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Physiological response of adipocytes to weight loss and maintenance
Metabolic processes in adipose tissue are dysregulated in obese subjects and, in response to weight loss, either normalize or change in favor of weight regain. To determine changes in adipocyte glucose and fatty acid metabolism in relation to changes in adipocyte size during weight loss and maintena...
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Published in: | PloS one 2013-03, Vol.8 (3), p.e58011 |
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description | Metabolic processes in adipose tissue are dysregulated in obese subjects and, in response to weight loss, either normalize or change in favor of weight regain.
To determine changes in adipocyte glucose and fatty acid metabolism in relation to changes in adipocyte size during weight loss and maintenance.
Twenty-eight healthy subjects (12 males), age 20-50 y, and BMI 28-35 kg/m(2), followed a very low energy diet for 2 months, followed by a 10-month period of weight maintenance. Body weight, body composition (deuterium dilution and BodPod), protein levels (Western blot) and adipocyte size were assessed prior to and after weight loss and after the 10-month follow-up.
A 10% weight loss resulted in a 16% decrease in adipocyte size. A marker for glycolysis decreased (AldoC) during weight loss in association with adipocyte shrinking, and remained decreased during follow-up in association with weight maintenance. A marker for fatty acid transport increased (FABP4) during weight loss and remained increased during follow-up. Markers for mitochondrial beta-oxidation (HADHsc) and lipolysis (ATGL) were only increased after the 10-month follow-up. During weight loss HADHsc and ATGL were coordinately regulated, which became weaker during follow-up due to adipocyte size-related changes in HADHsc expression. AldoC was the major denominator of adipocyte size and body weight, whereas changes in ATGL during weight loss contributed to body weight during follow-up. Upregulation of ATGL and HADHsc occured in the absence of a negative energy balance and was triggered by adipocyte shrinkage or indicated preadipocyte differentiation.
Markers for adipocyte glucose and fatty acid metabolism are changed in response to weight loss in line with normalization from a dysregulated obese status to an improved metabolic status.
ClinicalTrials.gov NCT01015508. |
doi_str_mv | 10.1371/journal.pone.0058011 |
format | article |
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To determine changes in adipocyte glucose and fatty acid metabolism in relation to changes in adipocyte size during weight loss and maintenance.
Twenty-eight healthy subjects (12 males), age 20-50 y, and BMI 28-35 kg/m(2), followed a very low energy diet for 2 months, followed by a 10-month period of weight maintenance. Body weight, body composition (deuterium dilution and BodPod), protein levels (Western blot) and adipocyte size were assessed prior to and after weight loss and after the 10-month follow-up.
A 10% weight loss resulted in a 16% decrease in adipocyte size. A marker for glycolysis decreased (AldoC) during weight loss in association with adipocyte shrinking, and remained decreased during follow-up in association with weight maintenance. A marker for fatty acid transport increased (FABP4) during weight loss and remained increased during follow-up. Markers for mitochondrial beta-oxidation (HADHsc) and lipolysis (ATGL) were only increased after the 10-month follow-up. During weight loss HADHsc and ATGL were coordinately regulated, which became weaker during follow-up due to adipocyte size-related changes in HADHsc expression. AldoC was the major denominator of adipocyte size and body weight, whereas changes in ATGL during weight loss contributed to body weight during follow-up. Upregulation of ATGL and HADHsc occured in the absence of a negative energy balance and was triggered by adipocyte shrinkage or indicated preadipocyte differentiation.
Markers for adipocyte glucose and fatty acid metabolism are changed in response to weight loss in line with normalization from a dysregulated obese status to an improved metabolic status.
ClinicalTrials.gov NCT01015508.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0058011</identifier><identifier>PMID: 23505452</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adipocytes ; Adipocytes - physiology ; Adipose tissue ; Adiposity ; Adult ; Autophagy ; Biology ; Body composition ; Body composition (biology) ; Body mass ; Body Mass Index ; Body size ; Body weight ; Body weight changes ; Body weight loss ; Deuterium ; Dilution ; Energy ; Energy balance ; Energy Metabolism ; Fatty acids ; Fatty Acids - metabolism ; Female ; Gene expression ; Glucose ; Glucose - metabolism ; Glycolysis ; Humans ; Lipase - metabolism ; Lipids ; Lipolysis ; Maintenance ; Male ; Males ; Markers ; Medicine ; Metabolism ; Middle Aged ; Mitochondria ; Nutrition research ; Obesity ; Oxidation ; Physiological aspects ; Physiology ; Proteins ; Proteins - metabolism ; Proteomics ; Shrinkage ; Studies ; Toxicology ; Weight control ; Weight loss ; Weight Loss - physiology ; Young Adult</subject><ispartof>PloS one, 2013-03, Vol.8 (3), p.e58011</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Verhoef et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Verhoef et al 2013 Verhoef et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-165ddbe36f3f9ec3f5b707e1bc25277b509c50894c7b9cd4db82750494bed8873</citedby><cites>FETCH-LOGICAL-c692t-165ddbe36f3f9ec3f5b707e1bc25277b509c50894c7b9cd4db82750494bed8873</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1330881584/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1330881584?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23505452$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Votruba, Susanne Breuer</contributor><creatorcontrib>Verhoef, Sanne P M</creatorcontrib><creatorcontrib>Camps, Stefan G J A</creatorcontrib><creatorcontrib>Bouwman, Freek G</creatorcontrib><creatorcontrib>Mariman, Edwin C M</creatorcontrib><creatorcontrib>Westerterp, Klaas R</creatorcontrib><title>Physiological response of adipocytes to weight loss and maintenance</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Metabolic processes in adipose tissue are dysregulated in obese subjects and, in response to weight loss, either normalize or change in favor of weight regain.
To determine changes in adipocyte glucose and fatty acid metabolism in relation to changes in adipocyte size during weight loss and maintenance.
Twenty-eight healthy subjects (12 males), age 20-50 y, and BMI 28-35 kg/m(2), followed a very low energy diet for 2 months, followed by a 10-month period of weight maintenance. Body weight, body composition (deuterium dilution and BodPod), protein levels (Western blot) and adipocyte size were assessed prior to and after weight loss and after the 10-month follow-up.
A 10% weight loss resulted in a 16% decrease in adipocyte size. A marker for glycolysis decreased (AldoC) during weight loss in association with adipocyte shrinking, and remained decreased during follow-up in association with weight maintenance. A marker for fatty acid transport increased (FABP4) during weight loss and remained increased during follow-up. Markers for mitochondrial beta-oxidation (HADHsc) and lipolysis (ATGL) were only increased after the 10-month follow-up. During weight loss HADHsc and ATGL were coordinately regulated, which became weaker during follow-up due to adipocyte size-related changes in HADHsc expression. AldoC was the major denominator of adipocyte size and body weight, whereas changes in ATGL during weight loss contributed to body weight during follow-up. Upregulation of ATGL and HADHsc occured in the absence of a negative energy balance and was triggered by adipocyte shrinkage or indicated preadipocyte differentiation.
Markers for adipocyte glucose and fatty acid metabolism are changed in response to weight loss in line with normalization from a dysregulated obese status to an improved metabolic status.
ClinicalTrials.gov NCT01015508.</description><subject>Adipocytes</subject><subject>Adipocytes - physiology</subject><subject>Adipose tissue</subject><subject>Adiposity</subject><subject>Adult</subject><subject>Autophagy</subject><subject>Biology</subject><subject>Body composition</subject><subject>Body composition (biology)</subject><subject>Body mass</subject><subject>Body Mass Index</subject><subject>Body size</subject><subject>Body weight</subject><subject>Body weight changes</subject><subject>Body weight loss</subject><subject>Deuterium</subject><subject>Dilution</subject><subject>Energy</subject><subject>Energy balance</subject><subject>Energy Metabolism</subject><subject>Fatty acids</subject><subject>Fatty Acids - metabolism</subject><subject>Female</subject><subject>Gene expression</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Glycolysis</subject><subject>Humans</subject><subject>Lipase - metabolism</subject><subject>Lipids</subject><subject>Lipolysis</subject><subject>Maintenance</subject><subject>Male</subject><subject>Males</subject><subject>Markers</subject><subject>Medicine</subject><subject>Metabolism</subject><subject>Middle Aged</subject><subject>Mitochondria</subject><subject>Nutrition research</subject><subject>Obesity</subject><subject>Oxidation</subject><subject>Physiological aspects</subject><subject>Physiology</subject><subject>Proteins</subject><subject>Proteins - metabolism</subject><subject>Proteomics</subject><subject>Shrinkage</subject><subject>Studies</subject><subject>Toxicology</subject><subject>Weight control</subject><subject>Weight loss</subject><subject>Weight Loss - physiology</subject><subject>Young Adult</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl2L1DAUhoso7rr6D0QLguDFjPlskhthGfwYWFjx6zak6UknQ6cZm1Sdf2_W6S5TUJBcJJw8583Jy1sUTzFaYirw620Yh950y33oYYkQlwjje8U5VpQsKoLo_ZPzWfEoxm2GqKyqh8UZoRxxxsl5sfq4OUQfutB6a7pygJj1IpTBlabx-2APCWKZQvkTfLtJZRdiLE3flDvj-wS96S08Lh4400V4Mu0Xxdd3b7-sPiyurt-vV5dXC1spkha44k1TA60cdQosdbwWSACuLeFEiJojZTmSillRK9uwppZEcMQUq6GRUtCL4vlRd5-n0NP_o8aUIikxlywT6yPRBLPV-8HvzHDQwXj9pxCGVpsheduBhso1RgguBUJMGKJc5ZgTguAabPYma72ZXhvrHTQW-jSYbiY6v-n9Rrfhh6ZcYcZUFngxCQzh-wgx_WPkiWpNnsr3LmQxu_PR6ksmJFUMSZKp5V-ovBrYeZsT4HyuzxpezRoyk-BXas0Yo15__vT_7PW3OfvyhN2A6dImhm5MPsdmDrIjaIccmQHcnXMY6ZsA37qhbwKspwDntmenrt813SaW_gboP-rT</recordid><startdate>20130307</startdate><enddate>20130307</enddate><creator>Verhoef, Sanne P M</creator><creator>Camps, Stefan G J A</creator><creator>Bouwman, Freek G</creator><creator>Mariman, Edwin C M</creator><creator>Westerterp, Klaas R</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20130307</creationdate><title>Physiological response of adipocytes to weight loss and maintenance</title><author>Verhoef, Sanne P M ; Camps, Stefan G J A ; Bouwman, Freek G ; Mariman, Edwin C M ; Westerterp, Klaas R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-165ddbe36f3f9ec3f5b707e1bc25277b509c50894c7b9cd4db82750494bed8873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adipocytes</topic><topic>Adipocytes - 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metabolism</topic><topic>Proteomics</topic><topic>Shrinkage</topic><topic>Studies</topic><topic>Toxicology</topic><topic>Weight control</topic><topic>Weight loss</topic><topic>Weight Loss - physiology</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Verhoef, Sanne P M</creatorcontrib><creatorcontrib>Camps, Stefan G J A</creatorcontrib><creatorcontrib>Bouwman, Freek G</creatorcontrib><creatorcontrib>Mariman, Edwin C M</creatorcontrib><creatorcontrib>Westerterp, Klaas R</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Opposing Viewpoints Resource Center</collection><collection>Science (Gale in Context)</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>Advanced Technologies & Aerospace Database (1962 - 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To determine changes in adipocyte glucose and fatty acid metabolism in relation to changes in adipocyte size during weight loss and maintenance.
Twenty-eight healthy subjects (12 males), age 20-50 y, and BMI 28-35 kg/m(2), followed a very low energy diet for 2 months, followed by a 10-month period of weight maintenance. Body weight, body composition (deuterium dilution and BodPod), protein levels (Western blot) and adipocyte size were assessed prior to and after weight loss and after the 10-month follow-up.
A 10% weight loss resulted in a 16% decrease in adipocyte size. A marker for glycolysis decreased (AldoC) during weight loss in association with adipocyte shrinking, and remained decreased during follow-up in association with weight maintenance. A marker for fatty acid transport increased (FABP4) during weight loss and remained increased during follow-up. Markers for mitochondrial beta-oxidation (HADHsc) and lipolysis (ATGL) were only increased after the 10-month follow-up. During weight loss HADHsc and ATGL were coordinately regulated, which became weaker during follow-up due to adipocyte size-related changes in HADHsc expression. AldoC was the major denominator of adipocyte size and body weight, whereas changes in ATGL during weight loss contributed to body weight during follow-up. Upregulation of ATGL and HADHsc occured in the absence of a negative energy balance and was triggered by adipocyte shrinkage or indicated preadipocyte differentiation.
Markers for adipocyte glucose and fatty acid metabolism are changed in response to weight loss in line with normalization from a dysregulated obese status to an improved metabolic status.
ClinicalTrials.gov NCT01015508.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23505452</pmid><doi>10.1371/journal.pone.0058011</doi><tpages>e58011</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adipocytes Adipocytes - physiology Adipose tissue Adiposity Adult Autophagy Biology Body composition Body composition (biology) Body mass Body Mass Index Body size Body weight Body weight changes Body weight loss Deuterium Dilution Energy Energy balance Energy Metabolism Fatty acids Fatty Acids - metabolism Female Gene expression Glucose Glucose - metabolism Glycolysis Humans Lipase - metabolism Lipids Lipolysis Maintenance Male Males Markers Medicine Metabolism Middle Aged Mitochondria Nutrition research Obesity Oxidation Physiological aspects Physiology Proteins Proteins - metabolism Proteomics Shrinkage Studies Toxicology Weight control Weight loss Weight Loss - physiology Young Adult |
title | Physiological response of adipocytes to weight loss and maintenance |
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