin at this age; and (3) no neurochemical signs of hypothalamic CCKergic dysregulation in this animal model at the age of weaning.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Biological and medical sciences</subject><subject>Birth Weight</subject><subject>Body Weight</subject><subject>Cholecystokinin-8S</subject><subject>Dietary Proteins - administration & dosage</subject><subject>Disease Models, Animal</subject><subject>Eating</subject><subject>Female</subject><subject>Hypothalamus</subject><subject>Hypothalamus - metabolism</subject><subject>Insulin Resistance</subject><subject>Leptin</subject><subject>Male</subject><subject>Maternal malnutrition</subject><subject>Maternal-Fetal Exchange</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Nutrition Disorders - complications</subject><subject>Nutrition Disorders - metabolism</subject><subject>Obesity - etiology</subject><subject>Offspring</subject><subject>Other nutritional diseases (malnutrition, nutritional and vitamin deficiencies...)</subject><subject>Pregnancy</subject><subject>Pregnancy Complications - metabolism</subject><subject>Rat</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Sincalide - analogs & derivatives</subject><subject>Sincalide - metabolism</subject><issn>0167-0115</issn><issn>1873-1686</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1vEzEQhq0K1IbSn1DkA0JwWGrHu-v1qaoivqRKHFrO1sSeJQavHWxvIf8ep4mAGwePJeuZ8TsPIZecveWM91d3tciGcd69VuoNY2zoGnFCFnyQouH90D8hiz_IGXmW8zfGeCelOCVnnPVdPe2C5NUmejS7XOJ3F1xohjvq8QF9pi5Q67JJWJBudttYNuBhcoaG2Xh0NI70J0LwLnylCUqm-GsbM1paIp2gYArg6TbFgnXSBD7MJbniYnhOno7gM14c73Py5f27-9XH5vbzh0-rm9vGCMVKI6y1zMh2gCUgiCWOCoVQgwQ7tGuUSzSSYQu2NyjXa2a5FW19UMJ0I8NOnJNXh7k1xI8Zc9FT3Qe9h4BxzrpXbbXV8wp2B9CkmHPCUW-TmyDtNGd6b1s_2tZ7lVop_Whbi9r34vjBvJ7Q_tN10FuBl0cAsgE_JgjG5b_cUrSd3Ae9PmBVOz44TDobh8GgdQlN0Ta6_yT5Dbgjnw4</recordid><startdate>19991223</startdate><enddate>19991223</enddate><creator>Plagemann, Andreas</creator><creator>Rittel, Fanny</creator><creator>Waas, Thomas</creator><creator>Harder, Thomas</creator><creator>Rohde, Wolfgang</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>7X8</scope></search><sort><creationdate>19991223</creationdate><title>Cholecystokinin-8S levels in discrete hypothalamic nuclei of weanling rats exposed to maternal protein malnutrition</title><author>Plagemann, Andreas ; Rittel, Fanny ; Waas, Thomas ; Harder, Thomas ; Rohde, Wolfgang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-3ddd0c748a2aea32ef9e33987ad84be72ec70e4ad6ce7bb0d1d340e493c5f0e53</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>Birth Weight</topic><topic>Body Weight</topic><topic>Cholecystokinin-8S</topic><topic>Dietary Proteins - administration & dosage</topic><topic>Disease Models, Animal</topic><topic>Eating</topic><topic>Female</topic><topic>Hypothalamus</topic><topic>Hypothalamus - metabolism</topic><topic>Insulin Resistance</topic><topic>Leptin</topic><topic>Male</topic><topic>Maternal malnutrition</topic><topic>Maternal-Fetal Exchange</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Nutrition Disorders - complications</topic><topic>Nutrition Disorders - metabolism</topic><topic>Obesity - etiology</topic><topic>Offspring</topic><topic>Other nutritional diseases (malnutrition, nutritional and vitamin deficiencies...)</topic><topic>Pregnancy</topic><topic>Pregnancy Complications - metabolism</topic><topic>Rat</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Sincalide - analogs & derivatives</topic><topic>Sincalide - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Plagemann, Andreas</creatorcontrib><creatorcontrib>Rittel, Fanny</creatorcontrib><creatorcontrib>Waas, Thomas</creatorcontrib><creatorcontrib>Harder, Thomas</creatorcontrib><creatorcontrib>Rohde, Wolfgang</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>MEDLINE - Academic</collection><jtitle>Regulatory peptides</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Plagemann, Andreas</au><au>Rittel, Fanny</au><au>Waas, Thomas</au><au>Harder, Thomas</au><au>Rohde, Wolfgang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cholecystokinin-8S levels in discrete hypothalamic nuclei of weanling rats exposed to maternal protein malnutrition</atitle><jtitle>Regulatory peptides</jtitle><addtitle>Regul Pept</addtitle><date>1999-12-23</date><risdate>1999</risdate><volume>85</volume><issue>2</issue><spage>109</spage><epage>113</epage><pages>109-113</pages><issn>0167-0115</issn><eissn>1873-1686</eissn><coden>REPPDY</coden><abstract>Perinatal malnutrition and growth retardation at birth are suggested to be important risk factors for the development of overweight and syndrome X in later life. Underlying mechanisms are unknown. Body weight and food intake are regulated, e.g. by hypothalamic neuropeptidergic systems which are thought to be highly vulnerable to persisting malorganization due to perinatal malnutrition. To investigate possible consequences for hypothalamic cholecystokinin-8S (CCK-8S) in the offspring, pregnant Wistar rats were fed an 8% protein diet during pregnancy and lactation (low-protein group; LP) while control mothers (CO) received a 17% protein isocaloric standard diet. LP offspring displayed underweight at birth (
P<0.05) and during suckling (
P<0.001), while leptin levels were not altered. At weaning, under basal conditions CCK-8S was decreased in LP offspring in the paraventricular hypothalamic nucleus and arcuate hypothalamic nucleus (
P<0.05), as well as in the dorsomedial hypothalamic nucleus, lateral hypothalamic area and ventromedial hypothalamic nucleus (
P<0.01). In summary, these data indicate (1) an inhibition of the satiety peptide CCK-8S in main regulators of body weight and food intake in low-protein malnourished newborn rats; (2) no direct relationship of hypothalamic CCK-8S to circulating leptin at this age; and (3) no neurochemical signs of hypothalamic CCKergic dysregulation in this animal model at the age of weaning.</abstract><cop>Shannon</cop><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>10651064</pmid><doi>10.1016/S0167-0115(99)00085-3</doi><tpages>5</tpages></addata></record> |
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| subjects | Animals Animals, Newborn Biological and medical sciences Birth Weight Body Weight Cholecystokinin-8S Dietary Proteins - administration & dosage Disease Models, Animal Eating Female Hypothalamus Hypothalamus - metabolism Insulin Resistance Leptin Male Maternal malnutrition Maternal-Fetal Exchange Medical sciences Metabolic diseases Nutrition Disorders - complications Nutrition Disorders - metabolism Obesity - etiology Offspring Other nutritional diseases (malnutrition, nutritional and vitamin deficiencies...) Pregnancy Pregnancy Complications - metabolism Rat Rats Rats, Wistar Sincalide - analogs & derivatives Sincalide - metabolism |
| title | Cholecystokinin-8S levels in discrete hypothalamic nuclei of weanling rats exposed to maternal protein malnutrition |
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