Subcutaneous adipose tissue layers as a stable correlate of leptin in response to short term energy restriction in obese girls
We studied the relationship of subcutaneous adipose tissue layers (SAT-layers) measured at 15 specified body sites with leptin before and after a weight loss program for three weeks. In 70 obese girls, SAT-layers were measured by means of the optical device, lipometer. Fat mass (FM) was estimated by...
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container_title | International Journal of Obesity |
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creator | Sudi, K M Gallistl, S Tröbinger, M Weinhandl, G Aigner, R Payerl, D Tafeit, E Möller, R Borkenstein, M H |
description | We studied the relationship of subcutaneous adipose tissue layers (SAT-layers) measured at 15 specified body sites with leptin before and after a weight loss program for three weeks.
In 70 obese girls, SAT-layers were measured by means of the optical device, lipometer. Fat mass (FM) was estimated by means of bioelectrical impedance.
At the beginning of the study, all estimates of adiposity, insulin, and SAT-layers from the upper body (from 1-neck to 6-lateral chest) were correlated to leptin at a P-value of |
doi_str_mv | 10.1038/sj.ijo.0801697 |
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In 70 obese girls, SAT-layers were measured by means of the optical device, lipometer. Fat mass (FM) was estimated by means of bioelectrical impedance.
At the beginning of the study, all estimates of adiposity, insulin, and SAT-layers from the upper body (from 1-neck to 6-lateral chest) were correlated to leptin at a P-value of<0.0001. Percentage FM together with SAT-layer 4-upper back and insulin explained 75% of the variation in leptin (P<0.0001). After three weeks, estimates of adiposity and leptin were reduced (all P<0.0001). Most SAT-layers were reduced, but SAT-layers 8-lower abdomen and 9-lower back were significantly increased. Changes in leptin were best explained by initial leptin, but percentage change (Delta) in insulin, Delta SAT-layer 1-neck, and Delta SAT-layer 3-biceps contributed to the Delta leptin (adj. r(2)=0.47, P<0.0001). In the weight-reduced state, circulating leptin was best explained by three SAT-layers and insulin (adj. r(2)=0.67, P<0.0001).
The results suggest that Delta changes in leptin are attributable to changes in the endocrine state and subcutaneous fat, and SAT-layers may serve as a stable correlate of leptin in the weight-reduced state.</description><identifier>ISSN: 0307-0565</identifier><identifier>EISSN: 1476-5497</identifier><identifier>DOI: 10.1038/sj.ijo.0801697</identifier><identifier>PMID: 11466587</identifier><language>eng</language><publisher>England: Nature Publishing Group</publisher><subject>Abdomen ; Adipose tissue ; Adipose Tissue - metabolism ; Adipose Tissue - physiology ; Body fat ; Body Mass Index ; Body Weight - physiology ; Child ; Diet, Reducing ; Electric Impedance ; Female ; Humans ; Insulin ; Insulin - blood ; Leptin - blood ; Obesity ; Obesity - metabolism ; Pediatrics ; Weight control</subject><ispartof>International Journal of Obesity, 2001-05, Vol.25 Suppl 1 (S1), p.S43-S45</ispartof><rights>Copyright Nature Publishing Group May 2001</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c359t-3f3721c89711aac51e78f61942971c43489878af9d0fac5e95a35445976d1133</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11466587$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sudi, K M</creatorcontrib><creatorcontrib>Gallistl, S</creatorcontrib><creatorcontrib>Tröbinger, M</creatorcontrib><creatorcontrib>Weinhandl, G</creatorcontrib><creatorcontrib>Aigner, R</creatorcontrib><creatorcontrib>Payerl, D</creatorcontrib><creatorcontrib>Tafeit, E</creatorcontrib><creatorcontrib>Möller, R</creatorcontrib><creatorcontrib>Borkenstein, M H</creatorcontrib><title>Subcutaneous adipose tissue layers as a stable correlate of leptin in response to short term energy restriction in obese girls</title><title>International Journal of Obesity</title><addtitle>Int J Obes Relat Metab Disord</addtitle><description>We studied the relationship of subcutaneous adipose tissue layers (SAT-layers) measured at 15 specified body sites with leptin before and after a weight loss program for three weeks.
In 70 obese girls, SAT-layers were measured by means of the optical device, lipometer. Fat mass (FM) was estimated by means of bioelectrical impedance.
At the beginning of the study, all estimates of adiposity, insulin, and SAT-layers from the upper body (from 1-neck to 6-lateral chest) were correlated to leptin at a P-value of<0.0001. Percentage FM together with SAT-layer 4-upper back and insulin explained 75% of the variation in leptin (P<0.0001). After three weeks, estimates of adiposity and leptin were reduced (all P<0.0001). Most SAT-layers were reduced, but SAT-layers 8-lower abdomen and 9-lower back were significantly increased. Changes in leptin were best explained by initial leptin, but percentage change (Delta) in insulin, Delta SAT-layer 1-neck, and Delta SAT-layer 3-biceps contributed to the Delta leptin (adj. r(2)=0.47, P<0.0001). In the weight-reduced state, circulating leptin was best explained by three SAT-layers and insulin (adj. r(2)=0.67, P<0.0001).
The results suggest that Delta changes in leptin are attributable to changes in the endocrine state and subcutaneous fat, and SAT-layers may serve as a stable correlate of leptin in the weight-reduced state.</description><subject>Abdomen</subject><subject>Adipose tissue</subject><subject>Adipose Tissue - metabolism</subject><subject>Adipose Tissue - physiology</subject><subject>Body fat</subject><subject>Body Mass Index</subject><subject>Body Weight - physiology</subject><subject>Child</subject><subject>Diet, Reducing</subject><subject>Electric Impedance</subject><subject>Female</subject><subject>Humans</subject><subject>Insulin</subject><subject>Insulin - blood</subject><subject>Leptin - blood</subject><subject>Obesity</subject><subject>Obesity - metabolism</subject><subject>Pediatrics</subject><subject>Weight control</subject><issn>0307-0565</issn><issn>1476-5497</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkc1LAzEQxYMotlavHiV48bQ12SSbzVHELyh4sPeQprM1y3azJtlDL_7tprYgCAMDM783vOEhdE3JnBJW38d27lo_JzWhlZInaEq5rArBlTxFU8KILIioxARdxNgSQoQg5TmaUMqrStRyir4_xpUdk-nBjxGbtRt8BJxcjCPgzuwg5GkuHJNZdYCtDwE6kwD7BncwJNfjXAHi4Pu90uP46UPCCcIWQw9hs9tvU3A2Of8L-xVkcuNCFy_RWWO6CFfHPkPL56fl42uxeH95e3xYFJYJlQrWMFlSWytJqTFWUJB1U1HFyzyxnPFa1bI2jVqTJq9BCcME50LJak0pYzN0dzg7BP81Zjd666KFrjv8raVQLGNCZvL2H9n6MfTZmy6pKiulBM_Q_ADZ4GMM0OghuK0JO02J3seiY6tzLPoYSxbcHK-Oqy2s__BjDuwH0-aKcw</recordid><startdate>20010501</startdate><enddate>20010501</enddate><creator>Sudi, K M</creator><creator>Gallistl, S</creator><creator>Tröbinger, M</creator><creator>Weinhandl, G</creator><creator>Aigner, R</creator><creator>Payerl, D</creator><creator>Tafeit, E</creator><creator>Möller, R</creator><creator>Borkenstein, M H</creator><general>Nature Publishing Group</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>7T2</scope><scope>7TK</scope><scope>7TS</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7U2</scope></search><sort><creationdate>20010501</creationdate><title>Subcutaneous adipose tissue layers as a stable correlate of leptin in response to short term energy restriction in obese girls</title><author>Sudi, K M ; Gallistl, S ; Tröbinger, M ; Weinhandl, G ; Aigner, R ; Payerl, D ; Tafeit, E ; Möller, R ; Borkenstein, M H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c359t-3f3721c89711aac51e78f61942971c43489878af9d0fac5e95a35445976d1133</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Abdomen</topic><topic>Adipose tissue</topic><topic>Adipose Tissue - metabolism</topic><topic>Adipose Tissue - physiology</topic><topic>Body fat</topic><topic>Body Mass Index</topic><topic>Body Weight - physiology</topic><topic>Child</topic><topic>Diet, Reducing</topic><topic>Electric Impedance</topic><topic>Female</topic><topic>Humans</topic><topic>Insulin</topic><topic>Insulin - blood</topic><topic>Leptin - blood</topic><topic>Obesity</topic><topic>Obesity - metabolism</topic><topic>Pediatrics</topic><topic>Weight control</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sudi, K M</creatorcontrib><creatorcontrib>Gallistl, S</creatorcontrib><creatorcontrib>Tröbinger, M</creatorcontrib><creatorcontrib>Weinhandl, G</creatorcontrib><creatorcontrib>Aigner, R</creatorcontrib><creatorcontrib>Payerl, D</creatorcontrib><creatorcontrib>Tafeit, E</creatorcontrib><creatorcontrib>Möller, R</creatorcontrib><creatorcontrib>Borkenstein, M H</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>Health and Safety Science Abstracts (Full archive)</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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 Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>Biological Science Database</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 One Psychology</collection><collection>ProQuest Central Basic</collection><collection>Safety Science and Risk</collection><jtitle>International Journal of Obesity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sudi, K M</au><au>Gallistl, S</au><au>Tröbinger, M</au><au>Weinhandl, G</au><au>Aigner, R</au><au>Payerl, D</au><au>Tafeit, E</au><au>Möller, R</au><au>Borkenstein, M H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Subcutaneous adipose tissue layers as a stable correlate of leptin in response to short term energy restriction in obese girls</atitle><jtitle>International Journal of Obesity</jtitle><addtitle>Int J Obes Relat Metab Disord</addtitle><date>2001-05-01</date><risdate>2001</risdate><volume>25 Suppl 1</volume><issue>S1</issue><spage>S43</spage><epage>S45</epage><pages>S43-S45</pages><issn>0307-0565</issn><eissn>1476-5497</eissn><abstract>We studied the relationship of subcutaneous adipose tissue layers (SAT-layers) measured at 15 specified body sites with leptin before and after a weight loss program for three weeks.
In 70 obese girls, SAT-layers were measured by means of the optical device, lipometer. Fat mass (FM) was estimated by means of bioelectrical impedance.
At the beginning of the study, all estimates of adiposity, insulin, and SAT-layers from the upper body (from 1-neck to 6-lateral chest) were correlated to leptin at a P-value of<0.0001. Percentage FM together with SAT-layer 4-upper back and insulin explained 75% of the variation in leptin (P<0.0001). After three weeks, estimates of adiposity and leptin were reduced (all P<0.0001). Most SAT-layers were reduced, but SAT-layers 8-lower abdomen and 9-lower back were significantly increased. Changes in leptin were best explained by initial leptin, but percentage change (Delta) in insulin, Delta SAT-layer 1-neck, and Delta SAT-layer 3-biceps contributed to the Delta leptin (adj. r(2)=0.47, P<0.0001). In the weight-reduced state, circulating leptin was best explained by three SAT-layers and insulin (adj. r(2)=0.67, P<0.0001).
The results suggest that Delta changes in leptin are attributable to changes in the endocrine state and subcutaneous fat, and SAT-layers may serve as a stable correlate of leptin in the weight-reduced state.</abstract><cop>England</cop><pub>Nature Publishing Group</pub><pmid>11466587</pmid><doi>10.1038/sj.ijo.0801697</doi><oa>free_for_read</oa></addata></record> |
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subjects | Abdomen Adipose tissue Adipose Tissue - metabolism Adipose Tissue - physiology Body fat Body Mass Index Body Weight - physiology Child Diet, Reducing Electric Impedance Female Humans Insulin Insulin - blood Leptin - blood Obesity Obesity - metabolism Pediatrics Weight control |
title | Subcutaneous adipose tissue layers as a stable correlate of leptin in response to short term energy restriction in obese girls |
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